Ignet

Gene Information

Gene symbol: COL9A3

Gene name: collagen, type IX, alpha 3

HGNC ID: 2219

Synonyms: IDD, MED, EDM3, FLJ90759, DJ885L7.4.1

Related Genes

#	Gene Symbol	Number of hits
1	ALB	1 hits
2	APOA1	1 hits
3	AXPC1	1 hits
4	CD4	1 hits
5	CPB2	1 hits
6	FCP1	1 hits
7	GIP	1 hits
8	HLA-A	1 hits
9	IDDM2	1 hits
10	IL10	1 hits
11	INS	1 hits
12	LPAL2	1 hits
13	LPL	1 hits
14	MBNL1	1 hits
15	PDCD1	1 hits
16	TNFRSF10A	1 hits
17	TNFRSF25	1 hits
18	ZDHHC23	1 hits

Related Sentences

#	PMID	Sentence
1	2140181	Urinary (CPU) and plasma C peptide values at baseline (CP0) and under stimulation with glucagon were determined in healthy subjects (n = 17) and in insulin-dependent (IDD, n = 45) and non insulin-dependent (NIDD, n = 32) diabetics.
2	2140181	SD) was found on the one hand between the IDD group (CPU = 5.58 +/- 5.58 nmol/24 h; CP = 0.14 +/- 0.08 nmol/l; maximum C peptide value after stimulation (CPmax) = 0.33 +/- 0.31 nmol/l; C peptide delta (delta CP) = 0.14 +/- 0.14 nmol/l; area under the curve (A) = 5.00 +/- 4.84) and the NIDD group (CPU = 15.47 +/- 8.22 nmol/24 h; CP = 0.64 +/- 0.28 nmol/l; CPmax = 1.14 +/- 0.44 nmol/l; delta CP = 0.50 +/- 0.31 nmol/l; A = 17.5 +/- 5.86) and on the other hand between the IDD group and the control group (CPU = 18.20 +/- 8.40 nmol/24 h; CP = 0.41 +/- 0.11 nmol/l; CPmax = 1.00 +/- 0.31 nmol/l; delta CP = 0.69 +/- 0.20 nmol/l; A = 17.10 +/- 4.45).
3	2377077	These data suggest that in both IDD and NIDD patients, there may be a relation between these modifications in the RBC lipid composition and rheological impairment of the RBC.
4	2648798	No significant differences were seen between lean and obese NIDDs and IDDs.
5	2676279	During the last 25 years the concept of a chronic autoimmune process leading to the development of insulin dependent diabetes (IDD) has emerged.
6	2676279	The initial description of linkage disequilibrium of HLA DR3 and DR4 alleles with IDD has now progressed to the molecular level with the identification of residue 57 of the HLA DQ beta chain as crucial to the genetic predisposition to IDD.
7	2676279	However, some therapies in the animal models, not typically considered immunologic, such as protein restriction and insulin therapy, have prevented IDD.
8	2676279	During the last 25 years the concept of a chronic autoimmune process leading to the development of insulin dependent diabetes (IDD) has emerged.
9	2676279	The initial description of linkage disequilibrium of HLA DR3 and DR4 alleles with IDD has now progressed to the molecular level with the identification of residue 57 of the HLA DQ beta chain as crucial to the genetic predisposition to IDD.
10	2676279	However, some therapies in the animal models, not typically considered immunologic, such as protein restriction and insulin therapy, have prevented IDD.
11	2676279	During the last 25 years the concept of a chronic autoimmune process leading to the development of insulin dependent diabetes (IDD) has emerged.
12	2676279	The initial description of linkage disequilibrium of HLA DR3 and DR4 alleles with IDD has now progressed to the molecular level with the identification of residue 57 of the HLA DQ beta chain as crucial to the genetic predisposition to IDD.
13	2676279	However, some therapies in the animal models, not typically considered immunologic, such as protein restriction and insulin therapy, have prevented IDD.
14	2677232	The maximal in crement of serum C-peptide (delta CP) after glucagon stimulation in the controls was higher than in IDD and NIDD (p less than 0.01), and there was a gap between IDD (less than or equal to 0.69 ng/ml) and NIDD (1.20 ng/ml).
