Ignet

Gene Information

Gene symbol: ADRA1D

Gene name: adrenoceptor alpha 1D

HGNC ID: 280

Synonyms: ADRA1R, ADRA1A, ADRA1

Related Genes

#	Gene Symbol	Number of hits
1	A2M	1 hits
2	ACE	1 hits
3	ADIPOQ	1 hits
4	AGL	1 hits
5	AGT	1 hits
6	ALB	1 hits
7	ALPI	1 hits
8	APLP2	1 hits
9	APOA1	1 hits
10	ATP1A1	1 hits
11	BGLAP	1 hits
12	CFB	1 hits
13	CGB	1 hits
14	COL19A1	1 hits
15	COL1A1	1 hits
16	COL4A4	1 hits
17	COL4A5	1 hits
18	CP	1 hits
19	CRP	1 hits
20	EDN1	1 hits
21	ELN	1 hits
22	FXYD1	1 hits
23	GNAZ	1 hits
24	HP	1 hits
25	HTR1A	1 hits
26	IL13RA2	1 hits
27	IL4R	1 hits
28	IL6	1 hits
29	INS	1 hits
30	LPAL2	1 hits
31	MGAM	1 hits
32	NOS3	1 hits
33	NPHS1	1 hits
34	ORM1	1 hits
35	ORM2	1 hits
36	PLCB1	1 hits
37	PRKAA1	1 hits
38	PTH	1 hits
39	PYGM	1 hits
40	RUNX1T1	1 hits
41	SERPINA1	1 hits
42	SERPINA3	1 hits
43	SERPINF2	1 hits
44	SI	1 hits
45	SLC12A1	1 hits
46	SLC2A4	1 hits
47	STN	1 hits
48	TF	1 hits
49	TTR	1 hits

Related Sentences

#	PMID	Sentence
1	75	The phosphorylated form of liver glycogen phosphorylase (alpha-1,4-glucan : orthophosphate alpha-glucosyl-transferase, EC 2.4.1.1) (phosphorylase a) is active and easily measured while the dephosphorylated form (phosphorylase b), in contrast to the muscle enzyme, has been reported to be essentially inactive even in the presence of AMP.
2	2478861	In this study, albumin and five acute phase proteins--alpha-1 acid glycoprotein, alpha-1 antitrypsin, haptoglobin, ceruloplasmin, and C-reactive protein--were measured.
3	2478861	Haptoglobin, alpha-1 acid glycoprotein, and C-reactive protein increased markedly in both diabetes and glucose intolerance; ceruloplasmin and alpha-1 antitrypsin increased more marginally.
4	2478861	When diabetics were divided into those with and without clinically detectable evidence of microvascular sequelae, elevation of haptoglobin, C-reactive protein and alpha-1 acid glycoprotein, and depression of albumin were found to progress with number of sequelae.
5	2478861	In this study, albumin and five acute phase proteins--alpha-1 acid glycoprotein, alpha-1 antitrypsin, haptoglobin, ceruloplasmin, and C-reactive protein--were measured.
6	2478861	Haptoglobin, alpha-1 acid glycoprotein, and C-reactive protein increased markedly in both diabetes and glucose intolerance; ceruloplasmin and alpha-1 antitrypsin increased more marginally.
7	2478861	When diabetics were divided into those with and without clinically detectable evidence of microvascular sequelae, elevation of haptoglobin, C-reactive protein and alpha-1 acid glycoprotein, and depression of albumin were found to progress with number of sequelae.
8	2478861	In this study, albumin and five acute phase proteins--alpha-1 acid glycoprotein, alpha-1 antitrypsin, haptoglobin, ceruloplasmin, and C-reactive protein--were measured.
9	2478861	Haptoglobin, alpha-1 acid glycoprotein, and C-reactive protein increased markedly in both diabetes and glucose intolerance; ceruloplasmin and alpha-1 antitrypsin increased more marginally.
10	2478861	When diabetics were divided into those with and without clinically detectable evidence of microvascular sequelae, elevation of haptoglobin, C-reactive protein and alpha-1 acid glycoprotein, and depression of albumin were found to progress with number of sequelae.
11	3117789	LE/2 and 3 do not react with transducin-alpha or Go alpha nor with the 41-kDa form of pertussis toxin substrate in brain, Gi alpha-1.
12	3490232	Early prediction of deep sternal wound infection after heart operations by alpha-1 acid glycoprotein and C-reactive protein measurements.
13	3490232	Serum C-reactive protein (CRP) and alpha 1-acid glycoprotein (AAG) levels were studied in 188 patients undergoing heart operations with cardiopulmonary bypass.
14	3490232	No correlation was found between CRP or AAG and duration of cardiopulmonary bypass, number of blood transfusions, or total protein levels on day 2.
