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BCL2 — RAF1

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: BCL2 → RAF1 (directlyIncreases, RAF1 Activity, BCL2 Activity)
  Evidence: This action releases activated NF-kB, which is then translocated to the nucleus where it mediates transcription of antiapoptotic factors.155,166 Other antiapoptotic effects of C-Raf are mediated by a mitochondrial pool of the protein, which, on stimulation, localizes to the mitochondrial membrane where the protein interacts with and phosphorylates Bcl-2, Bcl-2-associated athanogene, and other pro-apoptotic regulators, abrogating their pro-apoptotic effects.
• OpenBEL Selventa BEL large corpus: BCL2 → RAF1 (directlyIncreases, BCL2 Activity)
  Evidence: This action releases activated NF-kB, which is then translocated to the nucleus where it mediates transcription of antiapoptotic factors.155,166 Other antiapoptotic effects of C-Raf are mediated by a mitochondrial pool of the protein, which, on stimulation, localizes to the mitochondrial membrane where the protein interacts with and phosphorylates Bcl-2, Bcl-2-associated athanogene, and other pro-apoptotic regulators, abrogating their pro-apoptotic effects.

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: RAF1 — BCL2 (physical association, affinity chromatography technology) Jin et al., J Biol Chem 2005*
• IRef Biogrid Interaction: RAF1 — BCL2 (physical association, affinity chromatography technology) Mazzocca et al., Mol Pharmacol 2003*
• IRef Biogrid Interaction: RAF1 — BCL2 (direct interaction, two hybrid) Wang et al., Cell 1996*
• IRef Biogrid Interaction: RAF1 — BCL2 (physical association, affinity chromatography technology) Wang et al., Cell 1996*
• IRef Biogrid Interaction: RAF1 — BCL2 (direct interaction, pull down) Wang et al., Cell 1996*
• IRef Hprd Interaction: RAF1 — BCL2 (in vivo) Reed et al., Adv Exp Med Biol 1996*, Wang et al., Cell 1996*
• IRef Hprd Interaction: RAF1 — BCL2 (in vitro) Reed et al., Adv Exp Med Biol 1996*, Wang et al., Cell 1996*
• IRef Ophid Interaction: RAF1 — BCL2 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005
• IRef Ophid Interaction: RAF1 — BCL2 (aggregation, confirmational text mining) Reed et al., Adv Exp Med Biol 1996*
• STRING interaction: BCL2 — RAF1 (interaction, mapped from kegg_pathways)
• STRING interaction: BCL2 — RAF1 (interaction, mapped from kegg_pathways)
• STRING interaction: RAF1 — BCL2 (interaction, mapped from kegg_pathways)
• STRING interaction: RAF1 — BCL2 (interaction, mapped from kegg_pathways)

Text-mined interactions from Literome

Blagosklonny et al., Leukemia 1999 (Leukemia, Myeloid) : Although Lck tyrosine kinase has been recently implicated in Raf-1 activation during mitotic arrest, microtubule-active drugs induce Raf-1/Bcl-2 hyperphosphorylation and apoptosis in a Lck-deficient Jurkat cells
Nicolini et al., Neurochem Int 2003 (Brain Neoplasms...) : trans-Resveratrol reverses phosphorylation of Bcl-2 induced by paclitaxel and concomitantly blocks Raf-1 phosphorylation, also observed after paclitaxel exposure, thus suggesting that Bcl-2 inactivation may be dependent on the activation of the Raf/Ras cascade
Jin et al., J Biol Chem 2005 (MAP Kinase Signaling System) : Moreover, the mitochondrial translocation of Raf-1 and the interaction between Raf-1 and Bcl-2 are regulated by Raf-1 phosphorylation at Ser-338/Ser-339
Blagosklonny et al., Cancer Res 1996 (Breast Neoplasms...) : Taxol induced apoptosis and phosphorylation of Bcl-2 protein involves c-Raf-1 and represents a novel c-Raf-1 signal transduction pathway