15	2677232	In the controls, IDD and NIDD, the FCP was correlated well with delta CP (r = 0.61, 0.93 and 0.59) but not with fasting plasma glucose (r = 0.19, -0.08 and 0.23).
16	2677232	The maximal in crement of serum C-peptide (delta CP) after glucagon stimulation in the controls was higher than in IDD and NIDD (p less than 0.01), and there was a gap between IDD (less than or equal to 0.69 ng/ml) and NIDD (1.20 ng/ml).
17	2677232	In the controls, IDD and NIDD, the FCP was correlated well with delta CP (r = 0.61, 0.93 and 0.59) but not with fasting plasma glucose (r = 0.19, -0.08 and 0.23).
18	2881884	In contrast, the DQ3.DR4.b DQ beta haplotype was significantly decreased in IDD-associated DR4 chromosomes (P = 0.04).
19	2938403	Values for IDD and NIDD were 48.55 +/- 5.97 and 34.68 +/- 3.08 microgram/ml, respectively, for HRBC RIA test and 0.53 +/- 0.07 and 0.41 +/- 0.04 O.D., respectively, for PEG test, while control values were 26.63 +/- 2.12 microgram/ml for HRBC RIA test and 0.26 +/- 0.03 O.D. for PEG test.
20	2938403	An increase in the proportion of cells bearing surface IgG was observed in IDD and NIDD patients when compared to controls.
21	2938403	Values for IDD and NIDD were 48.55 +/- 5.97 and 34.68 +/- 3.08 microgram/ml, respectively, for HRBC RIA test and 0.53 +/- 0.07 and 0.41 +/- 0.04 O.D., respectively, for PEG test, while control values were 26.63 +/- 2.12 microgram/ml for HRBC RIA test and 0.26 +/- 0.03 O.D. for PEG test.
22	2938403	An increase in the proportion of cells bearing surface IgG was observed in IDD and NIDD patients when compared to controls.
23	2994452	Blending of cooked beans made no difference to plasma glucose, insulin, or GIP (gastric inhibitory polypeptide) responses in nondiabetics, NIDD (noninsulin-dependent diabetics), and IDD (insulin-dependent diabetics).
24	2994452	In NIDD and IDD, however, the reverse applied for plasma glucose.
25	3155150	Environmental agents have been implicated in the pathogenesis of insulin dependent diabetes (IDD).
26	3245392	Glycated serum proteins (GSP), stable glycated hemoglobin (HbA1c) together with some metabolic parameters were evaluated in 120 subjects, 30 with normal glucose tolerance (NGT), 30 with impaired glucose tolerance (IGT), 30 with non-insulin-dependent diabetes mellitus (NIDD), and 30 with insulin-dependent diabetes mellitus (IDD).
27	3245392	GSP levels were significantly higher in IGT, NIDD and IDD than in NGT.
28	3259888	Data from IDD and NIDD males, under and over 50 years of age, and of IDD and NIDD females, pre- and postmenopausal, were compared with the respective control group data after matching each diabetic subject to a non-diabetic one of identical age and menstrual history and of comparable body mass index.
29	3298936	The effect of highly purified natural porcine GIP on C-peptide release was examined in six type I (insulin-dependent) diabetics (IDD) with residual beta-cell function, six type II non-insulin-dependent) diabetics (NIDD), and six normal subjects.
30	3298936	In all subjects plasma, C-peptide increased more after 10 minutes of GIP infusion (IDD, 0.48 +/- 0.05; NIDD, 0.79 +/- 0.11; normal subjects, 2.27 +/- 0.29 nmol/L) than on the corresponding day with NaCl infusion (IDD, 0.35 +/- 0.03; NIDD, 0.62 +/- 0.08; normal subjects, 1.22 +/- 0.13 nmol/L, P less than .05 for all).
31	3298936	In the presence of a plasma glucose concentration of 8 mmol/L, physiologic concentrations of porcine GIP caused an immediate but impaired beta-cell response in IDD and NIDD patients.
32	3298936	The effect of highly purified natural porcine GIP on C-peptide release was examined in six type I (insulin-dependent) diabetics (IDD) with residual beta-cell function, six type II non-insulin-dependent) diabetics (NIDD), and six normal subjects.
