Ignet

Gene Information

Gene symbol: ADA

Gene name: adenosine deaminase

HGNC ID: 186

Related Genes

#	Gene Symbol	Number of hits
1	ABO	1 hits
2	ACE	1 hits
3	ACHE	1 hits
4	ACP1	1 hits
5	ACPP	1 hits
6	ADAR	1 hits
7	ADARB1	1 hits
8	ADCY10	1 hits
9	ADIPOQ	1 hits
10	ADK	1 hits
11	AK1	1 hits
12	AK2	1 hits
13	ALPI	1 hits
14	AMPD1	1 hits
15	APOC2	1 hits
16	AVP	1 hits
17	CAT	1 hits
18	COL1A1	1 hits
19	CPX	1 hits
20	CTSA	1 hits
21	CXCR4	1 hits
22	DHFR	1 hits
23	DPP4	1 hits
24	ENPEP	1 hits
25	FABP2	1 hits
26	GALNT3	1 hits
27	GCG	1 hits
28	GCK	1 hits
29	GCKR	1 hits
30	GGT1	1 hits
31	GHRH	1 hits
32	GLP1R	1 hits
33	GSTCD	1 hits
34	HNF4A	1 hits
35	HP	1 hits
36	IDDM2	1 hits
37	IL2	1 hits
38	INS	1 hits
39	INSR	1 hits
40	IRS1	1 hits
41	LEP	1 hits
42	LIPE	1 hits
43	LPAL2	1 hits
44	MPO	1 hits
45	NEU1	1 hits
46	NP	1 hits
47	NT5E	1 hits
48	PDGFA	1 hits
49	PGM1	1 hits
50	PLCB1	1 hits
51	PLCG1	1 hits
52	PPA1	1 hits
53	PTPRC	1 hits
54	RPN2	1 hits
55	SERPINF2	1 hits
56	SLC29A1	1 hits
57	SLC2A2	1 hits
58	SLC2A4	1 hits
59	SOD1	1 hits
60	SPINK1	1 hits
61	TNF	1 hits
62	VIPR1	1 hits

Related Sentences

#	PMID	Sentence
1	117108	No significant associations are seen when the MNSs, Kell, Lewis, Duffy, haptoglobin, red cell acid phosphatase, phosphoglucomutase, adenylate kinase, and adenosine deaminase distributions in these groups of subjects are compared
2	621091	Nine genetic polymorphic systems (ACP1, PGM1, ADA, AK, G-6-PD, Hp, ABO, Rh, MN), were studied in a series of 138 subjects affected by JOD.
3	621091	Differences between diabetic patients and controls were observed in the distribution of phenotypes of the red cell acid phosphatase (ACP1), and the ABO and MN blood groups.
4	696683	Adenosine deaminase was normal in most patients with extrahepatic obstruction and abnormal in most patients with parenchymal hepatic disease, and is potentially a useful test additional to the aminotransferases in routine diagnosis. 5'-Nucleotidase was more sensitive and specific than alkaline phosphatase in diagnosing hepatobiliary disorders.
5	1446805	Recently, linkage between the ADA gene locus and MODY, a subtype of NIDDM, has been reported.
6	1468454	Insulin-dependent diabetes mellitus and severe atopic dermatitis in a child with adenosine deaminase deficiency.
7	1468454	We report a 2.3-year-old girl with complete lack of adenosine deaminase (ADA) activity who presented with severe atopic dermatitis and insulin-dependent diabetes mellitus but only mild recurrent infections.
8	1468454	Insulin-dependent diabetes mellitus and severe atopic dermatitis in a child with adenosine deaminase deficiency.
9	1468454	We report a 2.3-year-old girl with complete lack of adenosine deaminase (ADA) activity who presented with severe atopic dermatitis and insulin-dependent diabetes mellitus but only mild recurrent infections.
10	1628771	No linkage to ADA or GLUT2 genes in two families.
11	1628771	We studied the linkage of MODY to two loci: ADA and GLUT2 in two large pedigrees with nonradioactive microsatellite polymorphic systems.
12	1628771	Formal linkage analysis excluded a tight linkage between ADA and MODY with a LOD score of -5.82 and -2.24 at a recombination fraction of 0.01 in the two families.
13	1628771	The LOD scores for GLUT2 were -7.79 and -1.9 at a recombination fraction of 0.001 in the two families, thus providing evidence against the involvement of GLUT2 in MODY.
14	1628771	No linkage to ADA or GLUT2 genes in two families.
15	1628771	We studied the linkage of MODY to two loci: ADA and GLUT2 in two large pedigrees with nonradioactive microsatellite polymorphic systems.
16	1628771	Formal linkage analysis excluded a tight linkage between ADA and MODY with a LOD score of -5.82 and -2.24 at a recombination fraction of 0.01 in the two families.
17	1628771	The LOD scores for GLUT2 were -7.79 and -1.9 at a recombination fraction of 0.001 in the two families, thus providing evidence against the involvement of GLUT2 in MODY.
18	1628771	No linkage to ADA or GLUT2 genes in two families.
19	1628771	We studied the linkage of MODY to two loci: ADA and GLUT2 in two large pedigrees with nonradioactive microsatellite polymorphic systems.
20	1628771	Formal linkage analysis excluded a tight linkage between ADA and MODY with a LOD score of -5.82 and -2.24 at a recombination fraction of 0.01 in the two families.
21	1628771	The LOD scores for GLUT2 were -7.79 and -1.9 at a recombination fraction of 0.001 in the two families, thus providing evidence against the involvement of GLUT2 in MODY.
22	1779465	Using the strategy of the second approach, Bell et al. recently reported that the gene responsible for MODY (maturity-onset diabetes of the young) is tightly linked to the adenosine deaminase gene on chromosome 20q.
23	1834379	The present study was designed to investigate whether the immunodeficiency in this animal may be associated with deficiency of purine nucleoside phosphorylase (PNP) and possibly adenosine deaminase (ADA).
24	1899928	Maturity-onset diabetes of the young (MODY) is a form of non-insulin-dependent diabetes mellitus characterized by an early age of onset, usually before 25 years of age, and an autosomal dominant mode of inheritance.
25	1899928	A DNA polymorphism in the adenosine deaminase gene (ADA) on the long arm of chromosome 20 was found to cosegregate with MODY.
26	1899928	The maximum logarithm of odds (lod score) for linkage between MODY and ADA was 5.25 at a recombination fraction of 0.00.
27	1899928	These results indicate that the odds are greater than 178,000:1 that the gene responsible for MODY in this family is tightly linked to the ADA gene on chromosome 20q.
28	1899928	Maturity-onset diabetes of the young (MODY) is a form of non-insulin-dependent diabetes mellitus characterized by an early age of onset, usually before 25 years of age, and an autosomal dominant mode of inheritance.
29	1899928	A DNA polymorphism in the adenosine deaminase gene (ADA) on the long arm of chromosome 20 was found to cosegregate with MODY.
30	1899928	The maximum logarithm of odds (lod score) for linkage between MODY and ADA was 5.25 at a recombination fraction of 0.00.
31	1899928	These results indicate that the odds are greater than 178,000:1 that the gene responsible for MODY in this family is tightly linked to the ADA gene on chromosome 20q.
32	1899928	Maturity-onset diabetes of the young (MODY) is a form of non-insulin-dependent diabetes mellitus characterized by an early age of onset, usually before 25 years of age, and an autosomal dominant mode of inheritance.
33	1899928	A DNA polymorphism in the adenosine deaminase gene (ADA) on the long arm of chromosome 20 was found to cosegregate with MODY.
34	1899928	The maximum logarithm of odds (lod score) for linkage between MODY and ADA was 5.25 at a recombination fraction of 0.00.
35	1899928	These results indicate that the odds are greater than 178,000:1 that the gene responsible for MODY in this family is tightly linked to the ADA gene on chromosome 20q.
36	2066107	Evidence of selective interaction between adenosine deaminase and acid phosphatase polymorphisms in fetuses carried by diabetic women.
37	2066107	Possible selective interaction between genetic polymorphisms of acid phosphatase locus 1 (ACP1) and adenosine deaminase (ADA) has been investigated in a sample of 211 infants from diabetic women, and in 350 consecutive infants from normal women.
38	2066107	Evidence of selective interaction between adenosine deaminase and acid phosphatase polymorphisms in fetuses carried by diabetic women.