15	7783662	As compared with the lean littermates, heart alpha-subunit-2 of inhibitory G protein (Gi alpha-2), liver Gi alpha-3, and adipocyte G1 alpha-1 and Gi alpha-3 were also reduced in ob/ob mice.
16	7804513	The new antihypertensive agents such as calcium antagonists, angiotensin converting enzyme inhibitors and post-synaptic alpha-1 receptor antagonists have proved to be neutral or to have positive effect on metabolic disturbances.
17	8281906	In man, dose-response relationships are not well established because the curves are obtained with groups of patients and they reflect an overall mean rather than the reality of each individual patient. 2) Secondary regulatory adaptive mechanism such as: down regulation of beta, 5-HT2, alpha-2 receptors--increased reactivity of 5-HT1A, alpha-1 and dopaminergic systems.
18	8599075	Plasma zinc, C-reactive protein, alpha-1 acid glycoprotein, haptoglobin, prealbumin, transferrin, and iron have also been determined in some patients.
19	8599075	We also found a significant positive correlation between urinary zinc and acute phase proteins alpha-1 acid glycoprotein (rs = 0.4649, P < 0.005), haptoglobin (rs = 0.4688, P < 0.005) and C-reactive protein (rs = 0.3636, P < 0.025), as well as a negative correlation with plasma zinc (rs = 0.3640, P < 0.025).
20	8599075	Plasma zinc, C-reactive protein, alpha-1 acid glycoprotein, haptoglobin, prealbumin, transferrin, and iron have also been determined in some patients.
21	8599075	We also found a significant positive correlation between urinary zinc and acute phase proteins alpha-1 acid glycoprotein (rs = 0.4649, P < 0.005), haptoglobin (rs = 0.4688, P < 0.005) and C-reactive protein (rs = 0.3636, P < 0.025), as well as a negative correlation with plasma zinc (rs = 0.3640, P < 0.025).
22	8737033	Serum creatinine, creatinine clearance, urinary excretion of immunoglobulin G, albumin collagen IV (NC1), kappa and lambda chains, alpha-1 microglobulin and Tamm-Horsfall protein were evaluated.
23	8737033	The excretion rates of immunoglobulin G and albumin decreased, whereas the proximal and distal tubular function and the excretion of collagen IV did not change.
24	8916594	The levels of serum albumin, alpha-1 acid glycoprotein, alpha-1 antitrypsin and caeruloplasmin were not significantly different between the patients with retinopathy and controls.
25	8926953	Drug therapy means application of different groups of antihypertensive agents (selective beta-blockers, diuretics, angiotensin-converting enzyme inhibitors, calcium channel antagonists and postsynaptic alpha-1 blockers).
26	9096763	Serum alpha-1 antitrypsin level was 224 (normal 85-213) mg/dL and PI phenotype was M1.
27	9295306	In this study, we examined the potential role of serine/threonine protein phosphatase-1 (PP-1) and PP-2A in the mechanism of Na+/K+-ATPase activation by insulin in the rat skeletal muscle cell line L6.
28	9295306	Immunoprecipitation of the enzyme from 32P-labeled cells with an antibody directed against the alpha-1 subunit of the enzyme revealed a 60% decrease in 110-kDa protein phosphorylation in insulin-treated cells.
29	9295306	To further confirm the role of PP-1, we used L6 cell lines that overexpress the glycogen/SR-associated regulatory subunit of PP-1, PP-1G.
30	9295306	Overexpression of PP-1G resulted in a 3-fold increase in insulin-stimulated PP-1 catalytic activity.
31	9295306	Inhibition of phosphatidylinositol-3 kinase with wortmannin blocked insulin-stimulated PP-1 activation as well as the dephosphorylation and activation of Na+/K+-ATPase.
32	9295306	We conclude that insulin regulates the activity of Na+/K+-ATPase by promoting dephosphorylation of the alpha subunit via an insulin-stimulated PP-1 and that phosphatidylinositol-3 kinase-generated signals may mediate insulin activation of PP-1 and Na+/K+-ATPase.
33	9389420	Serum sialic acid was confirmed as a marker of the acute-phase response since serum concentrations were significantly related to established acute-phase proteins such as alpha-1 acid glycoprotein (r = 0.82, p < 0.0001).
34	9389420	There was a significant graded increase of serum sialic acid, alpha-1 acid glycoprotein, IL-6 and urinary albumin excretion rate amongst the three groups, with the lowest levels in non-diabetic subjects, intermediate levels in NIDDM patients without syndrome X and highest levels in NIDDM patients with syndrome X.
35	9389420	C-reactive protein and cortisol levels were also higher in syndrome X-positive compared to X-negative patients and serum amyloid A was higher in both diabetic groups than in the control group.
