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RAF1 — SRC

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: RAF1 → SRC (directlyIncreases, RAF1 Activity)
  Evidence: Y341 is phosphorylated by the Src family of non-RTKs, Janus kinase, and erythropoietin.
• Reactome Reaction: RAF1 → SRC (reaction) Cleghon et al., J Biol Chem 1994*
• Reactome Reaction: RAF1 → SRC (direct_complex) Cleghon et al., J Biol Chem 1994*

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: RAF1 — SRC (direct interaction, pull down) Cleghon et al., J Biol Chem 1994*
• IRef Biogrid Interaction: RAF1 — SRC (physical association, affinity chromatography technology) Cleghon et al., J Biol Chem 1994*
• MIPS CORUM CNK1-SRC-RAF1 complex: CNK1-SRC-RAF1 complex complex (CNKSR1-RAF1-SRC) Ziogas et al., J Biol Chem 2005*
• IRef Corum Interaction: Complex of RAF1-SRC-CNKSR1 (association, anti tag coimmunoprecipitation) Ziogas et al., J Biol Chem 2005*
• IRef Hprd Interaction: RAF1 — SRC (in vivo) Mason et al., EMBO J 1999, Park et al., FEBS Lett 2006*, Cleghon et al., J Biol Chem 1994*, Xia et al., Proc Natl Acad Sci U S A 1996*
• IRef Hprd Interaction: RAF1 — SRC (in vitro) Mason et al., EMBO J 1999, Park et al., FEBS Lett 2006*, Cleghon et al., J Biol Chem 1994*, Xia et al., Proc Natl Acad Sci U S A 1996*
• IRef Ophid Interaction: RAF1 — SRC (aggregation, confirmational text mining) Cleghon et al., J Biol Chem 1994*
• IRef Ophid Interaction: RAF1 — SRC (aggregation, interologs mapping) Brown et al., Bioinformatics 2005
• STRING interaction: SRC — RAF1 (interaction, mapped from kegg_pathways)
• STRING interaction: SRC — RAF1 (interaction, mapped from kegg_pathways)
• STRING interaction: RAF1 — SRC (interaction, mapped from kegg_pathways)
• STRING interaction: RAF1 — SRC (interaction, mapped from kegg_pathways)

Text-mined interactions from Literome

Grammatikakis et al., Mol Cell Biol 1999 : In addition, p50(cdc37) greatly potentiated v-Src mediated Raf-1 activation
Ziogas et al., J Biol Chem 2005 : CNK1 is a scaffold protein that regulates Src mediated Raf-1 activation ... Here we demonstrate that the connector enhancer of Ksr1, CNK1, mediates Src dependent tyrosine phosphorylation and activation of Raf-1 ... CNK1 regulates the activation of Raf-1 by Src in a concentration dependent manner typical for a scaffold protein
Mariappan et al., J Biol Chem 2005 : Studies with PP1/2 showed that phosphorylation of c-Src was required for tyrosine phosphorylation of Raf-1 , an upstream regulator of Erk
Dasgupta et al., J Clin Invest 2006 (Carcinoma, Non-Small-Cell Lung...) : Here we find that mitogenic effects of nicotine in non-small cell lung cancers ( NSCLCs ) are analogous to those of growth factors and involve activation of Src , induction of Rb-Raf-1 interaction, and phosphorylation of Rb. Analysis of human NSCLC tumors show enhanced levels of Rb-Raf-1 complexes compared with adjacent normal tissue
Congleton et al., Leukemia 2012 (Leukemia, Myeloid) : Src inhibitors, PP2 and dasatinib, increase retinoic acid induced association of Lyn and c-Raf ( S259 ) and enhance MAPK dependent differentiation of myeloid leukemia cells
Chow et al., J Biol Chem 1995 : These findings demonstrate that N-terminal deletions in Raf-1 do not necessarily result in constitutively elevated basal kinase activity and that the N-terminal regulatory domain is completely dispensable for Raf-1 activation by Src
Marais et al., EMBO J 1995 : We show that in mammalian cells activation of p74Raf-1 by oncogenic Src requires pp60Src to be myristoylated and the ability of p74Raf-1 to interact with p21Ras-GTP
Pumiglia et al., Mol Cell Biol 1995 : By contrast, deletion of this Ras binding site did not diminish activation of Raf-1 kinase by Src, implying that Src and Ras can activate Raf-1 through independent mechanisms
Bruder et al., Nucleic Acids Res 1993 : In addition to Raf, we show that v-Src , v-H-Ras and v-Mos activate HIV-LTR expression through the NF-kappa B binding sites and v-H-Ras induced HIV-LTR expression is mediated by Raf-1
Stokoe et al., EMBO J 1997 : Activation of c-Raf-1 by Ras and Src through different mechanisms : activation in vivo and in vitro ... Consistent with the results from other groups, we find that the activation of c-Raf-1 by Src in vivo occurs concomitant with tyrosine phosphorylation on c-Raf-1, and in vitro, activation of c-Raf-1 by Src requires the presence of ATP ... Therefore we propose that activation of c-Raf-1 by Ras or by Src occurs through different mechanisms
Zimmermann et al., Oncogene 1997 : Stimulation of Raf-1 activity by MEK1 is independent of Ras, Src and tyrosine phosphorylation of Raf-1
Müller et al., EMBO J 1998 : Both TNF and exogeneous C6-ceramide interfered with the mitogenic activation of Raf-1 and ERK by epidermal growth factor and down-regulated v-Src induced Raf-1 kinase activity