39	2066107	Possible selective interaction between genetic polymorphisms of acid phosphatase locus 1 (ACP1) and adenosine deaminase (ADA) has been investigated in a sample of 211 infants from diabetic women, and in 350 consecutive infants from normal women.
40	2146155	On the role of insulin in regulation of adenosine deaminase activity in rat tissues.
41	2146155	After administration of insulin adenosine deaminase activity was reduced in different skeletal muscle types, the heart and the liver.
42	2146155	On the role of insulin in regulation of adenosine deaminase activity in rat tissues.
43	2146155	After administration of insulin adenosine deaminase activity was reduced in different skeletal muscle types, the heart and the liver.
44	2256476	Beside cytoplasmic glutathione-S-transferase and lysosomal beta-N-acetyl-glucosaminidase (beta-NAG) the majority of kidney-related urine proteins derives from membrane surface components of the most vulnerable proximal tubule epithelia, among them ala-(leu-gly)-aminopeptidase, gamma-glutamyl transpeptidase (GGT), the tubular portion of angiotensinase A, the major brush border glycoprotein 'SGP-240' and adenosine-deaminase-binding protein.
45	2556341	We investigated possible relations among four common neonatal manifestations of diabetic pregnancy (macrosomia, hypoglycemia, hypocalcemia, jaundice) and four enzyme polymorphisms (PGM1, ADA, AK1, ACP1 in a sample of infants born of diabetic mothers.
46	2822032	Adipocytes were isolated from epididymal white fat and interscapular brown fat of male rats, and activities of 5'-nucleotidase, adenosine deaminase and adenosine kinase were measured in cell extracts. 2. 5'-Nucleotidase activity in white adipocytes was increased in streptozotocin-diabetes, decreased in hypothyroidism and increased with age.
47	3070044	Five mutated genes on chromosome 20 have a relation to disease: a mutation in the adenosine deaminase gene results in a deficiency of the enzyme and severe combined immune deficiency; mutations in the gene for the growth hormone releasing factor result in some forms of dwarfism; mutations in the closely linked genes for the hormones arginine vasopressin and oxytocin and their neurophysins are probably responsible for some diabetes insipidus; and mutations in the gene that regulates both alpha-neuraminidase and beta-galactosidase activities determine galactosialidosis.
48	3070044	Two genes that code for tyrosine kinases are on the chromosome, SRC1 the proto-oncogene and a gene (HCK) coding for haemopoietic kinase (an src-like kinase), but no direct relation to cancer has been shown for either of these kinases.
49	3070044	Twenty-four additional loci are assigned to the chromosome: five genes that code for binding proteins, one for a light chain of ferritin, genes for three enzymes (inosine triphosphatase, s-adenosylhomocysteine hydrolase, and sterol delta 24-reductase), one for each of a secretory protein and an opiate neuropeptide, a cell surface antigen, two fragile sites, and 10 DNA sequences (one satellite and nine unique) that detect RFLPs.
50	7037376	In both groups of sand rats adenosine deaminase did not increase the noradrenaline effect on adenylate cyclase.
51	7508874	Maturity-onset diabetes of the young (MODY) is a model for genetic studies of non-insulin-dependent diabetes mellitus.
52	7508874	We have identified 15 MODY families in which diabetes is not the result of mutations in the glucokinase gene.
53	7508874	Nine other candidate genes potentially implicated in insulin secretion or insulin action have been tested for linkage with MODY in these families, including glucokinase regulatory protein, hexokinase II, insulin receptor substrate 1, fatty acid-binding protein 2, glucagon-like peptide-1 receptor, apolipoprotein C-II, glycogen synthase, adenosine deaminase (a marker for the MODY gene on chromosome 20), and phosphoenolpyruvate carboxykinase.
54	7543243	In CFPAC-1 cells, this downregulation is dependent on the presence of adenosine, since pretreatment of the cells with adenosine deaminase blocks the CPX effect.
55	7680315	We report a patient with a clinical picture consisting of small birth weight, connatal hypoplastic anaemia, vacuolised bone marrow precursors, failure to thrive, and, subsequently, by insulin-dependent diabetes, renal Fanconi syndrome, lactic acidosis, complex organic aciduria, and elevation of haemoglobin F and of adenosine deaminase activity.
56	7705022	We have studied members of 19 families with familial Type 2 diabetes (including 10 European families, 6 families from the Indian subcontinent, and 3 families of Afro-Caribbean origin), 2 of which were of MODY type (and both European), with a glucokinase marker and a marker linked to ADA, to examine whether glucokinase, or the unknown defect on chromosome 20, are implicated in diabetes in our pedigrees.
57	7821197	Adenosine deaminase (ADA) is suggested to be an important enzyme for modulating the bioactivity of insulin, but its clinical significance in diabetes mellitus (DM) is not yet characterized.
58	7821197	We measured the serum levels of ADA isoenzymes (ADA1 and ADA2) in healthy donors (HD, n = 52), insulin-dependent diabetes mellitus (IDDM, n = 53) patients and non-insulin-dependent diabetes mellitus (NIDDM, n = 65) patients.
59	7821197	Adenosine deaminase (ADA) is suggested to be an important enzyme for modulating the bioactivity of insulin, but its clinical significance in diabetes mellitus (DM) is not yet characterized.
60	7821197	We measured the serum levels of ADA isoenzymes (ADA1 and ADA2) in healthy donors (HD, n = 52), insulin-dependent diabetes mellitus (IDDM, n = 53) patients and non-insulin-dependent diabetes mellitus (NIDDM, n = 65) patients.
61	7924873	Early-onset type 2 (non-insulin-dependent) diabetes mellitus is associated with glucokinase locus, but not with adenosine deaminase locus, in the Japanese population.
62	7924873	To investigate the possible contribution of glucokinase (GCK) and adenosine deaminase (ADA) loci to the genetic susceptibility to type 2 (non-insulin-dependent) diabetes mellitus, we studied the association of these loci with type 2 diabetes in the Japanese population.
63	7924873	Fifty patients with type 2 diabetes and 50 control subjects were analyzed for microsatellite polymorphism 3' to the GCK gene and PstI polymorphism in the ADA gene by polymerase chain reaction.
64	7924873	In contrast, there was no difference in allelic or genotypic frequencies of PstI polymorphism in the ADA gene between the two groups.
65	7924873	These results suggest that the GCK locus, but not the ADA locus, contributes to the genetic susceptibility to type 2 diabetes in Japanese.
66	7924873	Early-onset type 2 (non-insulin-dependent) diabetes mellitus is associated with glucokinase locus, but not with adenosine deaminase locus, in the Japanese population.
67	7924873	To investigate the possible contribution of glucokinase (GCK) and adenosine deaminase (ADA) loci to the genetic susceptibility to type 2 (non-insulin-dependent) diabetes mellitus, we studied the association of these loci with type 2 diabetes in the Japanese population.
68	7924873	Fifty patients with type 2 diabetes and 50 control subjects were analyzed for microsatellite polymorphism 3' to the GCK gene and PstI polymorphism in the ADA gene by polymerase chain reaction.
69	7924873	In contrast, there was no difference in allelic or genotypic frequencies of PstI polymorphism in the ADA gene between the two groups.
70	7924873	These results suggest that the GCK locus, but not the ADA locus, contributes to the genetic susceptibility to type 2 diabetes in Japanese.
71	7924873	Early-onset type 2 (non-insulin-dependent) diabetes mellitus is associated with glucokinase locus, but not with adenosine deaminase locus, in the Japanese population.
72	7924873	To investigate the possible contribution of glucokinase (GCK) and adenosine deaminase (ADA) loci to the genetic susceptibility to type 2 (non-insulin-dependent) diabetes mellitus, we studied the association of these loci with type 2 diabetes in the Japanese population.
73	7924873	Fifty patients with type 2 diabetes and 50 control subjects were analyzed for microsatellite polymorphism 3' to the GCK gene and PstI polymorphism in the ADA gene by polymerase chain reaction.
74	7924873	In contrast, there was no difference in allelic or genotypic frequencies of PstI polymorphism in the ADA gene between the two groups.
75	7924873	These results suggest that the GCK locus, but not the ADA locus, contributes to the genetic susceptibility to type 2 diabetes in Japanese.
76	7924873	Early-onset type 2 (non-insulin-dependent) diabetes mellitus is associated with glucokinase locus, but not with adenosine deaminase locus, in the Japanese population.
