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CCNH — CDK2

Pathways - manually collected, often from reviews:

• BioCarta cyclins and cell cycle regulation: CDK7/cyclin H complex (CDK7-CCNH) → CYCLIN A/CDK2 complex (CDK2-CCNA1) (modification, activates)
  
• KEGG Cell cycle: Complex of CCNH-CDK7 → CDK2 (protein-protein, phosphorylation)
• Reactome Reaction: CDK2 → CCNH (reaction) Aprelikova et al., J Biol Chem 1995

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: CCNH — CDK2 (direct interaction, enzymatic study) Garrett et al., Mol Cell Biol 2001*
• IRef Biogrid Interaction: CCNH — CDK2 (direct interaction, enzymatic study) Higashi et al., Eur J Biochem 1996
• IRef Biogrid Interaction: CCNH — CDK2 (direct interaction, enzymatic study) Xu et al., Biochemistry 1999*
• IRef Biogrid Interaction: CCNH — CDK2 (direct interaction, enzymatic study) Lolli et al., Structure 2004*
• IRef Biogrid Interaction: CCNH — CDK2 (physical association, affinity chromatography technology) Varjosalo et al., Nat Methods 2013
• IRef Hprd Interaction: CCNH — CDK2 (in vitro) Mandal et al., Oncogene 1998*
• IRef Intact Interaction: CCNH — CDK2 (physical association, two hybrid) Zariwala et al., Oncogene 1998
• IRef Intact Interaction: Complex of MNAT1-CDK7-CCNH-CDK2 (phosphorylation reaction, protein kinase assay) Tassan et al., EMBO J 1995*
• IRef Ophid Interaction: CCNH — CDK2 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Morisaki et al., Exp Cell Res 1999 : This cyclin D1-bound Cdk2 was not activated by CAK either in vivo or in vitro, implicating cyclin D1 as an inhibitor of Cdk2 activation
Kim et al., J Biol Chem 2001 : For example, CDK9 was not phosphorylated by CAK, whereas CDK2-cyclin A kinase activity was dramatically enhanced by CAK
Yao et al., Mol Cell Biol 2002 : Activation of the Bur1-Bur2 cyclin dependent kinase complex by Cak1
Hamada et al., Biochim Biophys Acta 1996 : Phorbol ester treatment does not reduce the protein level of p33CDK2 , but does inhibit serum stimulated increases in the CAK activity and CDK2 phosphorylation at Thr160
Ko et al., Mol Cell Biol 1997 : While CDK7-cyclin H is sufficient for phosphorylation of CDK2 , we show that p36MAT1 is required for efficient phosphorylation of p53 by CDK7-cyclin H, suggesting that p36MAT1 can act as a substrate specificity determining factor for CDK7-cyclin H
Mandal et al., Oncogene 1998 : We also demonstrated that IFN induced CKIs prevent CAK from activating the CDK-2 as immunodepletion of induced CKIs from the inhibitory extracts resulted in the restoration of CAK mediated activation of CDK-2