Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 28, Issue 8, Pages 2637-2647Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.01601-07
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Funding
- Howard Hughes Medical Institute Funding Source: Medline
- NHLBI NIH HHS [R01 HL093470, K08 HL071841, K08 HL077520] Funding Source: Medline
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Transient receptor potential (TRIP) channels are nonselective cation channels, several of which are expressed in striated muscle. Because the scaffolding protein Homer 1 has been implicated in TRP channel regulation, we hypothesized that Homer proteins play a significant role in skeletal muscle function. Mice lacking Homer I exhibited a myopathy characterized by decreased muscle fiber cross-sectional area and decreased skeletal muscle force generation. Homer I knockout myotubes displayed increased basal current density and spontaneous cation influx. This spontaneous cation influx in Homer I knockout myotubes was blocked by reexpression of Homer 1b, but not Homer la, and by gene silencing of TRPC1. Moreover, diminished Homer 1 expression in mouse models of Duchenne's muscular dystrophy suggests that loss of Homer I scaffolding of TRP channels may contribute to the increased stretch-activated channel activity observed in mdr myofibers. These findings provide direct evidence that Homer 1 functions as an important scaffold for TRP channels and regulates mechanotransduction in skeletal muscle.
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