◀ Back to SMAD2
MYC — SMAD2
Pathways - manually collected, often from reviews:
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OpenBEL Selventa BEL large corpus:
Complex of MYC-ZBTB17
→
SMAD2
(decreases, MYC/ZBTB17 Activity)
Seoane et al., Nat Cell Biol 2001
Evidence: Here we provide evidence that TGFbeta signalling prevents recruitment of Myc to the p15INK4b transcriptional initiator by Myc-interacting zinc-finger protein 1 (Miz-1). This relieves repression and enables transcriptional activation by a TGFbeta-induced Smad protein complex that recognizes an upstream p15INK4b promoter region and contacts Miz-1. (from Weinberg - Pathways in Human Cancer poster, SMAD = SMAD 2/3) (MIZ-1 = ZBTB17)
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KEGG Cell cycle:
Complex of SMAD2-SMAD3-SMAD4
→
MYC
(gene expression, repression)
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NCI Pathway Database Validated targets of C-MYC transcriptional repression:
SMAD2-3/SMAD4/MYC/Max/MIZ-1 complex (MYC-MAX-ZBTB17-SMAD2_SMAD3-SMAD4)
→
SMAD2-3/SMAD4 complex (SMAD2_SMAD3-SMAD4)
(modification, collaborate)
Feng et al., Mol Cell 2002
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Validated targets of C-MYC transcriptional repression:
SMAD2-3/SMAD4/MYC/Max/MIZ-1 complex (MYC-MAX-ZBTB17-SMAD2_SMAD3-SMAD4)
→
MYC/Max/MIZ-1 complex (MYC-MAX-ZBTB17)
(modification, collaborate)
Feng et al., Mol Cell 2002
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Validated targets of C-MYC transcriptional repression:
SMAD2-3/SMAD4 complex (SMAD2_SMAD3-SMAD4)
→
MYC/Max/MIZ-1 complex (MYC-MAX-ZBTB17)
(modification, collaborate)
Feng et al., Mol Cell 2002
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Regulation of nuclear SMAD2/3 signaling:
MYC/MIZ-1 complex (MYC-ZBTB17)
→
SMAD2-3/SMAD4/SP1/MIZ-1 complex (SMAD2_SMAD3-SMAD4-SP1-ZBTB17)
(transcription, inhibits)
Feng et al., EMBO J 2000, Seoane et al., Nat Cell Biol 2001, Matsuura et al., Nature 2004
Evidence: mutant phenotype, reporter gene, physical interaction
-
NCI Pathway Database Validated targets of C-MYC transcriptional repression:
SMAD2-3/SMAD4/MYC/Max/MIZ-1 complex (MYC-MAX-ZBTB17-SMAD2_SMAD3-SMAD4)
→
SMAD2-3/SMAD4/SP1 complex (SMAD2_SMAD3-SMAD4-SP1)
(transcription, inhibits)
Staller et al., Nat Cell Biol 2001, Seoane et al., Nat Cell Biol 2001, Feng et al., Mol Cell 2002
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 *
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IRef Biogrid Interaction:
MYC
—
SMAD2
(physical association, affinity chromatography technology)
Feng et al., Mol Cell 2002
-
IRef Biogrid Interaction:
MYC
—
SMAD2
(direct interaction, pull down)
Feng et al., Mol Cell 2002
-
IRef Biogrid Interaction:
MYC
—
SMAD2
(direct interaction, two hybrid)
Feng et al., Mol Cell 2002
-
IRef Hprd Interaction:
MYC
—
SMAD2
(in vitro)
Feng et al., Mol Cell 2002
-
IRef Hprd Interaction:
MYC
—
SMAD2
(two hybrid)
Feng et al., Mol Cell 2002
-
IRef Hprd Interaction:
MYC
—
SMAD2
(in vivo)
Feng et al., Mol Cell 2002
-
IRef Ophid Interaction:
SMAD2
—
MYC
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
Text-mined interactions from Literome
Berger et al., Surgery 2002
:
We also demonstrate that
Smad signaling is not
sufficient for TGF-beta mediated
c-Myc repression
Gomis et al., Cancer Cell 2006
(Breast Neoplasms...) :
We found the transcription factor C/EBPbeta to be essential for TGFbeta induction of the cell cycle inhibitor p15INK4b by a FoxO-Smad complex and
repression of
c-MYC by an
E2F4/5-Smad complex in human epithelial cells
Holien et al., Leukemia 2012
(Multiple Myeloma) :
Bone morphogenetic proteins induce apoptosis in multiple myeloma cells by
Smad dependent repression of
MYC