Gene interactions and pathways from curated databases and text-mining

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CCND1 — PIK3R1

Text-mined interactions from Literome

Dufourny et al., J Endocrinol 2000 (Breast Neoplasms) : Since transcriptional activation of the cyclin D1 promoter by EGF, E2 and TPA is independent of PI3-K activity, these findings suggest a post-transcriptional role for PI3-K in the regulation of cyclin D1 expression
Guillemot et al., J Biol Chem 2001 (MAP Kinase Signaling System) : Taken together, these findings demonstrate that Ang II-induced cyclin D1 up-regulation is mediated by the activation and specific interaction of Egr-1 with the -136 to -96 bp region of the cyclin D1 promoter and by activation of the -29 to +139 bp region, both in a p21(ras)/Raf-1/MEK/ERK dependent manner, and also involves PI3K and SHP-2
Timms et al., Oncogene 2002 (Breast Neoplasms...) : PI3K signalling also participated in cell cycle progression, since PI3K and MAPK coordinately regulated changes in cyclin D1 and cdk6 expression
Albanese et al., Mol Biol Cell 2003 : Mitogenic induction of G ( 1 ) -S phase progression and cyclin D1 expression was PI3K dependent , and cyclin D1 ( -/- ) cells showed reduced PI3K dependent S-phase entry ... PI3K dependent induction of cyclin D1 was blocked by inhibitors of PI3K/Akt/IkappaB/IKKalpha or beta-catenin signaling
Acosta et al., Mol Endocrinol 2003 : Moreover, we show that both c-Src/PI3K and c-Src/Fak/Erk1/2 pathways are involved in the up-regulation of c-myc and cyclin d1 expression mediated by PRL
Lin et al., Mol Pharmacol 2003 : PTX blocks Akt but not phosphatidylinositol 3-kinase (PI3K) activation in response to PDGF and abrogates cyclin D1 induction by PI3K , suggesting an effect of PTX on Akt itself
Zhang et al., Cancer Res 2004 (Rhabdomyosarcoma...) : Inhibition of either pathway reduced expression of cyclins D1, D2, and D3 in RMS lines, whereas only PI3K inhibitors blocked cyclin D1 , D2, and D3 expression in ET lines
Takasawa et al., FEBS Lett 2006 : The Reg/ATF-2 induced cyclin D1 promoter activation was attenuated by PI(3)K inhibitors such as LY294002 and wortmannin
Friedrichsen et al., J Endocrinol 2006 : We conclude that incretin induced beta-cell replication is dependent on cAMP/PKA, p42 MAPK and PI3K activities, which may involve transcriptional induction of cyclin D1
Yang et al., BMC cell biology 2006 : We found, however, that neither PI3K , AKT, GSK3, nor proliferative signaling activity in general is responsible for the S phase decline in cyclin D1 levels
Xing et al., American journal of physiology. Renal physiology 2008 : These data reveal that Src is a crucial mediator of RPTC proliferation and Src mediated proliferation is associated with PI3K dependent upregulation of cyclin D1 and PI3K independent downregulation of p27 and p57
Zhang et al., Experimental biology and medicine (Maywood, N.J.) 2010 : These findings demonstrate for the first time that PI3K/Akt dependent cyclin D1 activation plays an essential role in HDL induced EPC proliferation, migration and angiogenesis
Li et al., PloS one 2012 : Pharmacological inhibition of JAK/STAT3, PI3K/Akt or MEK/ERK signaling by AG490, Wortmannin or U0126, respectively, reduced leptin induced cyclin D1 expression and NP cell proliferation