◀ Back to MYC
MYC — SMAD4
Pathways - manually collected, often from reviews:
-
FastForward regulation:
SMAD4
→
MYC
(transcriptional regulation, decrease)
Chen et al., Cell 2002
Evidence: REG, PROMACTIVITY, DNABINDING
-
FastForward regulation:
SMAD4
→
MYC
(transcriptional regulation, increase)
Lim et al., Proc Natl Acad Sci U S A 2006*
Evidence: REG, PROMACTIVITY, DNABINDING
-
FastForward regulation:
SMAD4, LEF1
→
MYC
(transcriptional regulation, increase)
Lim et al., Proc Natl Acad Sci U S A 2006*
Evidence: PROMACTIVITY
-
KEGG Cell cycle:
Complex of SMAD2-SMAD3-SMAD4
→
MYC
(gene expression, repression)
-
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 Validated targets of C-MYC transcriptional activation:
SMAD3/SMAD4 complex (SMAD3-SMAD4)
→
MYC/Max complex (MYC-MAX)
(transcription, activates)
Smith et al., Oncogene 2009*
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Regulation of nuclear SMAD2/3 signaling:
MYC/MIZ-1 complex (MYC-ZBTB17)
→
SMAD3/SMAD4 complex (SMAD3-SMAD4)
(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 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
-
WikiPathways Hepatitis C and Hepatocellular Carcinoma:
SMAD3/SMAD4
→
MYC
(mim-inhibition)
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