77	7924873	To investigate the possible contribution of glucokinase (GCK) and adenosine deaminase (ADA) loci to the genetic susceptibility to type 2 (non-insulin-dependent) diabetes mellitus, we studied the association of these loci with type 2 diabetes in the Japanese population.
78	7924873	Fifty patients with type 2 diabetes and 50 control subjects were analyzed for microsatellite polymorphism 3' to the GCK gene and PstI polymorphism in the ADA gene by polymerase chain reaction.
79	7924873	In contrast, there was no difference in allelic or genotypic frequencies of PstI polymorphism in the ADA gene between the two groups.
80	7924873	These results suggest that the GCK locus, but not the ADA locus, contributes to the genetic susceptibility to type 2 diabetes in Japanese.
81	7924873	Early-onset type 2 (non-insulin-dependent) diabetes mellitus is associated with glucokinase locus, but not with adenosine deaminase locus, in the Japanese population.
82	7924873	To investigate the possible contribution of glucokinase (GCK) and adenosine deaminase (ADA) loci to the genetic susceptibility to type 2 (non-insulin-dependent) diabetes mellitus, we studied the association of these loci with type 2 diabetes in the Japanese population.
83	7924873	Fifty patients with type 2 diabetes and 50 control subjects were analyzed for microsatellite polymorphism 3' to the GCK gene and PstI polymorphism in the ADA gene by polymerase chain reaction.
84	7924873	In contrast, there was no difference in allelic or genotypic frequencies of PstI polymorphism in the ADA gene between the two groups.
85	7924873	These results suggest that the GCK locus, but not the ADA locus, contributes to the genetic susceptibility to type 2 diabetes in Japanese.
86	7955566	We performed limiting dilution culture of T cells from a patient affected by primary immunodeficiency as a result of complete lack of adenosine deaminase (ADA) activity and also affected by insulin-dependent diabetes mellitus (type I diabetes).
87	7955566	These T cells displayed ADA enzymatic activity and produced interleukin-2 after engagement of their T cell receptor (TCR)/CD3 complex.
88	7955566	We performed limiting dilution culture of T cells from a patient affected by primary immunodeficiency as a result of complete lack of adenosine deaminase (ADA) activity and also affected by insulin-dependent diabetes mellitus (type I diabetes).
89	7955566	These T cells displayed ADA enzymatic activity and produced interleukin-2 after engagement of their T cell receptor (TCR)/CD3 complex.
90	8094595	New dinucleotide repeat polymorphisms associated with the D20S17, PPGB, and ADA loci have been identified and mapped.
91	8216350	The effect of the adenosine deaminase (ADA) inhibitor 2'-deoxycoformycin (dCF) on the development of insulin-dependent diabetes mellitus (IDDM) was assessed in the BB Wistar rat.
92	8216350	Although the protective effect of dCF against IDDM was likely produced by immunosuppression, the different dCF dosages had similar effects on ADA suppression in spleen or thymus and on dATP accumulation in these organs.
93	8216350	The effect of the adenosine deaminase (ADA) inhibitor 2'-deoxycoformycin (dCF) on the development of insulin-dependent diabetes mellitus (IDDM) was assessed in the BB Wistar rat.
94	8216350	Although the protective effect of dCF against IDDM was likely produced by immunosuppression, the different dCF dosages had similar effects on ADA suppression in spleen or thymus and on dATP accumulation in these organs.
95	8527305	The effects of wortmannin, a potent inhibitor of phosphatidylinositol 3-kinase, on insulin-stimulated glucose transport, GLUT4 translocation, antilipolysis, and DNA synthesis.
96	8527305	Insulin-stimulated translocation of GLUT4 in isolated rat adipocytes was markedly inhibited by wortmannin.
97	8527305	Wortmannin had no effect on either basal or insulin-stimulated glucose utilization in L6 myocytes, a skeletal muscle cell line in which GLUT1 is the predominant transporter isoform.
98	8527305	Wortmannin also partially antagonized the antilipolytic effect of insulin on adenosine deaminase-stimulated lipolysis in isolated rat adipocytes.
99	8527305	We conclude that PI 3-kinase activation is necessary for maximum insulin-stimulated glucose transport, translocation of GLUT4, antilipolysis and DNA synthesis.
100	8591819	We assessed polymorphic markers close to the genes for glucokinase, hexokinase II, adenosine deaminase, pituitary adenylate cyclase-activating polypeptide receptor, and glucagon-like peptide-1 receptor.
101	9217288	We have previously reported that weekly administration of the adenosine deaminase inhibitor, 2'-deoxycoformycin (dCF), reduces the incidence of insulin-dependent diabetes mellitus (IDDM) in the BB Wistar rat, and this effect is likely due to immunosuppression by dCF.
102	9285775	Several candidate genes for non-insulin-dependent diabetes mellitus (NIDDM) map on chromosome 20, including the phosphoenolpyruvate carboxykinase gene (PCK1) and one of the maturity onset diabetes of the young genes (MODY1).
103	9285775	Moreover, another region spanning the ribophorin II (RPNII, phospholipase C (PLC1) and adenosine deaminase (ADA) loci suggested linkage with NIDDM (multipoint MLS of 1.81 in all NIDDM sib pairs, P = 0.003; MLS = 1.31, P = 0.012 when using a conservative weighting procedure).
104	9364370	We present a girl with severe combined immunodeficiency (SCID) from adenosine deaminase (ADA) deficiency who developed insulin dependent diabetes mellitus (IDDM).
105	9405929	Cytosolic low molecular weight acid phosphatase (ACP1) is a high polymorphic phosphotyrosine-protein-phosphatase involved in signal transduction.
106	9405929	Adenosine deaminase, ABO blood groups and several clinical variables have been also considered.
107	9792534	We found that, in rat epitrochlearis and soleus muscles, removing adenosine with adenosine deaminase or blocking its action with the adenosine receptor blocker CPDPX markedly reduces the responsiveness of glucose transport to stimulation by 1) insulin alone, 2) contractions alone, and 3) insulin and contractions in combination.
108	9792534	Measurement of the increase in GLUT4 at the cell surface in response to a maximally effective insulin stimulus in the epitrochlearis muscle, using the exofacial label ATB-[3H]BMPA, showed that adenosine deaminase treatment markedly reduces cell-surface GLUT4 labeling.
109	9792534	The reduction in cell-surface GLUT4 labeling was similar in magnitude to the decrease in maximally insulin-stimulated glucose transport activity in adenosine deaminase-treated muscles.
110	9792534	These results show that adenosine potentiates insulin- and contraction-stimulated glucose transport in skeletal muscle by enhancing the increase in GLUT4 at the cell surface and raise the possibility that decreased adenosine production or action could play a causative role in insulin resistance.
111	9792534	We found that, in rat epitrochlearis and soleus muscles, removing adenosine with adenosine deaminase or blocking its action with the adenosine receptor blocker CPDPX markedly reduces the responsiveness of glucose transport to stimulation by 1) insulin alone, 2) contractions alone, and 3) insulin and contractions in combination.
112	9792534	Measurement of the increase in GLUT4 at the cell surface in response to a maximally effective insulin stimulus in the epitrochlearis muscle, using the exofacial label ATB-[3H]BMPA, showed that adenosine deaminase treatment markedly reduces cell-surface GLUT4 labeling.
113	9792534	The reduction in cell-surface GLUT4 labeling was similar in magnitude to the decrease in maximally insulin-stimulated glucose transport activity in adenosine deaminase-treated muscles.
114	9792534	These results show that adenosine potentiates insulin- and contraction-stimulated glucose transport in skeletal muscle by enhancing the increase in GLUT4 at the cell surface and raise the possibility that decreased adenosine production or action could play a causative role in insulin resistance.
115	9792534	We found that, in rat epitrochlearis and soleus muscles, removing adenosine with adenosine deaminase or blocking its action with the adenosine receptor blocker CPDPX markedly reduces the responsiveness of glucose transport to stimulation by 1) insulin alone, 2) contractions alone, and 3) insulin and contractions in combination.
116	9792534	Measurement of the increase in GLUT4 at the cell surface in response to a maximally effective insulin stimulus in the epitrochlearis muscle, using the exofacial label ATB-[3H]BMPA, showed that adenosine deaminase treatment markedly reduces cell-surface GLUT4 labeling.
117	9792534	The reduction in cell-surface GLUT4 labeling was similar in magnitude to the decrease in maximally insulin-stimulated glucose transport activity in adenosine deaminase-treated muscles.