36	9389420	Serum sialic acid was confirmed as a marker of the acute-phase response since serum concentrations were significantly related to established acute-phase proteins such as alpha-1 acid glycoprotein (r = 0.82, p < 0.0001).
37	9389420	There was a significant graded increase of serum sialic acid, alpha-1 acid glycoprotein, IL-6 and urinary albumin excretion rate amongst the three groups, with the lowest levels in non-diabetic subjects, intermediate levels in NIDDM patients without syndrome X and highest levels in NIDDM patients with syndrome X.
38	9389420	C-reactive protein and cortisol levels were also higher in syndrome X-positive compared to X-negative patients and serum amyloid A was higher in both diabetic groups than in the control group.
39	9400023	Instead, an increase in the activity of the G proteins or phospholipase C-beta coupled to the alpha-1 adrenoceptor may be mediating the enhanced responsiveness elicited by alpha-1 adrenoceptor stimulation in diabetic arteries.
40	9616209	Evidence for defects in the trafficking and translocation of GLUT4 glucose transporters in skeletal muscle as a cause of human insulin resistance.
41	9616209	Since muscle GLUT4 glucose transporter levels are normal in type 2 diabetes, we have tested the hypothesis that insulin resistance is due to impaired translocation of intracellular GLUT4 to sarcolemma.
42	9616209	In equilibrium fractions from basal muscle, GLUT4 was decreased by 25-29% in both 25 and 28% sucrose density fractions and increased twofold in both the 32% sucrose fraction and bottom pellet in diabetics compared with insulin-sensitive controls, without any differences in membrane markers (phospholemman, phosphalamban, dihydropyridine-binding complex alpha-1 subunit).
43	9616209	Thus, insulin resistance was associated with redistribution of GLUT4 to denser membrane vesicles.
44	9616209	No effects of insulin stimulation on GLUT4 localization were observed.
45	9616209	In non-equilibrium fractions, insulin led to small GLUT4 decrements in the 25 and 28% sucrose fractions and increased GLUT4 in the 32% sucrose fraction by 2.8-fold over basal in insulin-sensitive but only by 1.5-fold in both insulin-resistant and diabetic subgroups.
46	9616209	Similar to GLUT4, the insulin-regulated aminopeptidase (vp165) was redistributed to a dense membrane compartment and did not translocate in response to insulin in insulin-resistant subgroups.
47	9616209	In conclusion, insulin alters the subcellular localization of GLUT4 vesicles in human muscle, and this effect is impaired equally in insulin-resistant subjects with and without diabetes.
48	9616209	Based on these data, we propose that human insulin resistance involves a defect in GLUT4 traffic and targeting leading to accumulation in a dense membrane compartment from which insulin is unable to recruit GLUT4 to the cell surface.
49	9788546	All the diabetic BB rats were hyperglycemic, with an increase of plasma levels of fructosamine, alpha-1 acid glycoprotein, and fibrinogen, and a dramatic decrease of C-peptide level.
50	9794113	Although insulin has been shown to raise plasma concentrations of endothelin (ET) and up regulate vascular smooth muscle ETA receptor expression, the interaction of vanadate, an insulinomimetic agent, with the vascular ET system has not been investigated.
51	9794113	We compared the effects of oral vanadate treatment (0.5 mg/ml; p.o.) and insulin infusion (12 mU.kg-1.min-1 s.c.) for two weeks on plasma ET concentrations and vascular responses to endothelin-1 (ET-1) and the alpha-1 adrenoceptor agonist, methoxamine, in aortic ring preparations from streptozotocin (STZ) diabetic and non-diabetic adult male Sprague-Dawley rats.
52	9794114	Type II (non-insulin-dependent) diabetes mellitus is associated with increased blood concentrations of markers of the acute-phase response, including sialic acid, alpha-1 acid glycoprotein, serum amyloid A, C-reactive protein and cortisol, and the main cytokine mediator of the response, interleukin-6.
53	10480607	These purified human islet MVEC (HI-MVEC) express von Willebrand factor, take up high levels of acetylated LDL, and upregulate endothelial cell leukocyte adhesion molecule 1 in response to tumor necrosis factor-alpha.
54	10480607	We also demonstrate that alpha-1 proteinase inhibitor (Api) is expressed on HI-MVEC and specifically located at the area of cell-cell junctions.
55	10588921	We examined whether N-hydroxyethyl-1-deoxynojirimycin (miglitol), a new human anti-diabetic drug with effects to inhibit alpha-1, 6-glucosidase glycogen debranching enzyme and reduce the glycogenolytic rate as well as to inhibit alpha-1,4-glucosidase, could reduce infarct size in the rabbit heart.
56	11872361	Alpha-1 blockers, ACE-antagonists, long-acting Ca blockers including nifedipine CR, some form of beta-blockers, tilisolor, which is reported to increase blood flow, improve insulin sensitivity when blood pressure is better controlled.
