Gene interactions and pathways from curated databases and text-mining

◀ Back to CCND1

CCND1 — CDK1

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Chang et al., Int J Oncol 2000 (Neoplasms, Experimental) : Inhibition of cyclin D1 expression or induction of cyclin dependent kinase inhibitor p21WAF1 expression was found in mimosine treated lung cancer cells
Osborne et al., Br J Dermatol 2002 (Breast Neoplasms...) : 1,25 ( OH ) 2D3 has a major inhibitory effect on the G1/S checkpoint of the cell cycle by upregulating the cyclin dependent kinase inhibitors p27 and p21, and by inhibiting cyclin D1
Cheng et al., Cancer Sci 2004 (Carcinoma, Hepatocellular...) : Etodolac induced p21WAF1/Cip1 and p27Kip1 expression and inhibited CDK2, CDK4, CDC2 , cyclin A and cyclin B1 expression, but did not affect cyclin D1 or cyclin E. HGF and 10 % FBS induced ERK phosphorylation, but phosphorylation of p38, JNK and AKT was down-regulated by etodolac
Nelsen et al., J Biol Chem 2005 (Aneuploidy...) : Transient transfection of cyclin D1 also induced centrosome and mitotic spindle abnormalities in breast epithelial cells, suggesting that this may be a generalized effect
Lavine et al., Mol Endocrinol 2008 : Analysis of cyclin and cdk mRNA and protein abundance revealed that CCK overexpression increased cyclin A, cyclin B, cyclin E, cdk1 , and cdk2 with no change in cyclin D1 , cyclin D2, cyclin D3, cdk4, or cdk6 in mouse and human islets
Brennan et al., J Med Food 2012 (Adrenocortical Carcinoma) : BME treatment enhanced cellular tumor antigen p53, cyclin dependent kinase inhibitor 1A ( also called p21 ), and cyclic AMP dependent transcription factor-3 levels and inhibited G1/S-specific cyclin D1 , D2, and D3, and mitogen activated protein kinase 8 ( also called Janus kinase ) expression, suggesting an additional mechanism involving cell cycle regulation and cell survival
Kang et al., Apoptosis 2012 : Cell cycle analysis indicated thioridazine induced the down-regulation of cyclin D1 , cyclin A and CDK4, and the induction of p21 and p27, a cyclin dependent kinase inhibitor