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CALM3 — PCNA

Text-mined interactions from Literome

Choi et al., Circ Res 2006 : We next determined that this Ca2+-responsive kinase activity was dependent on a direct interaction between calmodulin (CaM), one of the major Ca2+-signal transducers of eukaryotic cells, and cyclin E. Pharmacological inhibition of CaM abrogated the Ca2+ sensitivity of cyclin E/CDK2 and retarded mouse VSMC proliferation by causing G1 arrest ... Taken together, these findings reveal CaM dependent cyclin E/CDK2 activity as a mediator of the known Ca2+ sensitivity of the G1/S transition of VSMC
Choi et al., Cell cycle (Georgetown, Tex.) 2006 : Having identified a CaM binding site on cyclin E1, our studies support a direct role for CaM in mediating Ca2+-sensitive cyclin E/CDK2 activity and G1 to S phase transitions in VSMC
Hui et al., Circ Res 2011 (Coronary Restenosis...) : Having discovered that calmodulin (CaM) dependent cyclin E/CDK2 activity underlies Ca ( 2+ ) -sensitive G ( 1 ) -to-S phase transitions in VSMCs, we sought to explore the physiological importance of the CaM-cyclin E interaction
Colomer et al., Biochem Biophys Res Commun 1994 : We report here that Ca2+ and calmodulin regulate the expression of cdk2, cdc2, cyclin B and the proliferating cell nuclear antigen ( a co-factor of DNA polymerase-delta ) in human T lymphocytes
Taulés et al., J Biol Chem 1998 : Calmodulin is essential for cyclin dependent kinase 4 (Cdk4) activity and nuclear accumulation of cyclin D1-Cdk4 during G1