Gene interactions and pathways from curated databases and text-mining

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CCND1 — PI3

Text-mined interactions from Literome

Gille et al., J Biol Chem 1999 : PI 3-kinase activity is required for the expression of endogenous cyclin D(1) and for S phase entry following serum stimulation of quiescent NIH 3T3 fibroblasts ... Activated PI 3-kinase induces cyclin D(1) transcription and E2F activity, at least in part mediated by the serine/threonine kinase Akt/PKB, and to a lesser extent the Rho family GTPase Rac
D'Amico et al., J Biol Chem 2000 (Breast Neoplasms) : Inhibition of the PI 3-kinase and AKT/protein kinase B, but not of the p38, ERK, or JNK signaling pathways, reduced ILK induction of cyclin D1 expression
Oh et al., Exp Mol Med 2002 (Colorectal Neoplasms...) : In this study, we have elucidated differential regulation of the zinc stimulated p21 ( CiP/WAF1 ) and cyclin D1 activation by inhibition of phosphoinositide 3-kinase (PI3K)
Kuemmerle et al., Am J Physiol Gastrointest Liver Physiol 2004 : IGF-I elicited a time dependent increase in cyclin D1 protein levels mediated jointly by ERK1/2 dependent and PI3-kinase dependent mechanisms
Ouyang et al., Carcinogenesis 2006 (Skin Neoplasms) : Furthermore, inhibition of PI-3K/Akt by overexpression of Deltap85 or DN-Akt blocked arsenite induced IKK phosphorylation, IkappaBalpha degradation and cyclin D1 expression, indicating that IKK/NFkappaB is the downstream transducer of arsenite triggered PI-3K/Akt cascade
Wu et al., Oncogene 2008 : Transcriptional activation of c-myc and cyclin D1 promoters by nuclear IRS-1 does not occur with a mutant, inactive IRS-1 protein ( deletion of the phosphotyrosine binding domain, PTB ) and does not require PI3-kinase activity
Ouyang et al., Environ Health Perspect 2008 (Cell Transformation, Neoplastic...) : Our results demonstrate that PI-3K/Akt mediated cyclin D1 expression is at least one key event implicated in the arsenite human skin carcinogenic effect
Fukushima et al., Endocrinology 2008 : In contrast, IGF-I dependent PI 3-kinase activation was required for the increase in cyclin D1 mRNA levels and degradation of p27 ( Kip1 )
Zhang et al., Life Sci 2013 (Asthma...) : In the present study, we determined whether Phosphoinositide 3-kinase (PI3K) and Notch signal pathways are involved in the expression of cyclinD1 , cyclinA and p27kip1 which were key molecules in controlling cell cycling from CD4 ( + ) T lymphocyte in animal model of asthma
Treinies et al., Mol Cell Biol 1999 : Activation of PI3-kinase is indirect, perhaps through autocrine growth factors, and is required for the induction of cyclin D1
Takuwa et al., Mol Cell Biol 1999 : These results indicate that the catalytic activity of PI 3-kinase is necessary, and could also be sufficient , for upregulation of cyclin D1 , with mTOR signaling being differentially required depending upon cellular conditions