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RBL2 — SMAD3

Pathways - manually collected, often from reviews:

• KEGG TGF-beta signaling pathway: Complex of SMAD2-SMAD3-SMAD4 → Complex of E2F4-E2F5-RBL1-RBL2-TFDP1 (protein-protein, activation)
  

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

Studies that report less than 10 interactions are marked with *

• MIPS Negatome - no physical interaction between proteins Interaction: SMAD3 — RBL2 (Absence of interaction, anti tag coimmunoprecipitation) Chen et al., Cell 2002
• MIPS Negatome - no physical interaction between proteins Interaction: RBL2 — SMAD3 (Absence of interaction, coimmunoprecipitation, MI:0110) Wirt et al., Cell division 2010*

Text-mined interactions from Literome

Kim et al., Mol Biol Cell 2008 : Loss and gain of function studies demonstrated that, once tyrosine phosphorylated via integrin signaling, p130Cas binds to Smad3 and reduces phosphorylation of Smad3 ... Thus, p130Cas mediated control of TGF-beta/Smad signaling may provide an additional clue to the mechanism underlying resistance to TGF-beta induced growth inhibition
Wendt et al., J Biol Chem 2009 (Breast Neoplasms...) : Importantly, depleting p130Cas expression in TbetaR-II expressing metastatic MECs significantly increased their activation of Smad2/3 , which ( i ) reestablished the physiologic balance between canonical and noncanonical TGF-beta signaling, and ( ii ) reversed cellular invasion and early mammary tumor cell dissemination stimulated by TGF-beta