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Gene Information
Gene symbol: ING1
Gene name: inhibitor of growth family, member 1
HGNC ID: 6062
Synonyms: p33ING1, p33ING1b, p24ING1c, p33, p47, p47ING1a
Related Genes
| # | Gene Symbol | Number of hits |
| 1 | AGT | 1 hits |
| 2 | APOB | 1 hits |
| 3 | CASP3 | 1 hits |
| 4 | CD40 | 1 hits |
| 5 | CYBB | 1 hits |
| 6 | F2RL1 | 1 hits |
| 7 | GORASP1 | 1 hits |
| 8 | MAPK8 | 1 hits |
| 9 | NFKBIA | 1 hits |
| 10 | NOX5 | 1 hits |
| 11 | PPARG | 1 hits |
| 12 | PPARGC1A | 1 hits |
| 13 | PRKAA1 | 1 hits |
| 14 | PRKCB1 | 1 hits |
| 15 | SCD | 1 hits |
| 16 | UCP3 | 1 hits |
| 17 | ZMPSTE24 | 1 hits |
Related Sentences
| # | PMID | Sentence |
| 1 | 21911753 | Levels of phosphorylated p47(phox), active Rac1, Nox activity, ROS generation, Jun NH(2)-terminal kinase (JNK) 1/2 phosphorylation, and caspase-3 activity were significantly higher in the ZDF islets than the lean control rat islets. |
| 2 | 17065350 | Diabetes increased NADPH oxidase activity and the expressions of p47(phox), Nox2, and Nox4 mRNA levels in the renal cortex and were unchanged in diabetic PKC-beta(-/-) mice. |
| 3 | 19081082 | We found that ANGII-induced superoxide generation via NAD(P)H oxidase activation and increased protein and mRNA levels of NAD(P)H oxidase subunits (p47(PHOX) and gp91(PHOX)). |
| 4 | 19592621 | In cultured cardiomyocytes, high glucose upregulated Rac1 and NADPH oxidase activity and induced apoptotic cell death, which were blocked by overexpression of a dominant negative mutant of Rac1, knockdown of gp91(phox) or p47(phox), or NADPH oxidase inhibitor. |
| 5 | 20972877 | These results indicate that PAR2 plays a pivotal role in endothelial dysfunction in type 2 diabetes by up-regulating the expression/production of TNF-? and activating NAD(P)H oxidase subunit p47(phox). |
| 6 | 19680556 | We re-sequenced all exons, intron-exon boundaries and selected conserved non-coding sequences of candidate genes involved in aging-related processes, including dietary restriction (PPARG, PPARGC1A, SIRT1, SIRT3, UCP2, UCP3), metabolism (IGF1R, APOB, SCD), autophagy (BECN1, FRAP1), stem cell activation (NOTCH1, DLL1), tumor suppression (TP53, CDKN2A, ING1), DNA methylation (TRDMT1, DNMT3A, DNMT3B) Progeria syndromes (LMNA, ZMPSTE24, KL) and stress response (CRYAB, HSPB2). |
| 7 | 19955485 | Wild-type EC and sh-mRNA-AGER1(+) EC, but not AGER1(+) EC, had high NOX p47(phox) and gp91(phox) activity, superoxide anions, and NF-kappaB p65 nuclear translocation in response to MG and N(epsilon)-carboxymethyl-lysine. |
| 8 | 20167927 | The markers of oxidative stress, NAD(P)H oxidase subunit expression (gp91(phox), p47(phox), p67(phox), NOX1 to -4), NAD(P)H oxidase-mediated superoxide production, 26S proteasome activity, IkappaBalpha degradation, and nuclear translocation of nuclear factor (NF)-kappaB (p50 and p65) were examined in cultured human umbilical vein endothelial cells and mouse aortas isolated from AMPKalpha2 deficient mice. |
| 9 | 20167927 | Analysis of aortic endothelial cells from AMPKalpha2(-/-) mice and human umbilical vein endothelial cells expressing dominant negative AMPK or AMPKalpha2-specific siRNA revealed that loss of AMPK activity increased NAD(P)H oxidase subunit expression (gp91(phox), p47(phox), p67(phox), NOX1 and -4), NAD(P)H oxidase-mediated superoxide production, 26S proteasome activity, IkappaBalpha degradation, and nuclear translocation of NF-kappaB (p50 and p65), whereas AMPK activation by AICAR or overexpression of constitutively active AMPK had the opposite effect. |