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RAF1 — RB1

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: Complex of RAF1-RB1 → SRC (increases) Dasgupta et al., J Clin Invest 2006*
  Evidence: A549 cells were transiently transfected with FLAG–Raf-1 and Myc-Rb in the presence of wt Src, dominant negative Src or constitutively activated Src (v-Src)....Figure 3G shows that the Rb–Raf-1 interaction is observed in cells transfected with WT and constitutively activated Src; however, dominant-negative Src inhibited the nicotine-induced Rb–Raf-1 binding.
• OpenBEL Selventa BEL large corpus: Complex of RAF1-RB1 → SRC (increases, RAF1/RB1 Activity) Dasgupta et al., J Clin Invest 2006*
  Evidence: A549 cells were transiently transfected with FLAG–Raf-1 and Myc-Rb in the presence of wt Src, dominant negative Src or constitutively activated Src (v-Src)....Figure 3G shows that the Rb–Raf-1 interaction is observed in cells transfected with WT and constitutively activated Src; however, dominant-negative Src inhibited the nicotine-induced Rb–Raf-1 binding.
• OpenBEL Selventa BEL large corpus: Complex of RAF1-RB1 (increases) Dasgupta et al., J Clin Invest 2006*
  Evidence: As shown in Figure 2A, quiescent A549 cells and HAECs did not have any detectable Rb–Raf-1 interaction, but stimulation with nicotine induced a robust Rb–Raf-1 interaction. The Rb–Raf-1 interaction was detected up to 2 hours after nicotine stimulation and dissipated within 4 hours. The binding between Rb and Raf-1 was also observed in lung cancer cell lines H23, H441, and H226 (Figure 2B) as well as in primary lung cells such as SAECs, NHBEs, and HMEC-Ls stimulated with 1 ?M nicotine (Figu...
• OpenBEL Selventa BEL large corpus: Complex of RAF1-RB1 (increases)
  Evidence: The mitogenic effects of nicotine resulted in enhanced recruitment of E2F1 and Raf-1 causing dissociation of Rb from these promoters...[90].
• OpenBEL Selventa BEL large corpus: Complex of RAF1-RB1 (increases)
  Evidence: Treatment of A549 cells with 1 mM nicotine (the mean plasma concentration of nicotine in smokers) was found to cause physical interaction of the retinoblastoma protein (Rb) with the signaling kinase Raf-1 [16]
• OpenBEL Selventa BEL large corpus: RB1 → RAF1 (directlyIncreases, RB1 Activity)
  Evidence: 157,167 The antiapoptotic effects of C-Raf are also mediated through the ankyrin-repeat protein Tvl-1 and apoptosis signal-regulated kinase-1.166,168,169 In addition, C-Raf phosphorylates Rb, p53, Cdc25, and other cell cycle regulatory proteins in metaphase.
• OpenBEL Selventa BEL large corpus: RB1 → RAF1 (directlyIncreases, RB1 Activity)
  Evidence: Raf1 can bind pRb and p130, which are not thereby dissociated from E2F complexes, although promoter inhibition is reversed (Wang et al., 1998). There was no detectable binding to p107. Binding to pRb is mediated by the Nterminal 28 amino acids of Raf1. The kinase activity of Raf1 was required to reverse the pRb-mediated promoter repression (Wang et al., 1998), but the phosphorylation sites on pRb remain to be described and therefore are not indicated in the diagram.

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

Studies that report less than 10 interactions are marked with *

• IRef Bind Interaction: RAF1 — RB1 Wang et al., Mol Cell Biol 1998*
• IRef Bind_translation Interaction: RAF1 — RB1 (experimental interaction detection) Wang et al., Mol Cell Biol 1998*
• IRef Bind_translation Interaction: RAF1 — RB1 (coimmunoprecipitation) Wang et al., Mol Cell Biol 1998*
• IRef Bind_translation Interaction: RAF1 — RB1 (affinity chromatography technology) Wang et al., Mol Cell Biol 1998*
• IRef Bind_translation Interaction: RAF1 — RB1 (two hybrid) Wang et al., Mol Cell Biol 1998*
• IRef Biogrid Interaction: RAF1 — RB1 (physical association, affinity chromatography technology) Dasgupta et al., Mol Cell Biol 2004*
• IRef Biogrid Interaction: RAF1 — RB1 (physical association, affinity chromatography technology) Wang et al., Mol Cell Biol 1998*
• IRef Biogrid Interaction: RAF1 — RB1 (direct interaction, two hybrid) Wang et al., Mol Cell Biol 1998*
• IRef Biogrid Interaction: RAF1 — RB1 (physical association, affinity chromatography technology) Singh et al., Mol Cancer Ther 2010*
• IRef Biogrid Interaction: RAF1 — RB1 (direct interaction, pull down) Wang et al., Mol Cell Biol 1998*
• IRef Biogrid Interaction: RAF1 — RB1 (direct interaction, enzymatic study) Dasgupta et al., Mol Cell Biol 2004*
• IRef Biogrid Interaction: RAF1 — RB1 (direct interaction, pull down) Wang et al., Mol Cell Biol 1999*
• IRef Biogrid Interaction: RAF1 — RB1 (direct interaction, pull down) Dasgupta et al., Mol Cell Biol 2004*
• IRef Hprd Interaction: RAF1 — RB1 (in vitro) Nakanishi et al., Biochem Biophys Res Commun 1999*, Wang et al., Mol Cell Biol 1998*
• IRef Hprd Interaction: RAF1 — RB1 (in vivo) Nakanishi et al., Biochem Biophys Res Commun 1999*, Wang et al., Mol Cell Biol 1998*
• IRef Intact Interaction: RAF1 — RB1 (physical association, anti bait coimmunoprecipitation) Singh et al., Mol Cancer Ther 2010*
• IRef Ophid Interaction: RAF1 — RB1 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005