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RUNX2 — SMAD4

Pathways - manually collected, often from reviews:

• NCI Pathway Database Regulation of nuclear SMAD2/3 signaling: RUNX2 (RUNX2) → SMAD3/SMAD4 complex (SMAD3-SMAD4) (modification, collaborate)
  Alliston et al., EMBO J 2001*
  Evidence: mutant phenotype, physical interaction
• NCI Pathway Database Regulation of nuclear SMAD2/3 signaling: RUNX2 (RUNX2) → SMAD3/SMAD4/RUNX2 complex (SMAD3-SMAD4-RUNX2) (modification, collaborate)
  Alliston et al., EMBO J 2001*
  Evidence: mutant phenotype, physical interaction
• NCI Pathway Database Regulation of nuclear SMAD2/3 signaling: SMAD3/SMAD4 complex (SMAD3-SMAD4) → SMAD3/SMAD4/RUNX2 complex (SMAD3-SMAD4-RUNX2) (modification, collaborate)
  Alliston et al., EMBO J 2001*
  Evidence: mutant phenotype, physical interaction
• WikiPathways Hypothesized Pathways in Pathogenesis of Cardiovascular Disease: SMAD4 → RUNX2 (mim-transcription-translation)

Text-mined interactions from Literome

Leboy et al., J Bone Joint Surg Am 2001 (Hypertrophy) : When chondrocytes were simultaneously transfected with both Runx2 and Smad 1 or 5, promoter activity was further increased, indicating that BMP stimulated Smad activity can be augmented by increasing the levels of Runx2
Lee et al., Oncogene 2002 (MAP Kinase Signaling System) : Both the Smad and p38 MAPK pathways play a crucial role in Runx2 expression following induction by transforming growth factor-beta and bone morphogenetic protein ... Runx2 is induced by the receptor activated Smad ; Runx2 mediates the blockage of myogenic differentiation and induces osteoblast differentiation in C2C12 pluripotent mesenchymal precursor cells ... However, Smad does not directly induce Runx2 expression ; an additional step of de novo protein synthesis is required
Li et al., Frontiers in bioscience : a journal and virtual library 2005 (Bone Diseases) : The rate of chondrocyte maturation is tightly regulated through the interactions of Smad mediated signaling, the Wnt signaling pathway, and the transcription factor Runx2
Shen et al., J Biol Chem 2006 : In previous studies we discovered that E3 ubiquitin ligase Smad ubiquitin regulatory factor 1 ( Smurf1 ) induces Runx2 degradation in a ubiquitin-proteasome dependent manner, and Smurf1 plays an important role in osteoblast function and bone formation
Phimphilai et al., J Bone Miner Res 2006 : However, RUNX2 did not increase the ability of this BMP to activate SMAD , ERK, p38, and JNK pathways ... However, RUNX2 did not increase the ability of this BMP to activate SMAD , ERK, p38, and JNK pathways
McCarthy et al., Proc Natl Acad Sci U S A 2008 : At levels that occur in conditioned medium from differentiating osteoblast cultures, the agonist directly drives gene expression through estrogen-sensitive response elements, activates the obligate osteoblast transcription factor Runx2 , and potently enhances Smad dependent gene expression in response to TGF-beta, but exhibits relatively lesser suppressive effects on gene expression through C/EBP and AP-1 binding protein transcription factors
Xue et al., Gene Ther 2010 (Ossification, Heterotopic) : We found that the Runx2- and Smad4-specific siRNAs inhibited the expression of Runx2 and Smad4 at the level of messenger RNA and protein
Lu et al., Zhong Nan Da Xue Xue Bao Yi Xue Ban 2013 : Downregulation of Smad4 suppressed the AKP activity and RUNX2 mRNA expression, indicating that Smad4 siRNA simulated at least in part the function of miR-125b as the regulator of MSCs osteogenic differentiation