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Gene Information

Gene symbol: GAPDH

Gene name: glyceraldehyde-3-phosphate dehydrogenase

HGNC ID: 4141

Related Genes

#	Gene Symbol	Number of hits
1	ADIPOQ	1 hits
2	BCL2L1	1 hits
3	BNIP3L	1 hits
4	CPE	1 hits
5	GCK	1 hits
6	GJA1	1 hits
7	GJB2	1 hits
8	INS	1 hits
9	PARP1	1 hits
10	PRKCA	1 hits
11	SLC2A1	1 hits
12	SOD2	1 hits
13	TP53	1 hits
14	UCP1	1 hits

Related Sentences

#	PMID	Sentence
1	1645683	Islets cultured at 3.3 mM glucose displayed a decreased activity of glucokinase compared with islets cultured at 28 mM glucose (23.3 +/- 12%), whereas there was no difference in hexokinase activity or the level of GAPDH mRNA.
2	1618927	Insulin regulates GAPDH gene transcription in a tissue-specific manner.
3	1625685	In ongoing studies aimed at elucidating the mechanism of insulin action on the expression of genes that modulate glucose utilization and cell growth, we have focused on the inductive effect of insulin on transcription of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and the early growth response gene, Egr-1.
4	1625685	We present evidence that supports the role of protein phosphorylation in mediating the effect of insulin on activation of Egr-1 and GAPDH gene transcription.
5	12663450	The expression of Nix and Bcl-xL proteins decreased relative to glyceraldehyde-3-phosphate dehydrogenase (GAPDH) control on the removal of erythropoietin (EPO) from the culture medium.
6	14523042	Both the hyperglycemia-induced decrease in activity of GAPDH and its poly(ADP-ribosyl)ation were prevented by overexpression of either uncoupling protein-1 (UCP-1) or manganese superoxide dismutase (MnSOD), which decrease hyperglycemia-induced superoxide.
7	14523042	Elevated glucose increased poly(ADP-ribosyl)ation of GAPDH in WT aortae, but not in the aortae from PARP-1-deficient mice.
8	15962096	Recent work has demonstrated that hyperglycemia-induced overproduction of superoxide by the mitochondrial electron-transport chain triggers several pathways of injury [(protein kinase C (PKC), hexosamine and polyol pathway fluxes, advanced glycation end product formation (AGE)] involved in the pathogenesis of diabetic complications by inhibiting glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity.
9	19035278	GAPDH, hnRNP D and hnRNP A/B bind specifically to the p53 CPEs and could potentially be involved in the post-transcriptional regulation of p53.
10	21315688	Further, KR-66344 suppressed adipocyte differentiation on cortisone-induced adipogenesis in 3T3-L1 cells is associated with the suppression of the cortisone-induced mRNA levels of FABP4, G3PD, PPAR?2 and Glut4, and 11?-HSD1 expression and activity.
11	21613414	Conversely, enhanced GLUT1 expression led to a 2.4-fold increase in binding of mTOR to its activator, Rheb, and a commensurate 2.1-fold decrease in binding of Rheb to glyceraldehyde 3-phosphate dehydrogenase (GAPDH) consistent with mediation of GLUT1 effects by a metabolic effect on GAPDH.
12	21613414	Thus, GLUT1 expression appears to augment mesangial cell growth and matrix protein accumulation via effects on glycolysis and decreased GAPDH interaction with Rheb.
13	21567444	Growth in high glucose did not alter relative Cx26 level, whereas Cx30 and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) were reduced by ?30%, and Cx43 increased ?1.9-fold.