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CDKN2B — SMAD3

Pathways - manually collected, often from reviews:

• KEGG Cell cycle: Complex of SMAD2-SMAD3-SMAD4 → CDKN2B (gene expression, expression)
• NCI Pathway Database Regulation of nuclear SMAD2/3 signaling: SMAD2-3/SMAD4/FOXO1-3a-4/CEBPB complex (SMAD2_SMAD3-SMAD4-FOXO3_FOXO4_FOXO1-CEBPB) → p15INK4b (CDKN2B) (transcription, activates) Gomis et al., Cancer Cell 2006
  Evidence: mutant phenotype, reporter gene, physical interaction

Text-mined interactions from Literome

Feng et al., EMBO J 2000 : Interference with, or deficiency in, Smad2, Smad3 or Smad4 functions also reduced or abolished the TGF-beta dependent p15(Ink4B) induction, whereas the absence of Sp1 reduced the basal and TGF-beta induced p15(Ink4B) transcription
Feng et al., Mol Cell 2002 : Direct interaction of c-Myc with Smad2 and Smad3 to inhibit TGF-beta mediated induction of the CDK inhibitor p15(Ink4B) ... Through its direct interaction with Smads, c-Myc binds to the Sp1-Smad complex on the promoter of the p15(Ink4B) gene, thereby inhibiting the TGF-beta induced transcriptional activity of Sp1 and Smad/Sp1 dependent transcription of the p15(Ink4B) gene
Wu et al., J Am Soc Nephrol 2005 : Using a unique system of conditionally immortalized podocytes, it is demonstrated that autocrine TGF-beta2 induces G0/G1 arrest and differentiation under nonpermissive culture through Smad3 dependent induction of the cyclin dependent kinase inhibitor p15(Ink4b) ( Cdkn2b )
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