Gene interactions and pathways from curated databases and text-mining

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CCND1 — INS

Text-mined interactions from Literome

Chappell et al., J Biol Chem 2001 (Breast Neoplasms) : In contrast to its potentiating action, a direct mitogenic effect of insulin in MCF-7 cells involves activation of phosphatidylinositol 3-kinase and increased expression of cyclin D1
Kim et al., Obes Res 2001 : Removing insulin from cultures resulted in a reduction in differentially elevated levels of cyclin D1
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
Mawson et al., Mol Cell Endocrinol 2005 (Breast Neoplasms) : These studies demonstrated that estrogen significantly increased both c-Myc and cyclin D1 protein, while insulin predominantly increased cyclin D1 levels ... Therefore, estrogen and insulin/IGF-1 differentially regulate c-Myc and cyclin D1 to cooperatively stimulate breast cancer cell proliferation
Sun et al., Oncogene 2009 : We found previously that in intestinal cells, insulin or insulin-like growth factor-1 stimulates c-Myc and cyclin D1 protein expression through both Akt dependent and Akt independent mechanisms ... Significantly, shRNA ( small hairpin RNA ) -mediated PAK-1 knockdown attenuated both basal and insulin stimulated c-Myc and cyclin D1 expression, associated with a marked reduction in extracellular signal regulated kinase activation and beta-cat phosphorylation at Ser675
Pongsavee et al., International journal of molecular sciences 2009 : It is presumed that estrogen and insulin/IGF-1 regulate c-Myc and cyclin D1 during breast cancer cell proliferation
Palaniappan et al., Mol Cell Endocrinol 2013 : Furthermore, insulin stimulated T-I cell proliferation and the expression of cell cycle regulatory proteins CDK4, CCND3 and PCNA were also blocked by rapamycin