MEF2: a calcium-dependent regulator of cell division, differentiation and death.
By T. McKinsey, Chun-li Zhang, E. Olson. TIBS -Trends in Biochemical Sciences. Regular ed, 2002
732 citations recorded by the source corpus.
Subfields: Genetics, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/71d953d2aa8760c79e99d252bb8903364149864c
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In Genetics
In Molecular Biology
- E. Olson
- J. Richardson
- Joseph A. Hill
- P. Hogan
- T. McKinsey
- Matthew J. Potthoff
- Chun-li Zhang
- D. Sinclair
Citations in the corpus
- SIRTUIN 1 AND SIRTUIN 3: PHYSIOLOGICAL MODULATORS OF METABOLISM (2012, background): “MEF2 is a family of transcription factors with important functions in muscle cell differentiation and apoptosis (216).”
- Histone Deacetylases 5 and 9 Govern Responsiveness of the Heart to a Subset of Stress Signals and Play Redundant Roles in Heart Development (2004, background): “Given the interaction between class II HDACs and MEF2 and the central role of MEF2 in the control of cardiomyocyte differentiation (29), the developmental cardiac defects in the double mutants may result from superactivation of MEF2 with consequent precocious differentiation and cell cycle withdrawa”
- MEF2: a central regulator of diverse developmental programs (2007, background): “…of MEF2 is tightly governed by class IIa HDACs, which associate with the MADS domain and promote the formation of multiprotein repressive complexes on MEF2-dependent genes (Bertos et al., 2001; de Ruijter et al., 2003; McKinsey et al., 2001; McKinsey et al., 2002a; McKinsey et al., 2002b) (Fig.”
- Class II histone deacetylases act as signal-responsive repressors of cardiac hypertrophy. (2002, background): “The N-terminal regions of class II HDACs alsotone deacetylases (HDACs), which repress MEF2 accontain two conserved CaMK phosphorylation sitestivity, are substrates for a stress-responsive kinase (McKinsey et al., 2000a, 2002).”
- Transcriptional regulation by calcium, calcineurin, and NFAT. (2003, background): “2002); the MADS-box protein MEF2 (for review, see Olson and Williams 2000; Crabtree and Olson 2002; McKinsey et al. 2002); and the nuclear receptor PPAR- (X.”