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MYC — RBL1

Pathways - manually collected, often from reviews:

• FastForward regulation: RBL1 → MYC (transcriptional regulation, increase) Chen et al., Cell 2002
  Evidence: REG, PROMACTIVITY, DNABINDING
• KEGG Cell cycle: Complex of E2F4-E2F5-RBL1-RBL2-TFDP1-TFDP2 → MYC (gene expression, repression)
• KEGG TGF-beta signaling pathway: Complex of E2F4-E2F5-RBL1-RBL2-TFDP1 → MYC (gene expression, repression)
• NCI Pathway Database Validated targets of C-MYC transcriptional repression: p107 (RBL1) → MYC/Max complex (MYC-MAX) (transcription, inhibits) Luo et al., Oncogene 2004*, Penn et al., EMBO J 1990*, Facchini et al., Mol Cell Biol 1997*
  Evidence: mutant phenotype, reporter gene, physical interaction

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: MYC — RBL1 (physical association, affinity chromatography technology) Beijersbergen et al., EMBO J 1994*
• IRef Hprd Interaction: MYC — RBL1 (in vivo) Beijersbergen et al., EMBO J 1994*
• IRef Ophid Interaction: RBL1 — MYC (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Hoang et al., Mol Cell Biol 1995 (Burkitt Lymphoma...) : A link between increased transforming activity of lymphoma derived MYC mutant alleles, their defective regulation by p107 , and altered phosphorylation of the c-Myc transactivation domain
Beijersbergen et al., EMBO J 1994 : Our data suggest that p107 can control c-Myc activity through direct binding to the transactivation domain and that c-Myc is a target for p107 mediated growth suppression