57	11872361	Insulin resistance has been observed in heart failure and is correlated with angiotensin II.
58	11891856	One of these characteristics is the expression of alpha-1 proteinase inhibitor (Api).
59	11891856	In this study, we observed its expression in nonobese diabetic (NOD) mouse IEC, in relation to the occurrence of type 1 diabetes and in response to cytokines, namely IL-1 beta and IL-10.
60	11891856	Furthermore, in cultured NOD IEC, Api expression is downregulated by the addition of IL-1 beta and is upregulated by IL-10; it is always absent in IL-10-deficient NOD mice and overexpressed in IL-10 transgenic NODs, thus further supporting that this cytokine upregulates Api expression.
61	11903396	Brain natriuretic peptide increases urinary albumin and alpha-1 microglobulin excretion in Type 1 diabetes mellitus.
62	12204809	Each statin except fluvastatin improved the HDL subpopulation profile by increasing the concentrations of the large, cholesterol-rich, LpA-I alpha-1 and prealpha-1 HDL subpopulations.
63	12497307	[Serum alpha-1 antitrypsin levels in patients with Cuban epidemic neuropathy].
64	12898314	Two forms of type II collagen, IIA and IIB, are known to be produced by alternative splicing of the Alpha(1) (II) procollagen gene.
65	12911121	The conference "Stem Cell Therapies in Reparative Medicine," held aboard the cruise vessel Majesty of the Seas (Miami, USA-Nassau, Bahamas, April 19-22, 2002), focused on the analysis of these problems from different perspectives, including developmental biology (cell proliferation, fate determination, and enrichment), immunology (allorejection and prevention of autoimmunity recurrence), and clinical therapy, emphasizing the impact of stem cell technologies on the emerging field of tissue engineering and the treatment of alpha-1 antitrypsin deficiency.
66	14593089	RGZ increased whole kidney protein abundance of the alpha-1 subunit of Na-K-ATPase, the bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2), the sodium hydrogen exchanger (NHE3), the aquaporins 2 and 3, and endothelial nitric-oxide synthase.
67	14712302	Recombinant adeno-associated virus-mediated alpha-1 antitrypsin gene therapy prevents type I diabetes in NOD mice.
68	14712302	To test the ability of AAT to modulate the development of type I diabetes, we performed a series of investigations involving recombinant adeno-associated virus vector (rAAV)-mediated gene delivery of human alpha-1 antitrypsin (hAAT) to nonobese diabetic (NOD) mice.
69	14712302	Recombinant AAV-expressing hAAT (rAAV2-CB-AT) was administered intramuscularly to 4-week-old female NOD mice (1 x 10(10) i.u.
70	14712302	This study suggests a potential therapeutic role for AAT in preventing type I diabetes as well as the ability of AAV gene therapy-based approaches to ameliorate disease effectively.
71	14712302	Recombinant adeno-associated virus-mediated alpha-1 antitrypsin gene therapy prevents type I diabetes in NOD mice.
72	14712302	To test the ability of AAT to modulate the development of type I diabetes, we performed a series of investigations involving recombinant adeno-associated virus vector (rAAV)-mediated gene delivery of human alpha-1 antitrypsin (hAAT) to nonobese diabetic (NOD) mice.
73	14712302	Recombinant AAV-expressing hAAT (rAAV2-CB-AT) was administered intramuscularly to 4-week-old female NOD mice (1 x 10(10) i.u.
74	14712302	This study suggests a potential therapeutic role for AAT in preventing type I diabetes as well as the ability of AAV gene therapy-based approaches to ameliorate disease effectively.
75	15082116	Elevated sympathetic activity may promote insulin resistance syndrome by activating alpha-1 adrenergic receptors on adipocytes.
76	15082116	An excess of free intracellular calcium can reduce the efficiency of insulin-mediated glucose transport by blocking the dephosphorylation of GLUT-4.
77	15082116	Classical isoforms of protein kinase C (PKC) can interfere with insulin signalling via serine phosphorylation of IRS-1 and the insulin receptor.
78	15082116	Parathyroid hormone (PTH), by activating phospholipase C-beta in adipocytes, can promote a sustained increase in intracellular free calcium in these cells, while also activating classical PKCs.
79	15082116	This may rationalize the fact that insulin resistance is a typical feature of hyperparathyroidism, as well as epidemiological evidence that regular ingestion of dairy products or of ethanol--which down-regulates PTH secretion--reduces risk for insulin resistance syndrome and diabetes.
80	15082116	Alpha-1 adrenergic receptors of adipocytes--like PTH receptors--also activate phospholipase C-beta, and thus have an effect analogous to PTH on intracellular free calcium and PKC activity in adipocytes.