33	3298936	In all subjects plasma, C-peptide increased more after 10 minutes of GIP infusion (IDD, 0.48 +/- 0.05; NIDD, 0.79 +/- 0.11; normal subjects, 2.27 +/- 0.29 nmol/L) than on the corresponding day with NaCl infusion (IDD, 0.35 +/- 0.03; NIDD, 0.62 +/- 0.08; normal subjects, 1.22 +/- 0.13 nmol/L, P less than .05 for all).
34	3298936	In the presence of a plasma glucose concentration of 8 mmol/L, physiologic concentrations of porcine GIP caused an immediate but impaired beta-cell response in IDD and NIDD patients.
35	3407375	We found that the chemiluminescence (CL) emitted by opsonized zymosan (Zop) stimulated neutrophils in IDD and NIDD patients was significantly increased when compared to healthy subjects (p less than 0.01 and p less than 0.02, respectively).
36	3407375	The percentage of neutrophils with functional C3b receptors was normal in diabetic patients; however, the proportion of phagocytic cells through Fc receptors was significantly decreased in both types of patients (p less than 0.05 and p less than 0.01 for IDD and NIDD, respectively).
37	3407375	We found that the chemiluminescence (CL) emitted by opsonized zymosan (Zop) stimulated neutrophils in IDD and NIDD patients was significantly increased when compared to healthy subjects (p less than 0.01 and p less than 0.02, respectively).
38	3407375	The percentage of neutrophils with functional C3b receptors was normal in diabetic patients; however, the proportion of phagocytic cells through Fc receptors was significantly decreased in both types of patients (p less than 0.05 and p less than 0.01 for IDD and NIDD, respectively).
39	3666672	Both IDD and NIDD patients had significantly higher values of chemiluminescence and CIC than normal controls.
40	3720498	Urinary albumin, measured by radioimmunoassay, was evaluated as a method to assess early renal impairment in 76 insulin (IDD) and 36 noninsulin (NIDD)-dependent diabetic patients.
41	3720498	Mean albumin excretion in IDD and NIDD patients was significantly higher at 23 and 12 micrograms/100 ml glomerular filtrate (GF) respectively, compared to 4 micrograms/100 ml GF in normal subjects (P less than 0.001 and P less than 0.05).
42	3720498	Albumin excretion was significantly increased in hypertensive IDD and NIDD patients.
43	3720498	Significant correlations between albumin excretion and age, duration of diabetes and creatinine clearance were observed, but albumin excretion did not correlate with hemoglobin A1C.
44	3720498	Urinary albumin, measured by radioimmunoassay, was evaluated as a method to assess early renal impairment in 76 insulin (IDD) and 36 noninsulin (NIDD)-dependent diabetic patients.
45	3720498	Mean albumin excretion in IDD and NIDD patients was significantly higher at 23 and 12 micrograms/100 ml glomerular filtrate (GF) respectively, compared to 4 micrograms/100 ml GF in normal subjects (P less than 0.001 and P less than 0.05).
46	3720498	Albumin excretion was significantly increased in hypertensive IDD and NIDD patients.
47	3720498	Significant correlations between albumin excretion and age, duration of diabetes and creatinine clearance were observed, but albumin excretion did not correlate with hemoglobin A1C.
48	3995872	These results indicate that the increase in capillary density and lipoprotein-lipase activity that occurs in healthy young individuals as an effect of endurance training does not take place in obese, NIDD and IDD patients.
49	6229255	Concentrations of HDL cholesterol, apolipoprotein (apo) A-I and apo A-II were found to be significantly decreased in patients with insulin-dependent diabetes (IDD) and non-insulin-dependent diabetes (NIDD) compared with carefully selected controls matched for sex, age and body weight.
50	6229255	No correlation between HbA1 and either HDL cholesterol or A-I and A-II was found in IDD and NIDD.
51	6229255	A positive correlation between HbA1 and either triglyceride or VLDL triglyceride was noted in IDD and NIDD.
52	6229255	There was also a positive correlation between insulin dosage in IDD and HDL cholesterol, apolipoprotein A-I and A-II.
