Ignet

Gene Information

Gene symbol: HDC

Gene name: histidine decarboxylase

HGNC ID: 4855

Related Genes

#	Gene Symbol	Number of hits
1	ABP1	1 hits
2	AIRE	1 hits
3	ALB	1 hits
4	ALPI	1 hits
5	CSAD	1 hits
6	CSF2	1 hits
7	CSF3	1 hits
8	DDC	1 hits
9	GAD1	1 hits
10	GAD2	1 hits
11	GAST	1 hits
12	IL12A	1 hits
13	IL18	1 hits
14	IL1B	1 hits
15	IL3	1 hits
16	INS	1 hits
17	LEP	1 hits
18	NFKB1	1 hits
19	PARP1	1 hits
20	PTH	1 hits
21	TNF	1 hits

Related Sentences

#	PMID	Sentence
1	2377078	In view of the observations that (1) plasma histamine concentrations are significantly higher in diabetic patients and diabetic rats than those in controls, and (2) tissue concentrations of histamine are elevated in rats with experimental diabetes, we have investigated histamine synthesis, as reflected by histidine decarboxylase (HDC) activity, and histamine catabolism, as reflected by histaminase activity, in various tissues of the diabetic rat.
2	2971025	We also examined effects of insulin and alpha-hydrazinohistidine (alpha HH) treatments on retinal histamine synthesis in this diabetic model. alpha HH is a specific inhibitor of histidine decarboxylase.
3	3159596	At least 15 diabetic animals received insulin (6-8 U/day) or alpha-hydrazinohistidine (alpha-HH) for the last week of the holding period. alpha-HH is a specific inhibitor of histidine decarboxylase (HD), the principle histamine-forming enzyme in mammals.
4	4018454	We examined the interrelationship between inhibition of aortic histamine synthesis through inhibition of aortic histidine decarboxylase and intra-aortic albumin accumulation in rats made diabetic by a jugular vein injection of 60 mg/kg of streptozotocin under ether anesthesia.
5	6651615	We studied rat aortic endothelial and smooth muscle cell de novo histamine synthesis mediated by histidine decarboxylase (HD) and the effects of its inhibition by alpha-hydrazinohistidine on the intracellular histamine content and intraaortic albumin accumulation in streptozotocin-induced diabetes.
6	6802115	We studied histamine metabolism, i.e., histidine decarboxylase (HD)-mediated synthesis and histaminase-mediated catabolism, in relation to intracellular histamine content in both aortic endothelial and subjacent smooth muscle cells of control and diabetic rats.
7	7669042	Depletion of islet histamine contents by the specific and irreversible inhibitor of L-histidine decarboxylase, alpha-fluoromethyl-[S] histidine increased islet insulin content but failed to influence the rate of insulin secretion.
8	10580415	These results indicate that leptin increases histamine turnover by affecting the posttranscriptional process of HDC formation or histamine release per se.
9	10580415	Systemic depletion of brain histamine levels by pretreatment with an intraperitoneal injection of 224 micromol/kg alpha-fluoromethylhistidine (FMH), a suicide inhibitor of HDC, attenuated the leptin-induced feeding suppression by 50.7% (P < 0.05).
10	10580415	These results indicate that leptin increases histamine turnover by affecting the posttranscriptional process of HDC formation or histamine release per se.
11	10580415	Systemic depletion of brain histamine levels by pretreatment with an intraperitoneal injection of 224 micromol/kg alpha-fluoromethylhistidine (FMH), a suicide inhibitor of HDC, attenuated the leptin-induced feeding suppression by 50.7% (P < 0.05).
12	10955282	Increases in gastric histidine decarboxylase activity and plasma gastrin level in streptozotocin-induced type 1 diabetic rats.
13	10955282	When the diabetic rats were administered with insulin for 3 d, the increased histidine decarboxylase activity returned to a normal level in addition to normalization of the plasma glucose level.
14	10955282	The plasma gastrin level in the fasting state was also significantly elevated in the diabetic rats, and the insulin treatment normalized the level.
15	10955282	These results suggest that the gastric histidine decarboxylase activity and plasma gastrin level are increased in connection with the depletion of insulin in streptozotocin-induced diabetic rats, and gastric acid secretion is stimulated at a basal level, presumably due to increases in the concentrations of histamine and gastrin in oxyntic mucosa.
16	10955282	Increases in gastric histidine decarboxylase activity and plasma gastrin level in streptozotocin-induced type 1 diabetic rats.
17	10955282	When the diabetic rats were administered with insulin for 3 d, the increased histidine decarboxylase activity returned to a normal level in addition to normalization of the plasma glucose level.
18	10955282	The plasma gastrin level in the fasting state was also significantly elevated in the diabetic rats, and the insulin treatment normalized the level.
