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HDAC4 — RUNX2

Pathways - manually collected, often from reviews:

• WikiPathways Endochondral Ossification: HDAC4 → RUNX2 (inhibition)

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: HDAC4 — RUNX2 (physical association, affinity chromatography technology) Shimizu et al., J Biol Chem 2010*
• IRef Biogrid Interaction: HDAC4 — RUNX2 (physical association, affinity chromatography technology) Jeon et al., J Biol Chem 2006*
• IRef Biogrid Interaction: HDAC4 — RUNX2 (physical association, affinity chromatography technology) Vega et al., Cell 2004*
• IRef Hprd Interaction: RUNX2 — HDAC4 (in vitro) Vega et al., Cell 2004*
• IRef Hprd Interaction: RUNX2 — HDAC4 (in vivo) Vega et al., Cell 2004*

Text-mined interactions from Literome

Vega et al., Cell 2004 (Hypertrophy...) : Here we report that HDAC4 , which is expressed in prehypertrophic chondrocytes, regulates chondrocyte hypertrophy and endochondral bone formation by interacting with and inhibiting the activity of Runx2 , a transcription factor necessary for chondrocyte hypertrophy
Kang et al., EMBO J 2005 : Accordingly, HDAC4 or 5 is required for efficient TGF-beta mediated inhibition of Runx2 function and is involved in osteoblast differentiation
Schroeder et al., J Bone Miner Res 2005 : These studies show that histone deacetylase activity regulates osteoblast differentiation and bone formation at least in part by enhancing Runx2 dependent transcriptional activation