53	6229255	Concentrations of HDL cholesterol, apolipoprotein (apo) A-I and apo A-II were found to be significantly decreased in patients with insulin-dependent diabetes (IDD) and non-insulin-dependent diabetes (NIDD) compared with carefully selected controls matched for sex, age and body weight.
54	6229255	No correlation between HbA1 and either HDL cholesterol or A-I and A-II was found in IDD and NIDD.
55	6229255	A positive correlation between HbA1 and either triglyceride or VLDL triglyceride was noted in IDD and NIDD.
56	6229255	There was also a positive correlation between insulin dosage in IDD and HDL cholesterol, apolipoprotein A-I and A-II.
57	6229255	Concentrations of HDL cholesterol, apolipoprotein (apo) A-I and apo A-II were found to be significantly decreased in patients with insulin-dependent diabetes (IDD) and non-insulin-dependent diabetes (NIDD) compared with carefully selected controls matched for sex, age and body weight.
58	6229255	No correlation between HbA1 and either HDL cholesterol or A-I and A-II was found in IDD and NIDD.
59	6229255	A positive correlation between HbA1 and either triglyceride or VLDL triglyceride was noted in IDD and NIDD.
60	6229255	There was also a positive correlation between insulin dosage in IDD and HDL cholesterol, apolipoprotein A-I and A-II.
61	6757023	These data are compatible with the theory of heterogeneity (genetic and/or environmental) of IDD and a possible relationship between IDD and NIDD.
62	6759247	The range of ages at the time of first appearance of PCA was the same as that of onset of insulin-dependent diabetes (IDD) in the BB rats, suggesting that the processes leading to PCA and IDD were occurring at the same time of life in these animals.
63	6820936	Peripheral tissue resistance to the action of insulin is present in all three diabetic conditions; it is moderate in NIDD and IDD and severe in DKA.
64	6820936	Basal hepatic glucose production in NIDD and IDD can be either normal or increased, and correlates closely with the fasting plasma glucose concentration.
65	6820936	Suppression of HGP by insulin is normal in NIDD and IDD but severely impaired in DKA.
66	6820936	Peripheral tissue resistance to the action of insulin is present in all three diabetic conditions; it is moderate in NIDD and IDD and severe in DKA.
67	6820936	Basal hepatic glucose production in NIDD and IDD can be either normal or increased, and correlates closely with the fasting plasma glucose concentration.
68	6820936	Suppression of HGP by insulin is normal in NIDD and IDD but severely impaired in DKA.
69	6820936	Peripheral tissue resistance to the action of insulin is present in all three diabetic conditions; it is moderate in NIDD and IDD and severe in DKA.
70	6820936	Basal hepatic glucose production in NIDD and IDD can be either normal or increased, and correlates closely with the fasting plasma glucose concentration.
71	6820936	Suppression of HGP by insulin is normal in NIDD and IDD but severely impaired in DKA.
72	6950819	Histocompatibility (HLA) antigens and genotypes B, D and DR were studied in large sample of Caucasian insulin dependent diabetic (IDD) probands.
73	6950819	The associations between IDD and B8, B15, Dw3, Dw4, and DR3, and DR4 were measured by relative risks (RR) and delta values.
74	6950819	Histocompatibility (HLA) antigens and genotypes B, D and DR were studied in large sample of Caucasian insulin dependent diabetic (IDD) probands.
75	6950819	The associations between IDD and B8, B15, Dw3, Dw4, and DR3, and DR4 were measured by relative risks (RR) and delta values.
76	7044630	An islet cell antibody negative form of insulin-dependent diabetes mellitus (IDD) associated with HLA antigens A9 and Bw16.
77	7044630	One hundred and sixty-six unrelated children and adolescents having growth-onset, insulin-dependent diabetes mellitus (IDD) were studied for pancreatic-cytoplasmic islet cell antibodies (ICA) at various times from the diagnosis of the disease.
78	7044630	An islet cell antibody negative form of insulin-dependent diabetes mellitus (IDD) associated with HLA antigens A9 and Bw16.
79	7044630	One hundred and sixty-six unrelated children and adolescents having growth-onset, insulin-dependent diabetes mellitus (IDD) were studied for pancreatic-cytoplasmic islet cell antibodies (ICA) at various times from the diagnosis of the disease.
