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E2F4 — TGFB1

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: Complex of E2F4-EP300 → TGFB1 (decreases)
  Evidence: TGF-beta signaling did not compete with E2F-4 for binding to TIE/E2F, but reduced p300 co-immunoprecipitating with E2F-4. Therefore, TGF-beta signaling may suppress c-myc promoter activity by dissociating p300 from E2F-4.
• OpenBEL Selventa BEL large corpus: Complex of E2F4-RB1 → TGFB1 (increases) Li et al., Proc Natl Acad Sci U S A 1997*
  Evidence: We show here that TGF-beta treatment of HaCaT cells induced the formation of E2F4-RB and E2F4-p107 complexes, which are capable of binding to E2F sites.

Text-mined interactions from Literome

Hu et al., Leukemia & lymphoma 2000 (Leukemia, Myeloid) : Since TGFbeta1 upregulates p130/E2F-4 complex formation and downregulates p107/E2F-4 complex formation, with E2F-4 levels remaining constant, our results suggest that E2F-4 is switched from p107 to pRb and p130 when cells exit from the cell cycle and arrest in G1 by TGFbeta1
Fan et al., J Cell Sci 2002 : In this study, we examined the downstream effects of TGF-beta1 induced apoptosis and the potential roles for pRb and E2F
Herzinger et al., Oncogene 1995 : We have studied the effect of TGF-beta 1 on protein binding to a transcription factor E2F consensus element in extracts from early passage human keratinocytes ( HFKs ) and a permanent human keratinocyte cell line ( HaCaT )
Bang et al., J Biol Chem 1996 : TGF-beta1 increased the binding of p107 to the transcription factor E2F , leading to decreased c-Myc protein levels
Birchenall-Roberts et al., Oncogene 1996 : Surprisingly, in 32D-abl cells, TGF-beta1 , a potent G1/S inhibitor of 32D-123 and 32D-abl cell growth, increased E2F transactivation as shown by increased c-myc promoter-CAT and GAL4-E2F-1 activity