Ignet

Gene Information

Gene symbol: IDH3B

Gene name: isocitrate dehydrogenase 3 (NAD+) beta

HGNC ID: 5385

Related Genes

#	Gene Symbol	Number of hits
1	ACLY	1 hits
2	AK2	1 hits
3	ALPI	1 hits
4	ATP5O	1 hits
5	CKB	1 hits
6	COX8B	1 hits
7	CS	1 hits
8	DES	1 hits
9	FASN	1 hits
10	G6PD	1 hits
11	GCK	1 hits
12	GLS	1 hits
13	GLS2	1 hits
14	GPD1	1 hits
15	H6PD	1 hits
16	HSPB1	1 hits
17	IDH1	1 hits
18	IL1B	1 hits
19	INS	1 hits
20	ME1	1 hits
21	MGLL	1 hits
22	MPST	1 hits
23	NQO1	1 hits
24	OGDH	1 hits
25	PDHB	1 hits
26	PGD	1 hits
27	PKLR	1 hits
28	TNNT2	1 hits

Related Sentences

#	PMID	Sentence
1	5067	The diabetes mellitus caused the following changes in the metabolism: reduction in the concentration of ATP and NADPH, increase in the lactate/pyruvate quotient to above 40, reduction in the ATP/ADP quotient to below 1, reduction in the level of activity of the hydrogen-conveying enzymes G-6-P-dehydrogenase, isocitrate dehydrogenase and malate dehydrogenase, increase in the level of activity of the alkaline phosphatase, reduction of the protein content.
2	35455	Impaired testosterone biosynthesis in Leydig cells from streptozotocin treated rats is correlated with the reduced activity of glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase and isocitrate dehydrogenase.
3	590651	These animals showed high levels of phosphoenolpyruvate carboxykinase and low levels of glucokinase, hexokinase, isocitrate dehydrogenase and malic enzyme, but normal levels of pyruvate kinase in the liver.
4	729537	With the exception of NADP-isocitrate dehydrogenase, insulin replacement therapy induced increased activities of the enzymes in streptozotocin-treated rats.
5	729537	Insulin appeared to have a specific effect on the activities of glucokinase, ATP-citrate lyase, malic enzyme, and glucose-6-P-dehydrogenase.
6	2501061	The demand for NADPH in drug oxidation reactions, caused by the induction phenomenon, was reflected in the elevated activities of the NADPH producing enzymes in pentose phosphate pathway and in the activities of isocitrate dehydrogenase and malic enzyme from mitochondrial oxidation reactions.
7	2501061	Hepatic glucose production rate was related to plasma glucose, NADPH producing enzyme activities and cytochrome P450 content in the obese and lean mice.
8	2666106	Differential sensitivity to beta-cell secretagogues in cultured rat pancreatic islets exposed to human interleukin-1 beta.
9	2666106	Interleukin-1 (IL-1) has been suggested to be one possible mediator of immunological damage of the beta-cells.
10	2666106	The activities of the glycolytic enzymes hexokinase, glucokinase, and glyceraldehyde 3-phosphate dehydrogenase, were similar in control and IL-1-exposed islets.
11	2666106	Treatment with IL-1 also did not impair the activities of NADH+- and NADPH+-dependent glutamate dehydrogenase, glutamate-aspartate transaminase, glutamate-alanine transaminase, citrate synthase, and NAD+-linked isocitrate dehydrogenase.
12	2666106	These combined observations suggest that exposure to IL-1 induces a preferential decrease in glucose-mediated insulin release and mitochondrial glucose metabolism.
13	2666106	It is conceivable that the IL-1-induced suppression and shift in islet metabolism can be an explanation for the beta-cell insensitivity to glucose observed in the early phases of human and experimental insulin-dependent diabetes mellitus.
14	9746330	The mechanism is the activation by Ca2+ of four mitochondrial dehydrogenases, viz. glycerol 3-phosphate dehydrogenase, the pyruvate dehydrogenase multienzyme complex (PDH), NAD-linked isocitrate dehydrogenase (NAD-IDH) and 2-oxoglutarate dehydrogenase (OGDH).
15	11517735	The activities of malic enzyme, NADP+ isocitrate dehydrogenase, Glucose 6-P-dehydrogenase and the transaminases were determined to assess any degree of metabolic alteration caused by diabetic nephropathy.
16	14969338	DA-11004 is a synthetic, potent NADP-dependent isocitrate dehydrogenase (IDPc) inhibitor where IC50 for IDPc is 1.49 microM.
17	15286407	The activities of NADP-linked enzymes; namely glucose-6-phosphate dehydrogenase (G6PDH), malic enzyme (ME), isocitrate dehydrogenase (ICDH), and the activities of lipogenic enzymes namely ATP-citrate lyase (ATP-CL) and fatty acid synthase (FAS) were decreased significantly in liver and increased in kidney during diabetes as compared to control.
18	15522197	Regulation of high glucose-induced apoptosis by mitochondrial NADP+-dependent isocitrate dehydrogenase.
19	15522197	Recently, we demonstrated that the control of mitochondrial redox balance and the cellular defense against oxidative damage is one of the primary functions of mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDPm) to supply NADPH for antioxidant systems.
20	15522197	Regulation of high glucose-induced apoptosis by mitochondrial NADP+-dependent isocitrate dehydrogenase.