80	7173496	Thyroid microsomal autoantibodies were more frequent in patients with IDD and PCA, than in those with IDD alone (Caucasian 46% versus 18%, black 25% versus 2.5%).
81	7612220	The first Idd locus recognized, Idd1, is linked to the major histocompatibility complex (MHC), and its inheritance and expression are a paradigm for the other non-MHC Idd genes.
82	7977341	This analysis allows us to confirm the involvement of INS in IDD, and the best-fitting model is a multiplicative (noninteractive) effect of HLA and INS, with a biallelic locus for INS and a complementation model for HLA.
83	8335082	Extended HLA haplotypes frequencies were estimated from the HLA, C2, Bf and C4 phenotypes of 74 patients with non-insulin-dependent diabetes (NIDD), 92 with juvenile rheumatoid arthritis (JRA), 44 with Berger's disease (BD), 83 with insulin-dependent diabetes (IDD), and 140 healthy controls.
84	8335082	The extended HLA haplotype B18 CF130 DR3 DQw2, which is common (around 10% phenotype frequency) in healthy Spaniards and in other populations of paleo-North African origin, was found to be significantly less frequent in NIDD, JRA and BD, whereas its frequency was normal in IDD (although DR3 DQw2 haplotypes were increased in the latter disease).
85	8335082	These data support the existence of a common HLA-linked pathogeneic mechanism in NIDD, JRA and BD, and point to a genetic difference between IDD and NIDD at the HLA level.
86	8335082	Extended HLA haplotypes frequencies were estimated from the HLA, C2, Bf and C4 phenotypes of 74 patients with non-insulin-dependent diabetes (NIDD), 92 with juvenile rheumatoid arthritis (JRA), 44 with Berger's disease (BD), 83 with insulin-dependent diabetes (IDD), and 140 healthy controls.
87	8335082	The extended HLA haplotype B18 CF130 DR3 DQw2, which is common (around 10% phenotype frequency) in healthy Spaniards and in other populations of paleo-North African origin, was found to be significantly less frequent in NIDD, JRA and BD, whereas its frequency was normal in IDD (although DR3 DQw2 haplotypes were increased in the latter disease).
88	8335082	These data support the existence of a common HLA-linked pathogeneic mechanism in NIDD, JRA and BD, and point to a genetic difference between IDD and NIDD at the HLA level.
89	8335082	Extended HLA haplotypes frequencies were estimated from the HLA, C2, Bf and C4 phenotypes of 74 patients with non-insulin-dependent diabetes (NIDD), 92 with juvenile rheumatoid arthritis (JRA), 44 with Berger's disease (BD), 83 with insulin-dependent diabetes (IDD), and 140 healthy controls.
90	8335082	The extended HLA haplotype B18 CF130 DR3 DQw2, which is common (around 10% phenotype frequency) in healthy Spaniards and in other populations of paleo-North African origin, was found to be significantly less frequent in NIDD, JRA and BD, whereas its frequency was normal in IDD (although DR3 DQw2 haplotypes were increased in the latter disease).
91	8335082	These data support the existence of a common HLA-linked pathogeneic mechanism in NIDD, JRA and BD, and point to a genetic difference between IDD and NIDD at the HLA level.
92	8462206	This method was applied to detect total body water (TBW), fat (FAT) and fat-free mass (FFM) in 80 normal subjects, 65 diabetic (45 insulin-dependent [IDD], 20 non insulin-dependent [NIDD]) and 34 uremic diabetic patients (20 IDD, 14 NIDD) submitted to hemodialysis three times a week.
93	8462206	Sixteen uremic subjects, randomly selected from both IDD and NIDD groups, tested at the beginning and at the end of the same hemodialytic session, showed a significant decrease of TBW which corresponded to the correction of their overhydratation.
94	8676087	Therefore, the ability of IL-10 to overcome the absence of all non-MHC diabetes susceptibility (Idd) alleles was studied in transgenic mice expressing pancreatic IL-10 backcrossed to B10.H2g7 congenic mice, which have no Idd alleles other than NOD MHC (H2g7).