19	10955282	These results suggest that the gastric histidine decarboxylase activity and plasma gastrin level are increased in connection with the depletion of insulin in streptozotocin-induced diabetic rats, and gastric acid secretion is stimulated at a basal level, presumably due to increases in the concentrations of histamine and gastrin in oxyntic mucosa.
20	10955282	Increases in gastric histidine decarboxylase activity and plasma gastrin level in streptozotocin-induced type 1 diabetic rats.
21	10955282	When the diabetic rats were administered with insulin for 3 d, the increased histidine decarboxylase activity returned to a normal level in addition to normalization of the plasma glucose level.
22	10955282	The plasma gastrin level in the fasting state was also significantly elevated in the diabetic rats, and the insulin treatment normalized the level.
23	10955282	These results suggest that the gastric histidine decarboxylase activity and plasma gastrin level are increased in connection with the depletion of insulin in streptozotocin-induced diabetic rats, and gastric acid secretion is stimulated at a basal level, presumably due to increases in the concentrations of histamine and gastrin in oxyntic mucosa.
24	11496827	However, the histamine-forming enzyme, histidine decarboxylase (HDC), is induced in a variety of tissues in response (i) to gram-positive and gram-negative bacterial components (lipopolysaccharides, peptidoglycan, and enterotoxin A) and (ii) to various cytokines (IL-1, IL-3, IL-12, IL-18, TNF, G-CSF, and GM-CSF).
25	12527411	When given to STZ-treated mice, nicotinamide, an inhibitor of poly(ADP-ribose) synthetase, reduced both the elevation of blood glucose and the elevations of HDC activity and histamine production.
26	12716972	Serum parameters confirming this indirect effect included elevated calcitriol, phosphorus, alkaline phosphatase, and receptor activator of NF-kappaB ligand concentrations, and suppressed parathyroid hormone concentrations in HDC(-/-) mice compared with WT mice.
27	15070923	The structurally related group II pyridoxal phosphate (PLP)-dependent amino acid decarboxylases glutamic acid decarboxylase (GAD), aromatic L-amino acid decarboxylase (AADC), and histidine decarboxylase (HDC) are known autoantigens in endocrine disorders.
28	15070923	We report, for the first time, the prevalence of serum autoantibody reactivity against cysteine sulfinic acid decarboxylase (CSAD), an enzyme that shares 50% amino acid identity with the 65- and 67-kDa isoforms of GAD (GAD-65 and GAD-67), in endocrine autoimmune disease.
29	15070923	Anti-CSAD antibodies cross-reacted with GAD-65, and the anti-CSAD-positive sera were also reactive with AADC and HDC.
30	15070923	The low frequency of anti-CSAD reactivity is in striking contrast to the prevalence of antibodies against GAD-65, AADC, and HDC in APS1 patients, suggesting that different mechanisms control the immunological tolerance toward CSAD and the other group II decarboxylases.
31	15070923	The structurally related group II pyridoxal phosphate (PLP)-dependent amino acid decarboxylases glutamic acid decarboxylase (GAD), aromatic L-amino acid decarboxylase (AADC), and histidine decarboxylase (HDC) are known autoantigens in endocrine disorders.
32	15070923	We report, for the first time, the prevalence of serum autoantibody reactivity against cysteine sulfinic acid decarboxylase (CSAD), an enzyme that shares 50% amino acid identity with the 65- and 67-kDa isoforms of GAD (GAD-65 and GAD-67), in endocrine autoimmune disease.
33	15070923	Anti-CSAD antibodies cross-reacted with GAD-65, and the anti-CSAD-positive sera were also reactive with AADC and HDC.
34	15070923	The low frequency of anti-CSAD reactivity is in striking contrast to the prevalence of antibodies against GAD-65, AADC, and HDC in APS1 patients, suggesting that different mechanisms control the immunological tolerance toward CSAD and the other group II decarboxylases.
35	15070923	The structurally related group II pyridoxal phosphate (PLP)-dependent amino acid decarboxylases glutamic acid decarboxylase (GAD), aromatic L-amino acid decarboxylase (AADC), and histidine decarboxylase (HDC) are known autoantigens in endocrine disorders.
36	15070923	We report, for the first time, the prevalence of serum autoantibody reactivity against cysteine sulfinic acid decarboxylase (CSAD), an enzyme that shares 50% amino acid identity with the 65- and 67-kDa isoforms of GAD (GAD-65 and GAD-67), in endocrine autoimmune disease.
37	15070923	Anti-CSAD antibodies cross-reacted with GAD-65, and the anti-CSAD-positive sera were also reactive with AADC and HDC.
38	15070923	The low frequency of anti-CSAD reactivity is in striking contrast to the prevalence of antibodies against GAD-65, AADC, and HDC in APS1 patients, suggesting that different mechanisms control the immunological tolerance toward CSAD and the other group II decarboxylases.