118	9792534	These results show that adenosine potentiates insulin- and contraction-stimulated glucose transport in skeletal muscle by enhancing the increase in GLUT4 at the cell surface and raise the possibility that decreased adenosine production or action could play a causative role in insulin resistance.
119	10459555	Adenosine deaminase and body mass index in non-insulin-dependent diabetes mellitus.
120	10459555	No significant effect on the relation between ADA and BMI has been observed for the following variables: sex, age at the time of study, age at onset, therapy with insulin, and dyslipidemia.
121	10459555	Adenosine deaminase and body mass index in non-insulin-dependent diabetes mellitus.
122	10459555	No significant effect on the relation between ADA and BMI has been observed for the following variables: sex, age at the time of study, age at onset, therapy with insulin, and dyslipidemia.
123	10480596	Long-term regulation of lipolysis and hormone-sensitive lipase by insulin and glucose.
124	10480596	We have therefore investigated the effect of prolonged high glucose and insulin on adipocyte lipolysis in basal conditions or with maximal concentrations of adenosine deaminase (ADA), dibutyryl cyclic-AMP (dbcAMP), or isoproterenol (ISO).
125	10480596	However, insulin plus glucose increased the rate of ADA-, dbcAMP-, and ISO-stimulated lipolysis by 40-65%, and the effect was maximal by 8 h.
126	10480596	Because the effect of insulin and glucose was evident whether lipolysis was stimulated by ADA, dbcAMP, or ISO, we hypothesized that the expression of the rate-limiting enzyme for lipolysis, hormone-sensitive lipase (HSL), was increased.
127	10480596	Our results show that insulin plus glucose-treated cells contain approximately 40% more HSL protein than control cells, in good agreement with the increase in maximally stimulated lipolysis.
128	10480596	We conclude that hyperglycemic-hyperinsulinemic conditions increase basal and maximal adipocyte lipolysis by a mechanism that is not glutamine-dependent and involves maintenance of cellular concentrations of HSL.
129	10480596	Long-term regulation of lipolysis and hormone-sensitive lipase by insulin and glucose.
130	10480596	We have therefore investigated the effect of prolonged high glucose and insulin on adipocyte lipolysis in basal conditions or with maximal concentrations of adenosine deaminase (ADA), dibutyryl cyclic-AMP (dbcAMP), or isoproterenol (ISO).
131	10480596	However, insulin plus glucose increased the rate of ADA-, dbcAMP-, and ISO-stimulated lipolysis by 40-65%, and the effect was maximal by 8 h.
132	10480596	Because the effect of insulin and glucose was evident whether lipolysis was stimulated by ADA, dbcAMP, or ISO, we hypothesized that the expression of the rate-limiting enzyme for lipolysis, hormone-sensitive lipase (HSL), was increased.
133	10480596	Our results show that insulin plus glucose-treated cells contain approximately 40% more HSL protein than control cells, in good agreement with the increase in maximally stimulated lipolysis.
134	10480596	We conclude that hyperglycemic-hyperinsulinemic conditions increase basal and maximal adipocyte lipolysis by a mechanism that is not glutamine-dependent and involves maintenance of cellular concentrations of HSL.
135	10480596	Long-term regulation of lipolysis and hormone-sensitive lipase by insulin and glucose.
136	10480596	We have therefore investigated the effect of prolonged high glucose and insulin on adipocyte lipolysis in basal conditions or with maximal concentrations of adenosine deaminase (ADA), dibutyryl cyclic-AMP (dbcAMP), or isoproterenol (ISO).
137	10480596	However, insulin plus glucose increased the rate of ADA-, dbcAMP-, and ISO-stimulated lipolysis by 40-65%, and the effect was maximal by 8 h.
138	10480596	Because the effect of insulin and glucose was evident whether lipolysis was stimulated by ADA, dbcAMP, or ISO, we hypothesized that the expression of the rate-limiting enzyme for lipolysis, hormone-sensitive lipase (HSL), was increased.
139	10480596	Our results show that insulin plus glucose-treated cells contain approximately 40% more HSL protein than control cells, in good agreement with the increase in maximally stimulated lipolysis.
140	10480596	We conclude that hyperglycemic-hyperinsulinemic conditions increase basal and maximal adipocyte lipolysis by a mechanism that is not glutamine-dependent and involves maintenance of cellular concentrations of HSL.
141	10527935	GLUT4 trafficking in insulin-stimulated rat adipose cells: evidence that heterotrimeric GTP-binding proteins regulate the fusion of docked GLUT4-containing vesicles.
142	10527935	Agents that activate the G-protein G(i) (e.g. adenosine) increase, and agents that activate G(s) [e.g. isoprenaline (isoproterenol)] decrease, steady-state insulin-stimulated glucose transport activity and cell-surface GLUT4 in isolated rat adipose cells without changing plasma membrane GLUT4 content.
143	10527935	Here we have further examined the effects of R(s)G(s) and R(i)G(i) ligands (in which R(s) and R(i) are G(s)- and G(i)-coupled receptors respectively) on insulin-stimulated cell-surface GLUT4 and the kinetics of GLUT4 trafficking in these same cells.
144	10527935	Rat adipose cells were preincubated for 2 min with or without isoprenaline (200 nM) and adenosine deaminase (1 unit/ml), to stimulate G(s) and decrease the stimulation of G(i) respectively, followed by 0-20 min with insulin (670 nM).
145	10527935	Treatment with isoprenaline and adenosine deaminase decreased insulin-stimulated glucose transport activity by 58%.
146	10527935	Treatment with isoprenaline and adenosine deaminase also resulted in similar decreases in insulin-stimulated cell-surface GLUT4 as assessed by both bis-mannose photolabelling of the substrate-binding site and biotinylation of the extracellular carbohydrate moiety when evaluated under similar experimental conditions.
147	10527935	After stimulation with insulin in the absence of G(s) and the presence of G(i) agents, a distinct sequence of plasma membrane events took place, starting with an increase in immunodetectable GLUT4, then an increase in the accessibility of GLUT4 to bis-mannose photolabel, and finally an increase in glucose transport activity.
148	10527935	Pretreatment with isoprenaline and adenosine deaminase before stimulation with insulin did not affect the time course of the increase in immunodetectable GLUT4 in the plasma membrane, but did delay both the increase in accessibility of GLUT4 to photolabel and the increase in glucose transport activity.
149	10527935	These results suggest that R(s)G(s) and R(i)G(i) modulate insulin-stimulated glucose transport by influencing the extent to which GLUT4 is associated with occluded vesicles attached to the plasma membrane during exocytosis, perhaps by regulating the fusion process through which the GLUT4 in docked vesicles becomes exposed on the cell surface.
150	10527935	GLUT4 trafficking in insulin-stimulated rat adipose cells: evidence that heterotrimeric GTP-binding proteins regulate the fusion of docked GLUT4-containing vesicles.
151	10527935	Agents that activate the G-protein G(i) (e.g. adenosine) increase, and agents that activate G(s) [e.g. isoprenaline (isoproterenol)] decrease, steady-state insulin-stimulated glucose transport activity and cell-surface GLUT4 in isolated rat adipose cells without changing plasma membrane GLUT4 content.
152	10527935	Here we have further examined the effects of R(s)G(s) and R(i)G(i) ligands (in which R(s) and R(i) are G(s)- and G(i)-coupled receptors respectively) on insulin-stimulated cell-surface GLUT4 and the kinetics of GLUT4 trafficking in these same cells.
153	10527935	Rat adipose cells were preincubated for 2 min with or without isoprenaline (200 nM) and adenosine deaminase (1 unit/ml), to stimulate G(s) and decrease the stimulation of G(i) respectively, followed by 0-20 min with insulin (670 nM).
154	10527935	Treatment with isoprenaline and adenosine deaminase decreased insulin-stimulated glucose transport activity by 58%.
155	10527935	Treatment with isoprenaline and adenosine deaminase also resulted in similar decreases in insulin-stimulated cell-surface GLUT4 as assessed by both bis-mannose photolabelling of the substrate-binding site and biotinylation of the extracellular carbohydrate moiety when evaluated under similar experimental conditions.
156	10527935	After stimulation with insulin in the absence of G(s) and the presence of G(i) agents, a distinct sequence of plasma membrane events took place, starting with an increase in immunodetectable GLUT4, then an increase in the accessibility of GLUT4 to bis-mannose photolabel, and finally an increase in glucose transport activity.
