Gene interactions and pathways from curated databases and text-mining

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RUNX2 — SMAD5

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

Studies that report less than 10 interactions are marked with *

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
Nishimura et al., Bone 2002 : These results suggest that the interactions with Smad1 or Smad5 are not essential for Cbfa1 to demonstrate its osteogenic actions ... On the other hand, Cbfa1 expression requires the activation of Smad1/Smad5 by BMP-2
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
Gupta et al., Molecular cancer 2012 (Bone Resorption...) : Localization of RUNX2 in the nucleus requires phosphorylation of Smad-5 by integrin avß3 signaling
Lv et al., Nan Fang Yi Ke Da Xue Xue Bao 2013 : Transfection of the BMSCs with Smad1 siRNA decreased the basal level of Smad1/5/8 protein expression, and also inhibited Sr-induced up-regulation of p-Smad1/5/8 and Runx2 expressions as well as Sr-induced enhancement of ALP activity and formation of mineralized nodules