95	8676087	These results suggest that IL-10 may be necessary and sufficient for producing autoimmune diabetes in conjunction with NOD MHC homozygosity and that some Idd genes may be related to the regulation of IL-10.
96	8676087	Therefore, the ability of IL-10 to overcome the absence of all non-MHC diabetes susceptibility (Idd) alleles was studied in transgenic mice expressing pancreatic IL-10 backcrossed to B10.H2g7 congenic mice, which have no Idd alleles other than NOD MHC (H2g7).
97	8676087	These results suggest that IL-10 may be necessary and sufficient for producing autoimmune diabetes in conjunction with NOD MHC homozygosity and that some Idd genes may be related to the regulation of IL-10.
98	8866558	Moreover, giant PVS expression in major histocompatibility complex (MHC) and Idd congenic mice is determined by the genetic background.
99	9519736	Idd1 has been mapped to a class II gene in the major histocompatibility complex (MHC), whereas the products and functions of the remaining Idd loci are unresolved.
100	9519736	To investigate how non-MHC Idd genes regulate islet inflammation and IDDM progression, NOD mice were compared with the nonobese diabetes-resistant (NOR) mouse, a related MHC-identical strain that possesses a subset of the NOD-derived alleles at the Idd loci.
101	9519736	Our data define distinct cellular stages of IDDM pathogenesis in which the impact of Idd genes can be readily analyzed.
102	9519736	Idd1 has been mapped to a class II gene in the major histocompatibility complex (MHC), whereas the products and functions of the remaining Idd loci are unresolved.
103	9519736	To investigate how non-MHC Idd genes regulate islet inflammation and IDDM progression, NOD mice were compared with the nonobese diabetes-resistant (NOR) mouse, a related MHC-identical strain that possesses a subset of the NOD-derived alleles at the Idd loci.
104	9519736	Our data define distinct cellular stages of IDDM pathogenesis in which the impact of Idd genes can be readily analyzed.
105	9519736	Idd1 has been mapped to a class II gene in the major histocompatibility complex (MHC), whereas the products and functions of the remaining Idd loci are unresolved.
106	9519736	To investigate how non-MHC Idd genes regulate islet inflammation and IDDM progression, NOD mice were compared with the nonobese diabetes-resistant (NOR) mouse, a related MHC-identical strain that possesses a subset of the NOD-derived alleles at the Idd loci.
107	9519736	Our data define distinct cellular stages of IDDM pathogenesis in which the impact of Idd genes can be readily analyzed.
108	9570569	NOR IDDM resistance was previously found to be largely controlled by the Idd13 locus within an approximately 24 cM segment on Chromosome 2 encompassing BKS-derived alleles for H3a, B2m, Il1, and Pcna.
109	9570569	Since trans-interactions between relatively common and functionally normal allelic variants may contribute to IDDM in NOD mice, the search for Idd genes in humans should not be limited to functionally defective variants.
110	16087865	Mice deficient in programmed cell death 1 (PD-1, Pdcd1), an immunoinhibitory receptor belonging to the CD28/cytotoxic T lymphocyte-associated antigen-4 family, spontaneously develop lupus-like autoimmune disease and autoimmune dilated cardiomyopathy on C57BL/6 and BALB/c backgrounds, respectively.
111	16087865	The diabetic incidence of NOD-Pdcd1-/- mice was controlled by five genetic loci, including three known recessive loci [Idd (insulin-dependent diabetes) 1, Idd17, and Idd20] and two previously unidentified dominant loci [Iddp (Idd under PD-1 deficiency) 1 and Iddp2].
112	18178847	Genome-wide microarray expression analysis of CD4+ T Cells from nonobese diabetic congenic mice identifies Cd55 (Daf1) and Acadl as candidate genes for type 1 diabetes.
113	18178847	NOD.Idd3/5 congenic mice have insulin-dependent diabetes (Idd) regions on chromosomes 1 (Idd5) and 3 (Idd3) derived from the nondiabetic strains B10 and B6, respectively.
114	18178847	To test the hypothesis that candidate Idd genes can be identified by differential gene expression between activated CD4+ T cells from the diabetes-susceptible NOD strain and the diabetes-resistant NOD.Idd3/5 congenic strain, genome-wide microarray expression analysis was performed using an empirical Bayes method.