157	10527935	Pretreatment with isoprenaline and adenosine deaminase before stimulation with insulin did not affect the time course of the increase in immunodetectable GLUT4 in the plasma membrane, but did delay both the increase in accessibility of GLUT4 to photolabel and the increase in glucose transport activity.
158	10527935	These results suggest that R(s)G(s) and R(i)G(i) modulate insulin-stimulated glucose transport by influencing the extent to which GLUT4 is associated with occluded vesicles attached to the plasma membrane during exocytosis, perhaps by regulating the fusion process through which the GLUT4 in docked vesicles becomes exposed on the cell surface.
159	10527935	GLUT4 trafficking in insulin-stimulated rat adipose cells: evidence that heterotrimeric GTP-binding proteins regulate the fusion of docked GLUT4-containing vesicles.
160	10527935	Agents that activate the G-protein G(i) (e.g. adenosine) increase, and agents that activate G(s) [e.g. isoprenaline (isoproterenol)] decrease, steady-state insulin-stimulated glucose transport activity and cell-surface GLUT4 in isolated rat adipose cells without changing plasma membrane GLUT4 content.
161	10527935	Here we have further examined the effects of R(s)G(s) and R(i)G(i) ligands (in which R(s) and R(i) are G(s)- and G(i)-coupled receptors respectively) on insulin-stimulated cell-surface GLUT4 and the kinetics of GLUT4 trafficking in these same cells.
162	10527935	Rat adipose cells were preincubated for 2 min with or without isoprenaline (200 nM) and adenosine deaminase (1 unit/ml), to stimulate G(s) and decrease the stimulation of G(i) respectively, followed by 0-20 min with insulin (670 nM).
163	10527935	Treatment with isoprenaline and adenosine deaminase decreased insulin-stimulated glucose transport activity by 58%.
164	10527935	Treatment with isoprenaline and adenosine deaminase also resulted in similar decreases in insulin-stimulated cell-surface GLUT4 as assessed by both bis-mannose photolabelling of the substrate-binding site and biotinylation of the extracellular carbohydrate moiety when evaluated under similar experimental conditions.
165	10527935	After stimulation with insulin in the absence of G(s) and the presence of G(i) agents, a distinct sequence of plasma membrane events took place, starting with an increase in immunodetectable GLUT4, then an increase in the accessibility of GLUT4 to bis-mannose photolabel, and finally an increase in glucose transport activity.
166	10527935	Pretreatment with isoprenaline and adenosine deaminase before stimulation with insulin did not affect the time course of the increase in immunodetectable GLUT4 in the plasma membrane, but did delay both the increase in accessibility of GLUT4 to photolabel and the increase in glucose transport activity.
167	10527935	These results suggest that R(s)G(s) and R(i)G(i) modulate insulin-stimulated glucose transport by influencing the extent to which GLUT4 is associated with occluded vesicles attached to the plasma membrane during exocytosis, perhaps by regulating the fusion process through which the GLUT4 in docked vesicles becomes exposed on the cell surface.
168	10527935	GLUT4 trafficking in insulin-stimulated rat adipose cells: evidence that heterotrimeric GTP-binding proteins regulate the fusion of docked GLUT4-containing vesicles.
169	10527935	Agents that activate the G-protein G(i) (e.g. adenosine) increase, and agents that activate G(s) [e.g. isoprenaline (isoproterenol)] decrease, steady-state insulin-stimulated glucose transport activity and cell-surface GLUT4 in isolated rat adipose cells without changing plasma membrane GLUT4 content.
170	10527935	Here we have further examined the effects of R(s)G(s) and R(i)G(i) ligands (in which R(s) and R(i) are G(s)- and G(i)-coupled receptors respectively) on insulin-stimulated cell-surface GLUT4 and the kinetics of GLUT4 trafficking in these same cells.
171	10527935	Rat adipose cells were preincubated for 2 min with or without isoprenaline (200 nM) and adenosine deaminase (1 unit/ml), to stimulate G(s) and decrease the stimulation of G(i) respectively, followed by 0-20 min with insulin (670 nM).
172	10527935	Treatment with isoprenaline and adenosine deaminase decreased insulin-stimulated glucose transport activity by 58%.
173	10527935	Treatment with isoprenaline and adenosine deaminase also resulted in similar decreases in insulin-stimulated cell-surface GLUT4 as assessed by both bis-mannose photolabelling of the substrate-binding site and biotinylation of the extracellular carbohydrate moiety when evaluated under similar experimental conditions.
174	10527935	After stimulation with insulin in the absence of G(s) and the presence of G(i) agents, a distinct sequence of plasma membrane events took place, starting with an increase in immunodetectable GLUT4, then an increase in the accessibility of GLUT4 to bis-mannose photolabel, and finally an increase in glucose transport activity.
175	10527935	Pretreatment with isoprenaline and adenosine deaminase before stimulation with insulin did not affect the time course of the increase in immunodetectable GLUT4 in the plasma membrane, but did delay both the increase in accessibility of GLUT4 to photolabel and the increase in glucose transport activity.
176	10527935	These results suggest that R(s)G(s) and R(i)G(i) modulate insulin-stimulated glucose transport by influencing the extent to which GLUT4 is associated with occluded vesicles attached to the plasma membrane during exocytosis, perhaps by regulating the fusion process through which the GLUT4 in docked vesicles becomes exposed on the cell surface.
177	10615945	Role of adenosine in insulin-stimulated release of leptin from isolated white adipocytes of Wistar rats.
178	10615945	Leptin, the ob gene product that can decrease caloric intake and increase energy expenditure, is functionally released by insulin from adipose tissue.
179	10615945	The present study investigated the role of adenosine in the release of leptin by insulin in isolated rat white adipocytes.
180	10615945	Release of leptin, measured by radioimmunoassay, from insulin-stimulated samples was seen after 30 min.
181	10615945	Adenosine deaminase, at concentrations sufficient to metabolize endogenous adenosine, decreased insulin-stimulated leptin release.
182	10615945	Also, the insulin-stimulated leptin release was completely blocked by the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX).
183	10615945	In the presence of U73312, a specific inhibitor of phospholipase C (PLC), CPA-stimulated leptin secretion from adipocytes was reduced in a concentration-dependent manner, but it was not affected by U73343, the negative control for U73312.
184	10615945	Moreover, chelerythrine and GF 109203X diminished the CPA-stimulated leptin secretion at concentrations sufficient to inhibit protein kinase C (PKC).
185	10615945	These results suggest that, in isolated white adipocytes, the released adenosine acts as a helper and/or a positive regulator for insulin in the release of leptin via an activation of adenosine A1 receptors that involves the PLC-PKC pathway.
186	10795176	Half of all fulfilled intentions occurred in a community served by an active ADA AAP Coalition.
187	11284388	In addition to, but independent of its serine type catalytic activity, DPPIV binds closely to the soluble extracellular enzyme adenosine deaminase.
188	11284388	Other known substrates which are subject in vitro to receptor-specific changes induced by DPPIV truncation include neuropeptides such as substance P, peptidE YY and neuropeptide Y.
189	11284388	On the other hand, DPPIV mediated cleavage of the N-terminal His-Ala or Tyr-Ala dipeptides from circulating incretin hormones like, glucagon-like peptides (GLP)-1 and -2, gastric inhibitory polypeptide (GIP), all members of the enteroglucagon/GRF superfamily, results in their biological inactivation in vitro and in vivo.
190	11284388	Administration of specific DPPIV inhibitors closes this pathway of incretin degradation and greatly enhances insulin secretion.
191	11834126	These contained the genes of interest and the amplifiable gene markers dihydrofolate reductase (DHFR) and adenosine deaminase (ADA), separated by an internal ribosome entry site isolated from the encephalomyocarditis virus.
192	12085822	HHS, ADA work to boost awareness of diabetes and cardiovascular risk.
193	12637816	HHS and ADA warn Americans of "prediabetes".
194	12892317	Dipeptidyl-peptidase IV/CD26 (DPP IV) is a cell-surface protease belonging to the prolyloligopeptidase family.
195	12892317	Apart from its catalytic activity, it interacts with several proteins, for instance, adenosine deaminase, the HIV gp120 protein, fibronectin, collagen, the chemokine receptor CXCR4, and the tyrosine phosphatase CD45.
196	12892317	The role of DPP IV/ CD26 within the immune system is a combination of its exopeptidase activity and its interactions with different molecules.
197	12892317	This enables DPP IV/CD26 to serve as a co-stimulatory molecule to influence T cell activity and to modulate chemotaxis.
