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CDKN1A — INS

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Kaneto et al., Diabetologia 1999 : As support for the implication of p21 in impairment of beta-cell function, the p21 overexpression in the islet cells suppressed the insulin gene transcription
Chie et al., J Protein Chem 1999 : We have previously found that a peptide corresponding to residues 35-47 of the ras-p21 protein, from its switch 1 effector domain region, strongly inhibits oocyte maturation induced by oncogenic p21, but not by insulin activated cellular wild-type p21
Lai et al., J Biol Chem 2001 (Breast Neoplasms) : Thus the ability of estradiol to antagonize the insulin induced increase in p21 gene expression, with consequent activation of cyclin E-Cdk2, is a central component of the synergistic stimulation of breast epithelial cell proliferation induced by simultaneous activation of the estrogen and insulin/IGF-I signaling pathways
Kovac et al., Cancer Chemother Pharmacol 2001 : In contrast, PNC2 plasmid had no effect on the ability of insulin activated normal cellular or wild-type ras-p21 to induce oocyte maturation, suggesting that it is selective for blocking the mitogenic effects of oncogenic ( Val 12 ) ras p21
Ranginwale et al., Exp Cell Res 2001 (MAP Kinase Signaling System) : Oncogenic ras ( Val 12-containing ) -p21 protein induces oocyte maturation by a pathway that is blocked by peptides from effector domains of ras-p21, i.e., residues 35-47 ( that block Val 12-p21 activated raf ) and 96-110 and 115-126, which do not affect the ability of insulin activated cellular p21 to induce maturation
Wakino et al., J Biol Chem 2001 : PPARgamma ligands troglitazone ( TRO, 10 microm ) and rosiglitazone ( RSG, 10 microm ) attenuated the induction of p21 ( Cip1 ) protein by platelet derived growth factor ( PDGF ) and insulin without affecting cognate mRNA levels in rat aortic smooth muscle cells ( RASMC ) ... TRO, RSG, and rottlerin inhibited PDGF induced expression of p21 ( Cip1 ), but they did not affect insulin induced expression of p21 ( Cip1 )
Hiromura et al., Kidney Int 2002 : Our results also showed that the CDK-inhibitor p21 was increased by insulin and that p21 up-regulation was PI3-kinase/Akt pathway dependent
Chen et al., J Protein Chem 2002 : In an accompanying paper, we present results from microinjection of peptides corresponding to each of these domains into oocytes induced to undergo maturation by oncogenic ras-p21 and by insulin activated wild-type cellular p21 to determine whether these domain peptides may be involved in ras signaling through GAP
Doisneau-Sixou et al., Endocr Relat Cancer 2003 (Breast Neoplasms) : Insulin and estrogen synergistically stimulate cell cycle progression, and the ability of estrogen to antagonize an insulin induced increase in p21 ( WAF1/CIP1 ) gene expression appears to underlie this effect
Nakajima et al., Biochem Biophys Res Commun 2004 : To assess the relationship between the induction of p21 and MAP kinase activity, we investigated the effect of these inhibitors on insulin induced p21 expression in ATDC5 cells
Kaburagi et al., Endocrinology 2004 (MAP Kinase Signaling System) : In this type of cell overexpressing IRS-1 or IRS-3, we showed that : 1 ) overexpression of IRS-3, but not IRS-1, suppressed the G1/S transition induced by insulin ; 2 ) IRS-3 was more preferentially localized to the nucleus than IRS-1 ; 3 ) phosphorylation of glycogen synthase kinase 3 and MAPK/ERK was unaffected by IRS-3 overexpression, whereas that of protein kinase B was enhanced by either IRS; 4 ) overexpressed IRS-3 suppressed cyclin D1 expression in response to insulin ; 5 ) among the signaling molecules regulating cyclin D1 expression, activation of the small G protein Ral was unchanged, whereas insulin induced gene expression of c-myc, a critical component for growth control and cell cycle progression, was suppressed by overexpressed IRS-3 ; and 6 ) insulin induced expression of p21 , a cyclin dependent kinase inhibitor, was decreased by overexpressed IRS-3
Qu et al., Frontiers in bioscience : a journal and virtual library 2006 : In prior studies, we have found that oncogenic ras-p21 protein induces oocyte maturation using pathways that differ from those activated by insulin induced wild-type ras-p21 ... Both oncogenic and wild-type ras-p21 require interactions with raf, but unlike oncogenic ras-p21, insulin activated wild-type ras-p21 does not depend completely on activation of MEK and MAP kinase ( MAPK or ERK ) on the raf kinase pathway
Adler et al., Ann Clin Lab Sci 2008 (Cell Transformation, Neoplastic...) : In contrast, in oocytes induced to mature with insulin , which requires activation of wild-type ras-p21 , phosphorylation of raf-Ser338 but not raf-Ser259 occurs
Barrett et al., Mol Cell Biol 1990 : Microinjection of c-mosxe antisense oligonucleotides inhibited germinal vesicle breakdown induced by p21 and totally abolished S6 kinase activation by insulin or progesterone but only partially inhibited activation by p21
Robinson et al., Endocrinology 1994 : Insulin and IGF-I increased the ratio of GTP/GTP + GDP by 31 +/- 9.0 % and 36 +/- 8.0 %, respectively, p21Ras activation by insulin and IGF-I was maximal within 5 min
Burgering et al., Mol Cell Biol 1993 : Expression of p21rasAsn-17 , a dominant negative mutant of p21ras that blocks p21ras activation by growth factors, inhibits activation of extracellular signal regulated kinase 2 ( ERK2 ) by insulin and platelet derived growth factor in rat-1 cells [ A. M. M. de Vries-Smits, B. M. T. Burgering, S. J. Leevers, C. J. Marshall, and J. L. Bos, Nature ( London ) 357 : 602-604, 1992 ]