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CDK2 — HDAC2
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
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Gene Ontology Complexes transcription factor complex:
transcription factor complex complex (ATF7IP-GSC-GCM1-MAFB-NKX2-1-NKX2-5-RARG-KLF4-FOXF1-FOXF2-FOXE3-LDB1-ZFHX3-GATA6-SNAI3-FOXH1-KAT5-AHR-EYA3-NFATC2-CRX-MED27-HES6-SKI-XRCC6-ARNTL-SUB1-JUN-SOX17-SCX-DMBX1-TCF4-TCF7-PDLIM1-TFEB-LBX1-TRRAP-NAA16-EPAS1-MGA-PTF1A-HOXD12-MEF2B-TFDP3-TFDP1-HDAC2-YY1-SMAD9-CLOCK-ONECUT3-SMAD5-SMAD6-SMAD7-SMAD1-SMAD2-PRKDC-RCOR2-NHLH2-REL-TBX5-ARNTL2-BSX-HOXA10-HOXB13-MED23-PUS1-TAL1-RBL1-RBL2-MINA-HMGA1-BARX2-LEF1-EP300-PMF1-ARID5A-WWTR1-LMO2-LMO4-TP73-ABT1-CDK2-DKFZp686M216-CREG1-CTNNB1-SOX9-HAND2-SOX2-TEAD2-MYOG-TEAD4-CEBPA-GFI1B-MYOD1-ALX1-NPAS4-TFAP2D-FIGLA-ALX4-ETS1-PROP1-ASCL3-HCLS1-MSX1-MSX2-SRA1-AJUBA-MTA2-SIN3A-POU3F2-POU3F1-BEX1-MLXIPL-NR2E3-PBX2-ANKRD1-E2F6-E2F5-E2F4-E2F3-E2F2-E2F1-E2F8-CREBBP-ATF5-ATF4-POU2F3)
Kaspar et al., J Biol Chem 1999, Wang et al., J Biol Chem 1999, Nagpal et al., J Biol Chem 1999, Blixt et al., Genes Dev 2000, Carlberg et al., Mol Cell Biol Res Commun 2000, Bae et al., Development 2000, Cairo et al., Hum Mol Genet 2001, Tutter et al., Genes Dev 2001, Willis et al., J Biol Chem 2002, Bayne et al., Mol Hum Reprod 2004, Schubert et al., J Biol Chem 2004, Han et al., J Mol Biol 2005, Rodriguez et al., EMBO J 2005, Han et al., Nucleic Acids Res 2005, Zhang et al., Mol Cell Biol 2007, Wong et al., Cell 2009, Stevens et al., Immunology 2009, Stefanovic et al., J Cell Biol 2009, Skokowa et al., Nat Med 2012, Ge et al., Cell 1994, Durocher et al., EMBO J 1997, Hogenesch et al., Proc Natl Acad Sci U S A 1998, Hellqvist et al., J Biol Chem 1998, Ryu et al., Nature 1999
Text-mined interactions from Literome
Kim et al., J Antibiot (Tokyo) 2000
(Colorectal Neoplasms) :
These results suggest that the suppression of
Cdk2 kinase activity due to p21 overexpression
play a critical role in
HDAC inhibitor induced growth inhibition
Hitomi et al., FEBS Lett 2003
:
Histone deacetylase (HDAC) inhibitors arrest human tumor cells at the G1 phase of the cell cycle and
activate the
cyclin dependent kinase inhibitor, p21 ( WAF1/Cip1 )
Li et al., Cancer Res 2010
(Colonic Neoplasms) :
HDAC depletion relieved
HDAC mediated transcriptional inhibition of the
cyclin dependent kinase inhibitors p21WAF1 and p27KIP2, significantly increasing their expression and triggering cell cycle arrest in the G(2) phase of the cell cycle
Findeisen et al., Arterioscler Thromb Vasc Biol 2011
(Disease Models, Animal...) :
HDAC inhibition
resulted in a transcriptional and posttranscriptional regulation of the
cyclin dependent kinase inhibitors p21 ( Cip1 ) and p27 ( Kip )
Veliz et al., Cancer Control 2012
(Leukemia, Lymphocytic, Chronic, B-Cell...) :
These investigational agents include rituximab, alemtuzumab, ofatumumab, bendamustine, high-dose methylprednisolone, lenalidomide, lumiliximab,
cyclin dependent kinase inhibitors, small modular immunopharmaceuticals, Bcl-2 inhibitors, and
histone deacetylase inhibitors