198	14652987	Given the research findings and the guidelines for glycemic control established by ADA and ACE, ASHP supports and encourages strict glycemic control in all appropriate patients with diabetes mellitus to reduce the progression of chronic complications.
199	14739077	After removal of insulin and excess of free NBD-FA, lipolysis is initiated by addition of isoproterenol and/or adenosine deaminase.
200	15168879	Adenosine deaminase (ADA) is suggested to be an important enzyme for modulating the bioactivity of insulin, but its clinical significance in diabetes mellitus (DM) is not yet characterized.
201	15168879	Our findings suggest that ADA may play a role in insulin effect and glycamic control.
202	15168879	On the other hand, increased activity of ADA in type 2 DM might be a marker for insulin indication.
203	15168879	Adenosine deaminase (ADA) is suggested to be an important enzyme for modulating the bioactivity of insulin, but its clinical significance in diabetes mellitus (DM) is not yet characterized.
204	15168879	Our findings suggest that ADA may play a role in insulin effect and glycamic control.
205	15168879	On the other hand, increased activity of ADA in type 2 DM might be a marker for insulin indication.
206	15168879	Adenosine deaminase (ADA) is suggested to be an important enzyme for modulating the bioactivity of insulin, but its clinical significance in diabetes mellitus (DM) is not yet characterized.
207	15168879	Our findings suggest that ADA may play a role in insulin effect and glycamic control.
208	15168879	On the other hand, increased activity of ADA in type 2 DM might be a marker for insulin indication.
209	15281007	Type 2 diabetes and the genetics of signal transduction: a study of interaction between adenosine deaminase and acid phosphatase locus 1 polymorphisms.
210	15281007	Acid phosphatase locus 1 (ACP1) is a highly polymorphic enzyme that has an important role in flavoenzyme activity and in the control of insulin receptor activity and band 3 protein phosphorylation status.
211	15281007	Based on the hypothesis that ACP1 counteracts insulin signaling by dephosphorylating the insulin receptor and that adenosine has an anti-insulin action, we reasoned that low ACP1 activity (low dephosphorylating action on insulin receptor) when associated with high ADA activity (low adenosine concentration) would result in a cumulative effect towards an increased glucose tolerance.
212	15281007	On the contrary, high ACP1 activity when associated with low ADA activity would result in a cumulative effect towards a decreased glucose tolerance.
213	15281007	There was a nonsignificant trend toward an increase in the proportion of subjects with the complex type with high ACP1 activity and low ADA activity (ie, B/B; A/C; B/C; C/C//ADA1/2 and 2/2) in type 2 diabetes relative to that observed in newborn infants from the same population.
214	15281007	High ACP1 activity/low ADA activity joint genotype was positively associated with high glycemic levels and with high body mass index (BMI) values.
215	15281007	Low ACP1 activity/high ADA activity joint genotype was also positively associated with dyslipidemia.
216	15281007	These findings suggest that both ACP1 and ADA contribute to the clinical manifestations of type 2 diabetes and probably also have a marginal influence on susceptibility to the disease.
217	15281007	Type 2 diabetes and the genetics of signal transduction: a study of interaction between adenosine deaminase and acid phosphatase locus 1 polymorphisms.
218	15281007	Acid phosphatase locus 1 (ACP1) is a highly polymorphic enzyme that has an important role in flavoenzyme activity and in the control of insulin receptor activity and band 3 protein phosphorylation status.
219	15281007	Based on the hypothesis that ACP1 counteracts insulin signaling by dephosphorylating the insulin receptor and that adenosine has an anti-insulin action, we reasoned that low ACP1 activity (low dephosphorylating action on insulin receptor) when associated with high ADA activity (low adenosine concentration) would result in a cumulative effect towards an increased glucose tolerance.
220	15281007	On the contrary, high ACP1 activity when associated with low ADA activity would result in a cumulative effect towards a decreased glucose tolerance.
221	15281007	There was a nonsignificant trend toward an increase in the proportion of subjects with the complex type with high ACP1 activity and low ADA activity (ie, B/B; A/C; B/C; C/C//ADA1/2 and 2/2) in type 2 diabetes relative to that observed in newborn infants from the same population.
222	15281007	High ACP1 activity/low ADA activity joint genotype was positively associated with high glycemic levels and with high body mass index (BMI) values.
223	15281007	Low ACP1 activity/high ADA activity joint genotype was also positively associated with dyslipidemia.
224	15281007	These findings suggest that both ACP1 and ADA contribute to the clinical manifestations of type 2 diabetes and probably also have a marginal influence on susceptibility to the disease.
225	15281007	Type 2 diabetes and the genetics of signal transduction: a study of interaction between adenosine deaminase and acid phosphatase locus 1 polymorphisms.
226	15281007	Acid phosphatase locus 1 (ACP1) is a highly polymorphic enzyme that has an important role in flavoenzyme activity and in the control of insulin receptor activity and band 3 protein phosphorylation status.
227	15281007	Based on the hypothesis that ACP1 counteracts insulin signaling by dephosphorylating the insulin receptor and that adenosine has an anti-insulin action, we reasoned that low ACP1 activity (low dephosphorylating action on insulin receptor) when associated with high ADA activity (low adenosine concentration) would result in a cumulative effect towards an increased glucose tolerance.
228	15281007	On the contrary, high ACP1 activity when associated with low ADA activity would result in a cumulative effect towards a decreased glucose tolerance.
229	15281007	There was a nonsignificant trend toward an increase in the proportion of subjects with the complex type with high ACP1 activity and low ADA activity (ie, B/B; A/C; B/C; C/C//ADA1/2 and 2/2) in type 2 diabetes relative to that observed in newborn infants from the same population.
230	15281007	High ACP1 activity/low ADA activity joint genotype was positively associated with high glycemic levels and with high body mass index (BMI) values.
231	15281007	Low ACP1 activity/high ADA activity joint genotype was also positively associated with dyslipidemia.
232	15281007	These findings suggest that both ACP1 and ADA contribute to the clinical manifestations of type 2 diabetes and probably also have a marginal influence on susceptibility to the disease.
233	15281007	Type 2 diabetes and the genetics of signal transduction: a study of interaction between adenosine deaminase and acid phosphatase locus 1 polymorphisms.
234	15281007	Acid phosphatase locus 1 (ACP1) is a highly polymorphic enzyme that has an important role in flavoenzyme activity and in the control of insulin receptor activity and band 3 protein phosphorylation status.
235	15281007	Based on the hypothesis that ACP1 counteracts insulin signaling by dephosphorylating the insulin receptor and that adenosine has an anti-insulin action, we reasoned that low ACP1 activity (low dephosphorylating action on insulin receptor) when associated with high ADA activity (low adenosine concentration) would result in a cumulative effect towards an increased glucose tolerance.
236	15281007	On the contrary, high ACP1 activity when associated with low ADA activity would result in a cumulative effect towards a decreased glucose tolerance.
237	15281007	There was a nonsignificant trend toward an increase in the proportion of subjects with the complex type with high ACP1 activity and low ADA activity (ie, B/B; A/C; B/C; C/C//ADA1/2 and 2/2) in type 2 diabetes relative to that observed in newborn infants from the same population.
238	15281007	High ACP1 activity/low ADA activity joint genotype was positively associated with high glycemic levels and with high body mass index (BMI) values.
239	15281007	Low ACP1 activity/high ADA activity joint genotype was also positively associated with dyslipidemia.
240	15281007	These findings suggest that both ACP1 and ADA contribute to the clinical manifestations of type 2 diabetes and probably also have a marginal influence on susceptibility to the disease.
241	15281007	Type 2 diabetes and the genetics of signal transduction: a study of interaction between adenosine deaminase and acid phosphatase locus 1 polymorphisms.
242	15281007	Acid phosphatase locus 1 (ACP1) is a highly polymorphic enzyme that has an important role in flavoenzyme activity and in the control of insulin receptor activity and band 3 protein phosphorylation status.
243	15281007	Based on the hypothesis that ACP1 counteracts insulin signaling by dephosphorylating the insulin receptor and that adenosine has an anti-insulin action, we reasoned that low ACP1 activity (low dephosphorylating action on insulin receptor) when associated with high ADA activity (low adenosine concentration) would result in a cumulative effect towards an increased glucose tolerance.
244	15281007	On the contrary, high ACP1 activity when associated with low ADA activity would result in a cumulative effect towards a decreased glucose tolerance.