81	15082116	This suggests that, via activation of alpha-1 adrenergic receptors, increased sympathetic activity in adipose tissue may promote insulin resistance syndrome.
82	15082116	In fact, measures which provoke increased sympathetic output--such as diuretic use and severe salt restriction--are known to compromise insulin sensitivity, whereas alpha-1 antagonist drugs, as well as drugs that act centrally to suppress sympathetic activity, typically have a favorable effect on insulin function.
83	15082116	When insulin resistance syndrome is associated with elevated sympathetic activity--for example, in hypertensives who are obese or on diuretic therapy--measures which down-regulate sympathetic activity, or, more specifically, alpha-1 adrenergic activity, may be warranted.
84	15082116	Elevated sympathetic activity may promote insulin resistance syndrome by activating alpha-1 adrenergic receptors on adipocytes.
85	15082116	An excess of free intracellular calcium can reduce the efficiency of insulin-mediated glucose transport by blocking the dephosphorylation of GLUT-4.
86	15082116	Classical isoforms of protein kinase C (PKC) can interfere with insulin signalling via serine phosphorylation of IRS-1 and the insulin receptor.
87	15082116	Parathyroid hormone (PTH), by activating phospholipase C-beta in adipocytes, can promote a sustained increase in intracellular free calcium in these cells, while also activating classical PKCs.
88	15082116	This may rationalize the fact that insulin resistance is a typical feature of hyperparathyroidism, as well as epidemiological evidence that regular ingestion of dairy products or of ethanol--which down-regulates PTH secretion--reduces risk for insulin resistance syndrome and diabetes.
89	15082116	Alpha-1 adrenergic receptors of adipocytes--like PTH receptors--also activate phospholipase C-beta, and thus have an effect analogous to PTH on intracellular free calcium and PKC activity in adipocytes.
90	15082116	This suggests that, via activation of alpha-1 adrenergic receptors, increased sympathetic activity in adipose tissue may promote insulin resistance syndrome.
91	15082116	In fact, measures which provoke increased sympathetic output--such as diuretic use and severe salt restriction--are known to compromise insulin sensitivity, whereas alpha-1 antagonist drugs, as well as drugs that act centrally to suppress sympathetic activity, typically have a favorable effect on insulin function.
92	15082116	When insulin resistance syndrome is associated with elevated sympathetic activity--for example, in hypertensives who are obese or on diuretic therapy--measures which down-regulate sympathetic activity, or, more specifically, alpha-1 adrenergic activity, may be warranted.
93	15082116	Elevated sympathetic activity may promote insulin resistance syndrome by activating alpha-1 adrenergic receptors on adipocytes.
94	15082116	An excess of free intracellular calcium can reduce the efficiency of insulin-mediated glucose transport by blocking the dephosphorylation of GLUT-4.
95	15082116	Classical isoforms of protein kinase C (PKC) can interfere with insulin signalling via serine phosphorylation of IRS-1 and the insulin receptor.
96	15082116	Parathyroid hormone (PTH), by activating phospholipase C-beta in adipocytes, can promote a sustained increase in intracellular free calcium in these cells, while also activating classical PKCs.
97	15082116	This may rationalize the fact that insulin resistance is a typical feature of hyperparathyroidism, as well as epidemiological evidence that regular ingestion of dairy products or of ethanol--which down-regulates PTH secretion--reduces risk for insulin resistance syndrome and diabetes.
98	15082116	Alpha-1 adrenergic receptors of adipocytes--like PTH receptors--also activate phospholipase C-beta, and thus have an effect analogous to PTH on intracellular free calcium and PKC activity in adipocytes.
99	15082116	This suggests that, via activation of alpha-1 adrenergic receptors, increased sympathetic activity in adipose tissue may promote insulin resistance syndrome.
100	15082116	In fact, measures which provoke increased sympathetic output--such as diuretic use and severe salt restriction--are known to compromise insulin sensitivity, whereas alpha-1 antagonist drugs, as well as drugs that act centrally to suppress sympathetic activity, typically have a favorable effect on insulin function.
101	15082116	When insulin resistance syndrome is associated with elevated sympathetic activity--for example, in hypertensives who are obese or on diuretic therapy--measures which down-regulate sympathetic activity, or, more specifically, alpha-1 adrenergic activity, may be warranted.
102	15082116	Elevated sympathetic activity may promote insulin resistance syndrome by activating alpha-1 adrenergic receptors on adipocytes.
103	15082116	An excess of free intracellular calcium can reduce the efficiency of insulin-mediated glucose transport by blocking the dephosphorylation of GLUT-4.
104	15082116	Classical isoforms of protein kinase C (PKC) can interfere with insulin signalling via serine phosphorylation of IRS-1 and the insulin receptor.
