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E2F8 — RBL2

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

Studies that report less than 10 interactions are marked with *

• 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

Wharton et al., J Biol Chem 2000 : In contrast, p130 became partially phosphorylated, accompanied by a marked increase in p130 dependent E2F DNA binding activity and a partial release of free E2F-4
Yamada et al., Cytokine 2002 : Our results indicate that blocking E2F dependent transactivation, but not the formation of p130-E2F transcriptional repressor complexes, is responsible for the inhibition of IL-3 dependent cell growth by p130
Genovese et al., Oncogene 2006 (Eye Neoplasms...) : The mechanisms of transcriptional activation and repression by the Rb gene family has been extensively investigated : pRb, pRb2/p130 and p107 interact with different E2F family factors and can inhibit E2F responsive promoters, interfering with progression of cell cycle, gene transcription, initiation of apoptotic process and cell differentiation
Dingar et al., J Mol Cell Cardiol 2012 : As analyzed by chromatin immunoprecipitation, the E2F4-p130-repressor directly blocks transcription of essential apoptosis related genes, E2F1 , Apaf-1, and p73a through recruitment of histone deacetylase 1 (HDAC1)
Zalvide et al., Mol Cell Biol 1998 : Furthermore, the J domain is required to override the repression of E2F activity mediated by p130 and pRB and to disrupt p130-E2F DNA binding complexes