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CDK2 — SPDYA

Pathways - manually collected, often from reviews:

• KEGG Progesterone-mediated oocyte maturation: SPDYA/SPDYC → CDK2 (protein-protein, activation)

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: CDK2 — SPDYA (physical association, affinity chromatography technology) McAndrew et al., Cell cycle (Georgetown, Tex.) 2007*
• IRef Biogrid Interaction: CDK2 — SPDYA (physical association, affinity chromatography technology) Gastwirt et al., J Biol Chem 2006*
• IRef Biogrid Interaction: CDK2 — SPDYA (physical association, affinity chromatography technology) Dinarina et al., FEBS Lett 2009*
• IRef Biogrid Interaction: CDK2 — SPDYA (physical association, affinity chromatography technology) Porter et al., J Cell Biol 2002*
• IRef Biogrid Interaction: CDK2 — SPDYA (physical association, affinity chromatography technology) Barnes et al., Cancer Res 2003*
• IRef Biogrid Interaction: CDK2 — SPDYA (physical association, affinity chromatography technology) Porter et al., Mol Biol Cell 2003*
• IRef Hprd Interaction: Complex of CDK2-CDKN1B-SPDYA-CDKN1B-SPDYA-CDK2-SPDYA-CDKN1B-CDK2 (in vivo) Porter et al., Mol Biol Cell 2003*
• IRef Hprd Interaction: CDK2 — SPDYA (in vivo) Porter et al., J Cell Biol 2002*, Barnes et al., Cancer Res 2003*

Text-mined interactions from Literome

Cheng et al., BMC biochemistry 2005 : These differences may accommodate the CAK independent activation of Cdk2 by Speedy/Ringo A2 and they raise the possibility that CDK-Speedy/Ringo A2 complexes could phosphorylate and regulate a subset of non-canonical CDK substrates, such as Cdc25 protein phosphatases, to control cell cycle progression
Zhang et al., J Mol Neurosci 2012 (Brain Neoplasms...) : Altered expression of Spy1 led to changes in cell cycle processes, cyclin dependent kinase 2 activity, and p27kip1 protein stabilization, ultimately disrupting cell growth rate ... Altered expression of Spy1 led to changes in cell cycle processes, cyclin dependent kinase 2 activity, and p27kip1 protein stabilization, ultimately disrupting cell growth rate