21	15522197	Recently, we demonstrated that the control of mitochondrial redox balance and the cellular defense against oxidative damage is one of the primary functions of mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDPm) to supply NADPH for antioxidant systems.
22	15528036	Glycation-induced inactivation of NADP(+)-dependent isocitrate dehydrogenase: implications for diabetes and aging.
23	15528036	Recently, we demonstrated that the control of cytosolic and mitochondrial redox balance and the cellular defense against oxidative damage is one of the primary functions of NADP(+)-dependent isocitrate dehydrogenase (ICDH), because it supplies NADPH for antioxidant systems.
24	15528036	Glycation-induced inactivation of NADP(+)-dependent isocitrate dehydrogenase: implications for diabetes and aging.
25	15528036	Recently, we demonstrated that the control of cytosolic and mitochondrial redox balance and the cellular defense against oxidative damage is one of the primary functions of NADP(+)-dependent isocitrate dehydrogenase (ICDH), because it supplies NADPH for antioxidant systems.
26	16461555	The activities of hexokinase, glucose-6-phosphate dehydrogenase (G6PDH), phosphofructokinase (PFK), citrate synthase, phosphate-dependent glutaminase, NAD+-linked and NADP+-linked isocitrate dehydrogenase were assayed.
27	16461555	The activities of G6PDH and glutaminase were decreased, whereas that of PFK was raised by the diabetic state.
28	17288254	Hypoglycemic coma induced by administration of a large dose of insulin, was accompanied by the increased rates of glycolysis, glycogenolysis, activity of lactate dehydrogenase, succinate dehydrogenase, isocitrate dehydrogenase, and increased concentration of glycogen.
29	18685954	Kidney and liver tissues were excised at the end of the study for assaying enzymatic activities of isocitrate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, NADH-dehydrogenase and cytochrome-c-oxidase.
30	20012373	Upregulation of cytosolic NADP+-dependent isocitrate dehydrogenase by hyperglycemia protects renal cells against oxidative stress.
31	20012373	We found that both expression and enzymatic activity of cytosolic NADP(+)-dependent isocitrate dehydrogenase (IDPc) were upregulated in the renal cortexes of diabetic rats and mice.
32	20012373	Upregulation of cytosolic NADP+-dependent isocitrate dehydrogenase by hyperglycemia protects renal cells against oxidative stress.
33	20012373	We found that both expression and enzymatic activity of cytosolic NADP(+)-dependent isocitrate dehydrogenase (IDPc) were upregulated in the renal cortexes of diabetic rats and mice.
34	20127051	Increased proteins were identified as monoglyceride lipase, adenylate kinase, Cu/Zn superoxide dismutase, phosphoglucomutase, aldolase, isocitrate dehydrogenase, cytochrome c oxidase, small heat shock Hsp27/B1, actin and 3-mercaptopyruvate sulfurtransferase.
35	21354350	Among the decreased proteins, 3 are involved in heart structure (one isoform of desmin, troponin T2 and α-cardiac actin), 3 are involved in energy metabolism (mitochondrial ATP synthase β subunit, adenylate kinase and creatine kinase) and one is a component of the citric acid cycle (isocitrate dehydrogenase 3).
36	23579026	In most animal cells, NADPH is produced predominantly by glucose-6-phosphate dehydrogenase (G6PD) in the oxidative phase of the pentose phosphate pathway and, to a lesser extent, by isocitrate dehydrogenase (IDH) and malic enzyme (ME).
37	23579026	In this study, the activities of isolated G6PD, IDH, and ME were inhibited by MGO (0-2.5mM, 2-3h, 37°C), in a dose- and time-dependent manner, with G6PD and IDH more sensitive to modification than ME.
38	23579026	Incubation with radiolabeled MGO (0-500µM, 0-3h, 37°C) demonstrated dose- and time-dependent adduction to G6PD and IDH.
39	23579026	Peptide mass mapping studies confirmed hydroimidazolone formation on multiple peptides in G6PD and IDH, including those critical for NADP(+) binding, and substrate binding, in the case of IDH.
40	23788641	Control of voltage-gated potassium channel Kv2.2 expression by pyruvate-isocitrate cycling regulates glucose-stimulated insulin secretion.
41	23788641	Recent studies have shown that the pyruvate-isocitrate cycling pathway, involving the mitochondrial citrate/isocitrate carrier and the cytosolic NADP-dependent isocitrate dehydrogenase (ICDc), is involved in control of glucose-stimulated insulin secretion (GSIS).
42	23788641	Here we demonstrate that pyruvate-isocitrate cycling regulates expression of the voltage-gated potassium channel family member Kv2.2 in islet β-cells. siRNA-mediated suppression of ICDc, citrate/isocitrate carrier, or Kv2.2 expression impaired GSIS, and the effect of ICDc knockdown was rescued by re-expression of Kv2.2.
43	23788641	Immunoprecipitation studies demonstrated interaction of Kv2.1 and Kv2.2, and co-overexpression of the two channels reduced outward K(+) current compared with overexpression of Kv2.1 alone.