105	15082116	Parathyroid hormone (PTH), by activating phospholipase C-beta in adipocytes, can promote a sustained increase in intracellular free calcium in these cells, while also activating classical PKCs.
106	15082116	This may rationalize the fact that insulin resistance is a typical feature of hyperparathyroidism, as well as epidemiological evidence that regular ingestion of dairy products or of ethanol--which down-regulates PTH secretion--reduces risk for insulin resistance syndrome and diabetes.
107	15082116	Alpha-1 adrenergic receptors of adipocytes--like PTH receptors--also activate phospholipase C-beta, and thus have an effect analogous to PTH on intracellular free calcium and PKC activity in adipocytes.
108	15082116	This suggests that, via activation of alpha-1 adrenergic receptors, increased sympathetic activity in adipose tissue may promote insulin resistance syndrome.
109	15082116	In fact, measures which provoke increased sympathetic output--such as diuretic use and severe salt restriction--are known to compromise insulin sensitivity, whereas alpha-1 antagonist drugs, as well as drugs that act centrally to suppress sympathetic activity, typically have a favorable effect on insulin function.
110	15082116	When insulin resistance syndrome is associated with elevated sympathetic activity--for example, in hypertensives who are obese or on diuretic therapy--measures which down-regulate sympathetic activity, or, more specifically, alpha-1 adrenergic activity, may be warranted.
111	15082116	Elevated sympathetic activity may promote insulin resistance syndrome by activating alpha-1 adrenergic receptors on adipocytes.
112	15082116	An excess of free intracellular calcium can reduce the efficiency of insulin-mediated glucose transport by blocking the dephosphorylation of GLUT-4.
113	15082116	Classical isoforms of protein kinase C (PKC) can interfere with insulin signalling via serine phosphorylation of IRS-1 and the insulin receptor.
114	15082116	Parathyroid hormone (PTH), by activating phospholipase C-beta in adipocytes, can promote a sustained increase in intracellular free calcium in these cells, while also activating classical PKCs.
115	15082116	This may rationalize the fact that insulin resistance is a typical feature of hyperparathyroidism, as well as epidemiological evidence that regular ingestion of dairy products or of ethanol--which down-regulates PTH secretion--reduces risk for insulin resistance syndrome and diabetes.
116	15082116	Alpha-1 adrenergic receptors of adipocytes--like PTH receptors--also activate phospholipase C-beta, and thus have an effect analogous to PTH on intracellular free calcium and PKC activity in adipocytes.
117	15082116	This suggests that, via activation of alpha-1 adrenergic receptors, increased sympathetic activity in adipose tissue may promote insulin resistance syndrome.
118	15082116	In fact, measures which provoke increased sympathetic output--such as diuretic use and severe salt restriction--are known to compromise insulin sensitivity, whereas alpha-1 antagonist drugs, as well as drugs that act centrally to suppress sympathetic activity, typically have a favorable effect on insulin function.
119	15082116	When insulin resistance syndrome is associated with elevated sympathetic activity--for example, in hypertensives who are obese or on diuretic therapy--measures which down-regulate sympathetic activity, or, more specifically, alpha-1 adrenergic activity, may be warranted.
120	15198370	The alpha-1 isoform of the enzyme predominant in red blood cells and nerve tissue is encoded by the ATP1A1 gene.
121	16436663	Reverse transcription-polymerase chain reaction analysis showed that relative gene expression levels of matrix metalloproteinases (MMP-2 and MMP-9) and transforming growth factor-beta1 were increased in parallel with calcification.
122	16436663	Gene expression of core binding factor alpha-1, an osteoblast-specific transcription factor, increased in parallel with elastin calcification and attained approximately 9.5-fold higher expression at 21 days compared to 3 days after implantation.
123	16436663	Similarly, mRNA levels of the bone markers osteopontin and alkaline phosphatase also increased progressively, but osteocalcin levels remained unchanged.
124	16611675	This region harbors positional candidate genes such as chorionic gonadotropin, alpha chain; collagen, type XIX, alpha-1; and protein-tyrosine phosphatase, type 4A, 1 that may play a role in fetal growth and development.
125	17301191	The spots were cut from the gel, and 20 were identified by mass spectrometry as charge forms of 11 plasma proteins: Orosomucoid, transferrin, alpha-1 microglobulin, zinc alpha-2 glycoprotein, alpha-1 antitrypsin, complement factor B, haptoglobin, transthyretin, plasma retinol binding protein, albumin, and hemopexin.
126	17403060	Cells were pretreated in vitro with IL-4, incubated with IL-1beta and interferon (IFN)-gamma and DNA fragmentation and nitrite production analysed by flow cytometry and Griess assay, respectively.
127	17403060	Expression of type I (IL-4R alpha and common gamma-chain) and type II (IL-4R alpha, IL-13R alpha-1) IL-4R mRNA transcripts, together with cell surface expression of IL-4R, was demonstrated.
