Histone deacetylase 4 controls chondrocyte hypertrophy during skeletogenesis.

By Rick B. Vega, Koichi Matsuda, Junyoung Oh, Ana C. Barbosa, Xiangli Yang, Eric Meadows, J. McAnally, Chris Pomajzl, J. Shelton, J. Richardson and 2 more. Cell, 2004

829 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/05e6d13f48a8d84c3f4b8431276ed2a4772b41cd

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. J. Massagué
2. J. Seoane
3. PA Marks
4. D. Wotton
5. Fanxin Long
6. Rusty L. Montgomery
7. M. Haberland
8. D. Ornitz

In Oncology

1. J. Seoane
2. J. Massagué
3. D. Wotton
4. Fanxin Long
5. E. Olson
6. S. Minucci
7. PA Marks
8. Pier Giuseppe Pelicci

Citations in the corpus

• Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer (2006, result): “Accordingly, the corresponding knockouts show — in contrast to what is observed in Hdac1 -null mice — hypertrophic growt”
• HDAC family: What are the cancer relevant targets? (2009, background): “Thus, Hdac4 is a central regulator of chondrocyte hypertrophy and endochondral bone formation [29], which acts in concert with MEF2C [30].”
• Smad transcription factors. (2005, background): “In part this specificity may come from the fact that HDAC4 itself is able to interact with Runx2 (Vega et al. 2004), again suggesting the formation of a specific Smad-containing repressor complex that targets certain gene responses.”
• The control of chondrogenesis (2006, background): “Histone deacetylase 4 (HDAC4), which is expressed later in prehypertrophic chondrocytes, prevents premature chondrocyte hypertrophy by interacting with Runx2 and inhibiting its activity [Vega et al., 2004].”
• Histone Deacetylase Inhibitors: Overview and Perspectives (2007, background): “HDAC4 knockout mice have defects in chondrocyte differentiation (14); HDAC5 and HDAC9 knockouts have cardiac defects (15).”
• Histone deacetylase 5 epigenetically controls behavioral adaptations to chronic emotional stimuli. (2007, neutral): “Unfortunately, HDAC4 knockout mice do not survive into adulthood and hence could not be included in this study (Vega et al., 2004).”
• Development of the endochondral skeleton. (2013, background): “The direct effect of RUNX2 on chondrocyte hypertrophy appears to be regulated by HDAC4, a member of the class II histone deacetylases (Vega et al. 2004).”
• Building strong bones: molecular regulation of the osteoblast lineage (2011, background): “For instance, histone deacetylase 4 (HDAC4) was shown to suppress RUNX2 function in chondrocytes to inhibit hypertroph”
• The many roles of histone deacetylases in development and physiology: implications for disease and therapy (2009, background): “HDAC4 is highly expressed in the brain and growth plates of the skeleto”
• MEF2: a central regulator of diverse developmental programs (2007, background): “…directly activates the expression of the homeodomain transcription factors DLX5 and DLX6, two transcription factors that are necessary for craniofacial development, and MEF2C acts synergistically with these factors to direct craniofacial development (Miller et al., 2007; Verzi et al., 2007) (Fig.”