115	18178847	The two genes with the greatest differential RNA expression on chromosome 1 were those encoding decay-accelerating factor (DAF, also known as CD55) and acyl-coenzyme A dehydrogenase, long chain, which are located in the Idd5.4 and Idd5.3 regions, respectively.
116	18178847	In the case of DAF, differential expression of mRNA was extended to the protein level; NOD CD4+ T cells expressed higher levels of cell surface DAF compared with NOD.Idd3/5 CD4+ T cells following activation with anti-CD3 and -CD28.
117	18178847	DAF up-regulation was IL-4 dependent and blocked under Th1 conditions.
118	18178847	Genome-wide microarray expression analysis of CD4+ T Cells from nonobese diabetic congenic mice identifies Cd55 (Daf1) and Acadl as candidate genes for type 1 diabetes.
119	18178847	NOD.Idd3/5 congenic mice have insulin-dependent diabetes (Idd) regions on chromosomes 1 (Idd5) and 3 (Idd3) derived from the nondiabetic strains B10 and B6, respectively.
120	18178847	To test the hypothesis that candidate Idd genes can be identified by differential gene expression between activated CD4+ T cells from the diabetes-susceptible NOD strain and the diabetes-resistant NOD.Idd3/5 congenic strain, genome-wide microarray expression analysis was performed using an empirical Bayes method.
121	18178847	The two genes with the greatest differential RNA expression on chromosome 1 were those encoding decay-accelerating factor (DAF, also known as CD55) and acyl-coenzyme A dehydrogenase, long chain, which are located in the Idd5.4 and Idd5.3 regions, respectively.
122	18178847	In the case of DAF, differential expression of mRNA was extended to the protein level; NOD CD4+ T cells expressed higher levels of cell surface DAF compared with NOD.Idd3/5 CD4+ T cells following activation with anti-CD3 and -CD28.
123	18178847	DAF up-regulation was IL-4 dependent and blocked under Th1 conditions.
124	22465205	Insulin-like growth factors (IGFs) are well-known regulators of embryonic growth and differentiation.
125	22465205	In rabbit blastocysts, embryonic IGF1 and IGF2 are specifically strong in the embryoblast (ICM).
126	22465205	Signalling of IGFs and insulin in blastocysts follows the classical pathway with Erk1/2 and Akt kinase activation.
127	22465205	Exp IDD was induced in female rabbits by alloxan treatment prior to mating.
128	22465205	In pregnant females, hepatic IGF1 expression and IGF1 serum levels were decreased while IGF1 and IGF2 were increased in endometrium.
129	22465205	In cultured control blastocysts supplemented with IGF1 or insulin in vitro for 1 or 12 h, IGF1 and insulin receptors as well as IGF1 and IGF2 were downregulated.
130	22465205	In cultured T1D blastocysts activation of Akt and Erk1/2 was impaired with lower amounts of total Akt and Erk1/2 protein and a reduced phosphorylation capacity after IGF1 supplementation.
131	22465205	Both, the endometrium and the blastocyst produce more IGF1 and IGF2.
132	22465205	The increased endogenous IGF1 and IGF2 expression by the blastocyst compensates for the loss of systemic insulin and IGF.
133	22732593	Autoimmune type 1 diabetes (T1D) in humans and NOD mice results from interactions between multiple susceptibility genes (termed Idd) located within and outside the MHC.
134	22732593	Despite sharing ∼88% of their genome with NOD mice, including the H2(g7) MHC haplotype and other important Idd genes, the closely related nonobese resistant (NOR) strain fails to develop T1D because of resistance alleles in residual genomic regions derived from C57BLKS mice mapping to chromosomes (Chr.) 1, 2, and 4.
135	22732593	Autoimmune type 1 diabetes (T1D) in humans and NOD mice results from interactions between multiple susceptibility genes (termed Idd) located within and outside the MHC.
136	22732593	Despite sharing ∼88% of their genome with NOD mice, including the H2(g7) MHC haplotype and other important Idd genes, the closely related nonobese resistant (NOR) strain fails to develop T1D because of resistance alleles in residual genomic regions derived from C57BLKS mice mapping to chromosomes (Chr.) 1, 2, and 4.