128	17403060	Pre-incubation with IL-4 reduced significantly cell death induced by IL-1beta alone or by a combination of IL-1beta and IFN-gamma, although this was not accompanied by a reduced production of nitrite.
129	18220689	Specific markers of islet microvasculature are alpha-1 proteinase inhibitor and nephrin, a highly specific barrier protein with adhesion and signalling function.
130	18374100	Alpha-1 antitrypsin treatment of spontaneously diabetic nonobese diabetic mice receiving islet allografts.
131	18374100	Alpha-1 antitrypsin (AAT) is a serine protease inhibitor able to prevent diabetes onset in nonobese diabetic (NOD) mice and to prolong islet allograft survival in a nonautoimmune murine model.
132	18374100	Alpha-1 antitrypsin treatment of spontaneously diabetic nonobese diabetic mice receiving islet allografts.
133	18374100	Alpha-1 antitrypsin (AAT) is a serine protease inhibitor able to prevent diabetes onset in nonobese diabetic (NOD) mice and to prolong islet allograft survival in a nonautoimmune murine model.
134	18374099	Prolonged islet allograft survival by alpha-1 antitrypsin: the role of humoral immunity.
135	18374099	Immunomodulatory properties have been recognized for human alpha-1 antitrypsin (hAAT).
136	18374099	Prolonged islet allograft survival by alpha-1 antitrypsin: the role of humoral immunity.
137	18374099	Immunomodulatory properties have been recognized for human alpha-1 antitrypsin (hAAT).
138	18408372	Alpha-1 antichymotrypsin gene signal peptide a/t polymorphism and primary intracerebral hemorrhage.
139	18818245	Both diabetes (C versus D7) and ANGII increased NKA alpha-1 protein level and enzyme activity (C versus CA, D7 versus D7A).
140	18818245	NKA alpha-1 Ser23 phosphorylation was higher both in D7 and ANGII-treated rats in the non-cytoskeletal fraction, while no signal was detected in the cytoskeletal fraction.
141	18818245	Control kidneys showed NKA alpha-1 immunopositivity on the basolateral membrane of proximal tubular cells, while both D7 and ANGII broadened NKA immunopositivity towards the cytoplasm.
142	18818245	Both diabetes (C versus D7) and ANGII increased NKA alpha-1 protein level and enzyme activity (C versus CA, D7 versus D7A).
143	18818245	NKA alpha-1 Ser23 phosphorylation was higher both in D7 and ANGII-treated rats in the non-cytoskeletal fraction, while no signal was detected in the cytoskeletal fraction.
144	18818245	Control kidneys showed NKA alpha-1 immunopositivity on the basolateral membrane of proximal tubular cells, while both D7 and ANGII broadened NKA immunopositivity towards the cytoplasm.
145	18818245	Both diabetes (C versus D7) and ANGII increased NKA alpha-1 protein level and enzyme activity (C versus CA, D7 versus D7A).
146	18818245	NKA alpha-1 Ser23 phosphorylation was higher both in D7 and ANGII-treated rats in the non-cytoskeletal fraction, while no signal was detected in the cytoskeletal fraction.
147	18818245	Control kidneys showed NKA alpha-1 immunopositivity on the basolateral membrane of proximal tubular cells, while both D7 and ANGII broadened NKA immunopositivity towards the cytoplasm.
148	18993152	Furthermore, niacin significantly increased the large alpha-1 apolipoprotein A-I-containing HDL subspecies (12 to 17 nm).
149	19165811	Ions at m/z 2049 and 1219 originate from the collagen alpha-1(I) chain precursor and from the collagen alpha-5 (IV) chain precursor, respectively, and, also in this case, their different expressions can be related to the pathologies under investigation.
150	19298540	Chromium picolinate inhibits resistin secretion in insulin-resistant 3T3-L1 adipocytes via activation of amp-activated protein kinase.
151	19298540	Using normal and insulin-resistant 3T3-L1 adipocytes, we examined the effects of CrPic on the gene transcription and secretion of adiponectin and resistin.
152	19298540	In addition, using immunoblotting, ELISA and real-time reverse transcription-polymerase chain reaction (RT-PCR), we investigated the effects of 10 nmol/L CrPic for 24 h on AMP-activated protein kinase (AMPK) to determine whether this pathway contributed to the regulation of adiponectin and resistin expression and secretion. 3.
153	19298540	Chromium picolinate did not modulate the expression of adiponectin and resistin; however, it did significantly inhibit the secretion of resistin, but not adiponectin, by normal and insulin-resistant 3T3-L1 adipocytes in vitro.
154	19298540	Furthermore, although CrPic markedly elevated levels of phosphorylated AMPK and acetyl CoA carboxylase in 3T3-L1 adipocytes, it had no effect on the levels of AMPK alpha-1 and alpha-2 mRNA transcripts.