245	15281007	There was a nonsignificant trend toward an increase in the proportion of subjects with the complex type with high ACP1 activity and low ADA activity (ie, B/B; A/C; B/C; C/C//ADA1/2 and 2/2) in type 2 diabetes relative to that observed in newborn infants from the same population.
246	15281007	High ACP1 activity/low ADA activity joint genotype was positively associated with high glycemic levels and with high body mass index (BMI) values.
247	15281007	Low ACP1 activity/high ADA activity joint genotype was also positively associated with dyslipidemia.
248	15281007	These findings suggest that both ACP1 and ADA contribute to the clinical manifestations of type 2 diabetes and probably also have a marginal influence on susceptibility to the disease.
249	15281007	Type 2 diabetes and the genetics of signal transduction: a study of interaction between adenosine deaminase and acid phosphatase locus 1 polymorphisms.
250	15281007	Acid phosphatase locus 1 (ACP1) is a highly polymorphic enzyme that has an important role in flavoenzyme activity and in the control of insulin receptor activity and band 3 protein phosphorylation status.
251	15281007	Based on the hypothesis that ACP1 counteracts insulin signaling by dephosphorylating the insulin receptor and that adenosine has an anti-insulin action, we reasoned that low ACP1 activity (low dephosphorylating action on insulin receptor) when associated with high ADA activity (low adenosine concentration) would result in a cumulative effect towards an increased glucose tolerance.
252	15281007	On the contrary, high ACP1 activity when associated with low ADA activity would result in a cumulative effect towards a decreased glucose tolerance.
253	15281007	There was a nonsignificant trend toward an increase in the proportion of subjects with the complex type with high ACP1 activity and low ADA activity (ie, B/B; A/C; B/C; C/C//ADA1/2 and 2/2) in type 2 diabetes relative to that observed in newborn infants from the same population.
254	15281007	High ACP1 activity/low ADA activity joint genotype was positively associated with high glycemic levels and with high body mass index (BMI) values.
255	15281007	Low ACP1 activity/high ADA activity joint genotype was also positively associated with dyslipidemia.
256	15281007	These findings suggest that both ACP1 and ADA contribute to the clinical manifestations of type 2 diabetes and probably also have a marginal influence on susceptibility to the disease.
257	15281007	Type 2 diabetes and the genetics of signal transduction: a study of interaction between adenosine deaminase and acid phosphatase locus 1 polymorphisms.
258	15281007	Acid phosphatase locus 1 (ACP1) is a highly polymorphic enzyme that has an important role in flavoenzyme activity and in the control of insulin receptor activity and band 3 protein phosphorylation status.
259	15281007	Based on the hypothesis that ACP1 counteracts insulin signaling by dephosphorylating the insulin receptor and that adenosine has an anti-insulin action, we reasoned that low ACP1 activity (low dephosphorylating action on insulin receptor) when associated with high ADA activity (low adenosine concentration) would result in a cumulative effect towards an increased glucose tolerance.
260	15281007	On the contrary, high ACP1 activity when associated with low ADA activity would result in a cumulative effect towards a decreased glucose tolerance.
261	15281007	There was a nonsignificant trend toward an increase in the proportion of subjects with the complex type with high ACP1 activity and low ADA activity (ie, B/B; A/C; B/C; C/C//ADA1/2 and 2/2) in type 2 diabetes relative to that observed in newborn infants from the same population.
262	15281007	High ACP1 activity/low ADA activity joint genotype was positively associated with high glycemic levels and with high body mass index (BMI) values.
263	15281007	Low ACP1 activity/high ADA activity joint genotype was also positively associated with dyslipidemia.
264	15281007	These findings suggest that both ACP1 and ADA contribute to the clinical manifestations of type 2 diabetes and probably also have a marginal influence on susceptibility to the disease.
265	16103269	Platelet-derived growth factor (PDGF)-BB (25 ng/mL) increased DNA synthesis ([3H]thymidine incorporation), cellular proliferation (cell number), collagen synthesis ([3H]proline incorporation), and mitogen-activated protein kinase (MAPK) activity, and these effects were attenuated by 2-chloroadenosine (nonselective AR agonist) and 5'-N-methylcarboxamidoadenosine (MECA; nonselective AR agonist), but not by N6-cyclopentyladenosine (selective A1 AR agonist), AB-N-MECA (selective A3 AR agonist), or CGS21680 (selective A(2A) AR agonist).
266	16103269	Antisense, but not sense or scrambled, oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory effects of 2-chloroadenosine, 5'-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides to the A(2B) receptor.
267	16277212	The content of malonic dialdehyde, diene conjugates, ketodienes, middle-weight molecules, primary and secondary products of lipid peroxidation (LPO), and Schiff bases and the activity of catalase, glutathione peroxidase, and adenosine deaminase in erytrocytes have been evaluated.
268	16369729	Isolated rat cardiomyocytes displayed the presence of detectable amounts of mRNA for ENT1, ENT2, CNT1, and CNT2.
269	16369729	The expression level of equilibrative transporters (ENT1, ENT2) decreased and of concentrative transporters (CNT1, CNT2) increased in myocytes isolated from diabetic rat.
270	16369729	The activity of ecto-5'-nucleotidase increased 2-fold in diabetic cells resulting in a rise of the activity ratio of ecto-5'-nucleotidase/adenosine deaminase from 28 to 56.These results indicate that in rat cardiomyocytes diabetes alters activities of adenosine metabolizing enzymes in such a way that conversion of AMP to IMP is favored in the cytosolic compartment, whereas the capability to produce adenosine extracellularly is increased.
271	18436980	The effect of experimental diabetes on the circadian pattern of adenosine deaminase and myeloperoxidase activities in rat liver.
272	18436980	This study investigated time-dependent variations in the activities of adenosine deaminase (ADA), an adenosine-metabolizing enzyme, and myeloperoxidase (MPO), an oxidation reaction-catalyzing enzyme, in control and streptozotocin (STZ)-induced diabetic rat liver.
273	18436980	The hepatic activity of ADA did not change depending on the STZ treatment whereas MPO activity was significantly higher in the diabetics than in the controls.
274	18436980	The effect of experimental diabetes on the circadian pattern of adenosine deaminase and myeloperoxidase activities in rat liver.
275	18436980	This study investigated time-dependent variations in the activities of adenosine deaminase (ADA), an adenosine-metabolizing enzyme, and myeloperoxidase (MPO), an oxidation reaction-catalyzing enzyme, in control and streptozotocin (STZ)-induced diabetic rat liver.
276	18436980	The hepatic activity of ADA did not change depending on the STZ treatment whereas MPO activity was significantly higher in the diabetics than in the controls.
277	18436980	The effect of experimental diabetes on the circadian pattern of adenosine deaminase and myeloperoxidase activities in rat liver.
278	18436980	This study investigated time-dependent variations in the activities of adenosine deaminase (ADA), an adenosine-metabolizing enzyme, and myeloperoxidase (MPO), an oxidation reaction-catalyzing enzyme, in control and streptozotocin (STZ)-induced diabetic rat liver.
279	18436980	The hepatic activity of ADA did not change depending on the STZ treatment whereas MPO activity was significantly higher in the diabetics than in the controls.
280	18924059	The monitoring of patients treated with atypics, which has been recommended in the APA/ADA Consensus Paper in light of these facts, is insufficiently established in clinical practice.
281	19738938	The activity of adenosine deaminase in the cytosolic fraction was very low and was not affected by different glucose concentration, but in the membrane fraction of cells cultured with 25 mM glucose it was decreased by about 35% comparing to the activity in cells maintained in 5 mM glucose, irrespective of insulin concentration.
282	19738938	Neither insulin nor glucose had an effect on adenosine kinase (AK) activity in SKW 6.4 cells or in human B cells isolated from peripheral blood.
283	19845893	AMP deaminase-1 (AMPD1, C34T) and adenosine deaminase (ADA, G22A), were analyzed.
284	19845893	There were no associations between AMPD1 C34T or ADA G22A genotypes and TNF-alpha or its receptors.
285	19845893	AMP deaminase-1 (AMPD1, C34T) and adenosine deaminase (ADA, G22A), were analyzed.
286	19845893	There were no associations between AMPD1 C34T or ADA G22A genotypes and TNF-alpha or its receptors.
287	20048219	Metabolic testing rates in 3 state Medicaid programs after FDA warnings and ADA/APA recommendations for second-generation antipsychotic drugs.
