Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0026850 (
muscular dystrophy
)
5,870
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In response to skeletal muscle injury, satellite cells, which function as a myogenic stem cell population, become activated, expand through proliferation, and ultimately fuse with each other and with damaged myofibers to promote muscle regeneration. Here, we show that members of the Myocardin family of transcriptional coactivators,
MASTR
and MRTF-A, are up-regulated in satellite cells in response to skeletal muscle injury and
muscular dystrophy
. Global and satellite cell-specific deletion of
MASTR
in mice impairs skeletal muscle regeneration. This impairment is substantially greater when MRTF-A is also deleted and is due to aberrant differentiation and excessive proliferation of satellite cells. These abnormalities mimic those associated with genetic deletion of MyoD, a master regulator of myogenesis, which is down-regulated in the absence of
MASTR
and MRTF-A. Consistent with an essential role of
MASTR
in transcriptional regulation of MyoD expression,
MASTR
activates a muscle-specific postnatal MyoD enhancer through associations with MEF2 and members of the Myocardin family. Our results provide new insights into the genetic circuitry of muscle regeneration and identify
MASTR
as a central regulator of this process.
...
PMID:MASTR directs MyoD-dependent satellite cell differentiation during skeletal muscle regeneration. 2227 50
