Ignet

Gene Information

Gene symbol: HTR2B

Gene name: 5-hydroxytryptamine (serotonin) receptor 2B, G protein-coupled

HGNC ID: 5294

Synonyms: 5-HT(2B), 5-HT2B

Related Genes

#	Gene Symbol	Number of hits
1	ADH1B	1 hits
2	ADIPOQ	1 hits
3	ALB	1 hits
4	CRH	1 hits
5	IDDM2	1 hits
6	INS	1 hits
7	JAK1	1 hits
8	JAK2	1 hits
9	NOS2A	1 hits
10	NOX5	1 hits
11	PRKCA	1 hits
12	PTGS2	1 hits
13	RHOD	1 hits
14	SOD1	1 hits
15	STAT1	1 hits
16	STAT3	1 hits
17	TPH1	1 hits

Related Sentences

#	PMID	Sentence
1	3139426	Intraplatelet serotonin (5-HT) content was determined in 23 patients with type I (insulin-dependent) diabetes mellitus (IDDM), 23 patients with type II (non-insulin-dependent) diabetes mellitus (NIDDM), 29 patients with peripheral vascular disease (PVD) and 34 age-matched normal subjects.
2	3063593	Insulin incubation in bathing medium for 4-5 hr enhances the decreased gastro-intestinal responses to sal, but not to 5-HT. 4.
3	1671378	DA turnover was significantly reduced in striatum and hypothalamus in all diabetic groups. 5-HT turnover was reduced in chronically hyperglycemic diabetic rats in all four brain regions but normalized in insulin-treated diabetic rats.
4	1506131	Control animals showed a large 5-HT concentration-dependent increase in leakage of albumin in V3 venules, but this response was inhibited in the Diabetic-Tone animals.
5	1279445	In addition, an alternative method was used to assess 5-HT activity in thyroidectomized (TX) rats, i.e. measurement of 5-HT disappearance after inhibition of tryptophan hydroxylase with p-chlorophenylalanine (PCPA).
6	7687210	The effects of insulin and/or tryptophan (Try) administration on Try, serotonin (5-HT), 5-hydroxyindolacetic acid (5-HIAA) in raphe nuclei and hypothalamus and serum levels of large neutral amino acids [Try, valine, isoleucine, leucine, tyrosine and phenylalanine, (LNAA)] was investigated in diabetic rats. 2.
7	8910254	Results suggest that the contractile response to 5-HT in DM is related to the altered Ca2+ signal transduction system via disturbed protein kinase C (PKC) activity, and that there are alterations of receptor characteristics and of the density in 5-HT receptor subtypes, especially 5-HT1A, during DM development.
8	8931100	NG-nitro-L-arginine methyl ester (100 nmol/l), an inhibitor of nitric oxide synthase, significantly potentiated the contractile response of 5-HT in normal as well as diabetic pulmonary arterial rings.
9	12971908	The results in the present study showed that: (1) the plasma levels of NOx in both diabetic rats were low compared to those in control rats, (2) the hippocampal NOx levels in both diabetic rats were almost the same as those in control rats, while the levels of 5-HT and DA were low in the diabetics, and (3) a sudden decrease in the plasma glucose level due to insulin administration reduced the NOx level as well as enhanced the 5-HT level in the diabetic hippocampus, a finding consistent with the results of 7 days administration of insulin.
10	15601754	Treatment of rat VSMCs with 5-HT (10(-6) M) resulted in time-dependent activation ( approximately 2-fold) of JAK2, JAK1, and STAT1, but not STAT3 (maximal at 5 min, returned to baseline by 30 min).
11	15601754	Treatment with the 5-HT2A receptor antagonist ketanserin (10 nM) inhibited JAK2 activation by 5-HT.
12	15601754	Treatment of streptozotocin-induced diabetic rats with ketanserin (5 mg.kg-1.day-1) reduced activation of JAK2 and STAT1 but not STAT3 in endothelium-denuded thoracic aorta in vivo. 5-HT (10(-6) M) treatment resulted in increased cell proliferation and increased DNA synthesis, which were inhibited by the JAK2 inhibitor AG490.
13	17097612	Serotonin (5-hydroxytryptamine; 5-HT) 2A receptors contribute to the effects of 5-HT on platelet aggregation and vascular smooth muscle cell proliferation, and are reportedly involved in decreases in plasma levels of adiponectin, an adipokine, in diabetic subjects.
14	17218444	Interestingly, milnacipran did not increase plasma corticosterone and blood glucose levels, whereas fenfluramine, which inhibits 5-HT reuptake and stimulates 5-HT release, significantly increased plasma corticosterone and blood glucose levels in association with increased hypothalamic CRH mRNA levels.
15	19859528	While serotonin (5-HT) co-localization with insulin in granules of pancreatic beta-cells was demonstrated more than three decades ago, its physiological role in the etiology of diabetes is still unclear.
16	19859528	We combined biochemical and electrophysiological analyses of mice selectively deficient in peripheral tryptophan hydroxylase (Tph1-/-) and 5-HT to show that intracellular 5-HT regulates insulin secretion.
17	19859528	Our results demonstrate that 5-HT regulates insulin secretion by serotonylation of GTPases within pancreatic beta-cells and suggest that intracellular 5-HT functions in various microenvironments via this mechanism in concert with the known receptor-mediated signaling.
18	20590603	In each group, there was no significant change in the 5-HT-induced contractions after inhibition of nitric oxide synthase (with N(G)-nitro-L-arginine), of cyclooxygenase (with indomethacin) or of protein kinase C (with chelerythrine).
19	20590603	Although the diabetes-related enhancement of the 5-HT response was preserved with each of these inhibitors, enhancement was abolished by a Rho kinase inhibitor (Y27632) and by Src kinase inhibitors (PP1 analogue or Src kinase inhibitor I). 5-HT-induced activation of RhoA, Rho kinase and Src kinase in mesenteric arteries was greater in the ob/ob than in the Lean group, but the expression of RhoA, Rho kinase isoforms and Src did not differ between these groups.
20	20956003	Selective inhibition of COX-2 markedly reduced the vasodilatation induced by AA in OZR, but not in LZR, without altering 5-HT or ACh responses.
21	21756530	Based on the results that EtOH could increase the 5-HT in non-DM rats than in DM rats while acetaldehyde worked on both rats, it is more likely that alcohol dehydrogenase 1B activity was decreased in DM rats.
22	21521772	The hyper-responsiveness to 5-HT was endothelium-independent and unaffected by inhibition of nitric-oxide synthase but prevented by indomethacin, the selective COX-2 inhibitor N-[2-(cyclohexyloxyl)-4-nitrophenyl]-methane sulfonamide (NS-398), superoxide dismutase, and the NADPH oxidase inhibitor apocynin or chronic treatment with insulin.