288	20805743	In this article, we confirm the positive association of acid phosphatase locus 1 (ACP1)A/adenosine deaminase locus 1 (ADA1)2 gametic type with type 1 diabetes (T1D) previously reported and show a negative correlation between the frequency of this gametic type with past malarial morbidity in Sardinia.
289	20805743	Because ADA12 allele decreases the activity of A allele and since low ACP1 activity decreases Zeta-chain-associated protein kinase with molecular weight 70 kDa (Zap70) activity resulting in weak T-cell receptor signalling an epistatic interaction involving ADA1, ACP1 and Zap70 seems a likely mechanism for the associations observed.
290	21198750	Human CD26 has dipeptidyl peptidase-4 (DPP IV) enzyme activity and binds to adenosine deaminase (ADA).
291	21198750	Wildtype soluble recombinant human CD26 (srhCD26), an enzyme inactive mutant (srhCD26E-) and an ADA non-binding mutant (srhCD26A-) were co-incubated in in vitro T-cell proliferation assays with peripheral blood mononuclear cells (PBMC) stimulated with phytohaemagglutinin (PHA), muromonab-CD3 or Herpes simplex virus antigen (HSV Ag).
292	21198750	Thus, effects of soluble human CD26 on human T-cell proliferation are mechanistically independent of both the enzyme activity and the ADA-binding capability of sCD26.
293	21198750	Human CD26 has dipeptidyl peptidase-4 (DPP IV) enzyme activity and binds to adenosine deaminase (ADA).
294	21198750	Wildtype soluble recombinant human CD26 (srhCD26), an enzyme inactive mutant (srhCD26E-) and an ADA non-binding mutant (srhCD26A-) were co-incubated in in vitro T-cell proliferation assays with peripheral blood mononuclear cells (PBMC) stimulated with phytohaemagglutinin (PHA), muromonab-CD3 or Herpes simplex virus antigen (HSV Ag).
295	21198750	Thus, effects of soluble human CD26 on human T-cell proliferation are mechanistically independent of both the enzyme activity and the ADA-binding capability of sCD26.
296	21198750	Human CD26 has dipeptidyl peptidase-4 (DPP IV) enzyme activity and binds to adenosine deaminase (ADA).
297	21198750	Wildtype soluble recombinant human CD26 (srhCD26), an enzyme inactive mutant (srhCD26E-) and an ADA non-binding mutant (srhCD26A-) were co-incubated in in vitro T-cell proliferation assays with peripheral blood mononuclear cells (PBMC) stimulated with phytohaemagglutinin (PHA), muromonab-CD3 or Herpes simplex virus antigen (HSV Ag).
298	21198750	Thus, effects of soluble human CD26 on human T-cell proliferation are mechanistically independent of both the enzyme activity and the ADA-binding capability of sCD26.
299	21614532	The main objective of this study was to investigate the CD26 expression and its relationship with adenosine deaminase (ADA), dipeptidyl peptidase IV (DPP-IV), γ-glutamyltransferase (GGT), and N-acetyl-β-glucosaminidase (NAG) activities in lymphocytes of type 2 diabetics (T2DM) patients.
300	21614532	We observed a decrease in CD26 expression and a significant increase in the ADA activity in T2DM patients when compared with control subjects.
301	21614532	There were no differences between activities of DPP-IV, NAG, and GGT in lymphocytes of T2DM patients and control subjects.
302	21614532	Moreover, a positive correlation was found between DPPIV and ADA activities.
303	21614532	The main objective of this study was to investigate the CD26 expression and its relationship with adenosine deaminase (ADA), dipeptidyl peptidase IV (DPP-IV), γ-glutamyltransferase (GGT), and N-acetyl-β-glucosaminidase (NAG) activities in lymphocytes of type 2 diabetics (T2DM) patients.
304	21614532	We observed a decrease in CD26 expression and a significant increase in the ADA activity in T2DM patients when compared with control subjects.
305	21614532	There were no differences between activities of DPP-IV, NAG, and GGT in lymphocytes of T2DM patients and control subjects.
306	21614532	Moreover, a positive correlation was found between DPPIV and ADA activities.
307	21614532	The main objective of this study was to investigate the CD26 expression and its relationship with adenosine deaminase (ADA), dipeptidyl peptidase IV (DPP-IV), γ-glutamyltransferase (GGT), and N-acetyl-β-glucosaminidase (NAG) activities in lymphocytes of type 2 diabetics (T2DM) patients.
308	21614532	We observed a decrease in CD26 expression and a significant increase in the ADA activity in T2DM patients when compared with control subjects.
309	21614532	There were no differences between activities of DPP-IV, NAG, and GGT in lymphocytes of T2DM patients and control subjects.
310	21614532	Moreover, a positive correlation was found between DPPIV and ADA activities.
311	21697546	The abundance of adenosine deaminase was considerably down-regulated in diabetic myotubes and as the protein binds propyl dipeptidase (DPP-IV), we speculate whether the reduced binding of adenosine deaminase to DPP-IV may contribute to the diabetic phenotype in vivo by leading to a higher level of free DPP-IV to bind and inactivate the anti-diabetic hormones, glucagon-like peptide-1 and glucose-dependent insulintropic polypeptide.
312	21737173	The aim of the present study was to investigate the effects of Syzygium cumini leaf extract (ASc), on Adenosine deaminase (ADA) and Acetylcholinesterase (AChE) activities, and also on oxidative stress parameters in erythrocytes hemolysates (RBCs) and erythrocytes membranes (ghosts) from type 2 diabetics patients (Type 2 DM) under in vitro conditions.
313	21737173	Non protein thiol groups (NP-SH), AChE, Catalase (CAT) and Superoxide Dismutase (SOD) activities were measure in RBCs.
314	21737173	The results demonstrated that ADA and AChE activities, besides TBARS levels were higher in erythrocytes of Type 2 DM, while SOD activity and NP-SH levels were decreased when compared to control group.
315	21737173	The aim of the present study was to investigate the effects of Syzygium cumini leaf extract (ASc), on Adenosine deaminase (ADA) and Acetylcholinesterase (AChE) activities, and also on oxidative stress parameters in erythrocytes hemolysates (RBCs) and erythrocytes membranes (ghosts) from type 2 diabetics patients (Type 2 DM) under in vitro conditions.
316	21737173	Non protein thiol groups (NP-SH), AChE, Catalase (CAT) and Superoxide Dismutase (SOD) activities were measure in RBCs.
317	21737173	The results demonstrated that ADA and AChE activities, besides TBARS levels were higher in erythrocytes of Type 2 DM, while SOD activity and NP-SH levels were decreased when compared to control group.
318	22210125	A single nucleotide polymorphism of the adenosine deaminase, RNA-specific gene is associated with the serum triglyceride level, abdominal circumference, and serum adiponectin concentration.
319	22956389	This study investigated the ex vivo effects of the moderate red wine (RW) and grape juice (GJ) consumption, and the in vitro effects of the resveratrol, caffeic acid, gallic acid, quercetin, and rutin on NTPDase (nucleoside triphosphate diphosphohydrolase), ecto-nucleotide pyrophosphatase/phosphodiesterase (E-NPP), 5'-nucleotidase, and adenosine deaminase (ADA) activities in platelets and platelet aggregation from streptozotocin-induced diabetic rats.
320	23685153	Extracellular concentrations of adenosine are regulated by the interplay of equiliberative nucleoside transporter (ENT)s with enzymes of adenosine metabolism including adenosine deaminase-1 (ADA1), adenosine kinase (AK) and CD73.
321	23840723	In this study, we used primary mixed cultures of rat retinal cells exposed to high glucose conditions, to mimic hyperglycemia, and a streptozotocin rat model of type 1 diabetes to determine the effect diabetes/hyperglycemia have on the expression and protein levels of adenosine receptors and of the enzymes adenosine deaminase and adenosine kinase.
322	23840723	Adenosine deaminase and adenosine kinase expression and protein levels showed a significant decrease in diabetic retinas 30 days after diabetes induction.
323	23840723	In this study, we used primary mixed cultures of rat retinal cells exposed to high glucose conditions, to mimic hyperglycemia, and a streptozotocin rat model of type 1 diabetes to determine the effect diabetes/hyperglycemia have on the expression and protein levels of adenosine receptors and of the enzymes adenosine deaminase and adenosine kinase.
324	23840723	Adenosine deaminase and adenosine kinase expression and protein levels showed a significant decrease in diabetic retinas 30 days after diabetes induction.