Gene interactions and pathways from curated databases and text-mining

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BCR — CCND2

Text-mined interactions from Literome

Deininger et al., Cancer Res 2001 (Blast Crisis...) : Inhibition of Bcr-Abl with STI571 resulted in down-regulation of cyclin D2 and reduction of the number of cells in S phase, although complete G1 arrest was not induced
Banerji et al., Oncogene 2001 (Lymphoma, B-Cell...) : We show that BCR stimulation of WEHI 231 cells results in down-regulation of cyclin D2 and up-regulation of p27 ( Kip1 ), which are associated with pocket protein hypophosphorylation and E2F inactivation
Piatelli et al., J Biol Chem 2002 : Inhibition of the MEK1/2-ERK pathway was sufficient to abrogate BCR induced cyclin D2 expression at the mRNA and protein levels ... Disruption of endogenous heat shock protein 90 (hsp90) function with geldanamycin abrogated BCR induced cyclin D2 expression and proliferation
Glassford et al., Oncogene 2003 (Calcium Signaling...) : Collectively, these data provide evidence for the concept that the B-cell signalosome ( p85alpha, Btk, BLNK and PLCgamma ) is involved in regulating cyclin D2 expression in response to BCR engagement ... Consistent with this, we also showed that the BCR mediated cyclin D2 induction could be abolished by pretreatment of resting B cells with specific inhibitors of capacitative Ca ( 2+ ) entry ( SK & F 96365 ) or PKC ( Gö6850 )
Glassford et al., Eur J Immunol 2005 : The inhibitors of PI3K activity, LY294002 and Wortmannin, also abrogate cyclin D2 induction by BCR cross linking, confirming that the class IA PI3K is necessary for cyclin D2 induction in response to BCR stimulation ... Furthermore, using both p85alpha-null and p110delta-null B cells and inhibitors of PI3K, this study demonstrates for the first time, that BCR cross linking induces cyclin D2 mRNA expression via transcriptional activation of the cyclin D2 promoter and that this transcriptional activation of cyclin D2 requires PI3K activity
Xing et al., J Exp Med 2005 : G5pr(-/-) B cells did not show abnormalities in the BCR mediated activation of Erks and NF-kappaB, cyclin D2 induction, or Akt activation