155	19298540	Importantly, inhibition of AMPK by 2 h pretreatment of cells with 20 micromol/L compound C completely abolished the CrPic-induced suppression of resistin secretion. 4.
156	19298540	In conclusion, the data suggest that CrPic inhibits resistin secretion via activation of AMPK in normal and insulin-resistant 3T3-L1 adipocytes.
157	19423691	This process involves increased activity of alkaline phosphatase and increased expression of core binding factor alpha-1, a bone-specific transcription factor, with the subsequent induction of osteocalcin.
158	19423691	In addition, osteoblastic transformation of HSMCs provoked by elevated Pi (assessed by upregulation of core binding factor alpha-1, osteocalcin, and alkaline phosphatase activity) was diminished by ferritin/ferroxidase activity.
159	19423691	We conclude that induction of the HO-1/ferritin system prevents Pi-mediated calcification and osteoblastic differentiation of human smooth muscle cells mainly via the ferroxidase activity of ferritin.
160	19423691	This process involves increased activity of alkaline phosphatase and increased expression of core binding factor alpha-1, a bone-specific transcription factor, with the subsequent induction of osteocalcin.
161	19423691	In addition, osteoblastic transformation of HSMCs provoked by elevated Pi (assessed by upregulation of core binding factor alpha-1, osteocalcin, and alkaline phosphatase activity) was diminished by ferritin/ferroxidase activity.
162	19423691	We conclude that induction of the HO-1/ferritin system prevents Pi-mediated calcification and osteoblastic differentiation of human smooth muscle cells mainly via the ferroxidase activity of ferritin.
163	20356844	Structural basis for substrate selectivity in human maltase-glucoamylase and sucrase-isomaltase N-terminal domains.
164	20356844	Human maltase-glucoamylase (MGAM) and sucrase-isomaltase (SI) are small intestinal enzymes that work concurrently to hydrolyze the mixture of linear alpha-1,4- and branched alpha-1,6-oligosaccharide substrates that typically make up terminal starch digestion products.
165	20356844	The N-terminal catalytic domain of human MGAM (ntMGAM) has a preference for short linear alpha-1,4-oligosaccharides, whereas N-terminal SI (ntSI) has a broader specificity for both alpha-1,4- and alpha-1,6-oligosaccharides.
166	20356844	Structural basis for substrate selectivity in human maltase-glucoamylase and sucrase-isomaltase N-terminal domains.
167	20356844	Human maltase-glucoamylase (MGAM) and sucrase-isomaltase (SI) are small intestinal enzymes that work concurrently to hydrolyze the mixture of linear alpha-1,4- and branched alpha-1,6-oligosaccharide substrates that typically make up terminal starch digestion products.
168	20356844	The N-terminal catalytic domain of human MGAM (ntMGAM) has a preference for short linear alpha-1,4-oligosaccharides, whereas N-terminal SI (ntSI) has a broader specificity for both alpha-1,4- and alpha-1,6-oligosaccharides.
169	20442402	Orosomucoid (ORM), also called alpha-1 acid glycoprotein, is an abundant plasma protein that is an immunomodulator induced by stressful conditions such as infections.
170	20442402	Adipose Orm levels were elevated by metabolic signals, including insulin, high glucose, and free fatty acid, as well as by the proinflammatory cytokine tumor necrosis factor-alpha, which is found in increased levels in the adipose tissue of morbid obese subjects.
171	20442402	In both adipocytes and macrophages, ORM suppressed proinflammatory gene expression and pathways such as NF-kappaB and mitogen-activated protein kinase signalings and reactive oxygen species generation.
172	20442402	Concomitantly, ORM relieved hyperglycemia-induced insulin resistance as well as tumor necrosis factor-alpha-mediated lipolysis in adipocytes.
173	20442402	Accordingly, ORM improved glucose and insulin tolerance in obese and diabetic db/db mice.
174	20692406	Culture of impure human islet fractions in the presence of alpha-1 antitrypsin prevents insulin cleavage and improves islet recovery.
175	21483580	Inflammatory markers, such as high sensitive C-reactive protein (hsCRP), ferritin, transferrin, albumin, alpha-1 acid glycoprotein (AAG), alpha-2 macroglobulin (AMG), alpha-1 anti-trypsin (AAT) and lipoprotein a [Lp(a)] were measured in coronary artery disease patients (CAD) and CAD patients with non-alcoholic steatohepatitis (NASH).
176	22058037	Human maltase-glucoamylase (MGAM) hydrolyzes linear alpha-1,4-linked oligosaccharide substrates, playing a crucial role in the production of glucose in the human lumen and acting as an efficient drug target for type 2 diabetes and obesity.