|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
8
|
|
pubmed:dateCreated |
2008-3-27
|
|
pubmed:abstractText |
Transient receptor potential (TRP) 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 1 exhibited a myopathy characterized by decreased muscle fiber cross-sectional area and decreased skeletal muscle force generation. Homer 1 knockout myotubes displayed increased basal current density and spontaneous cation influx. This spontaneous cation influx in Homer 1 knockout myotubes was blocked by reexpression of Homer 1b, but not Homer 1a, and by gene silencing of TRPC1. Moreover, diminished Homer 1 expression in mouse models of Duchenne's muscular dystrophy suggests that loss of Homer 1 scaffolding of TRP channels may contribute to the increased stretch-activated channel activity observed in mdx myofibers. These findings provide direct evidence that Homer 1 functions as an important scaffold for TRP channels and regulates mechanotransduction in skeletal muscle.
|
|
pubmed:grant |
|
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-10433269,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-10469838,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-10651798,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-11118290,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-11418862,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-11756499,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-11784787,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-12072556,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-12223488,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-12235126,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-12354790,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-12379179,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-12524440,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-12556452,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-12810060,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-12887973,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-14505576,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-14645704,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-14660561,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-14688372,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-15528244,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-15665854,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-15820394,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-15879175,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-15924139,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-16009351,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-16118847,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-16226241,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-16887806,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-16914674,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-17355963,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-1791181,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-3838314,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-7738032,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-8271194,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-8897840,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18268005-9808459
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Apr
|
|
pubmed:issn |
1098-5549
|
|
pubmed:author |
pubmed-author:BurchJarrettJ,
pubmed-author:EuJerry PJP,
pubmed-author:MeissnerGerhardG,
pubmed-author:RosenbergPaul BPB,
pubmed-author:SethMaliniM,
pubmed-author:ShahRipalR,
pubmed-author:StiberJonathan AJA,
pubmed-author:TruskeyGeorge AGA,
pubmed-author:WilliamsR SandersRS,
pubmed-author:WorleyPaul FPF,
pubmed-author:YamaguchiNaohiroN,
pubmed-author:ZhangSarahS,
pubmed-author:ZhangZhu-ShanZS
|
|
pubmed:issnType |
Electronic
|
|
pubmed:volume |
28
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
2637-47
|
|
pubmed:dateRevised |
2009-11-18
|
|
pubmed:meshHeading |
pubmed-meshheading:18268005-Animals,
pubmed-meshheading:18268005-Calcium Signaling,
pubmed-meshheading:18268005-Carrier Proteins,
pubmed-meshheading:18268005-Cells, Cultured,
pubmed-meshheading:18268005-Disease Models, Animal,
pubmed-meshheading:18268005-Gene Deletion,
pubmed-meshheading:18268005-Gene Expression Regulation,
pubmed-meshheading:18268005-Mice,
pubmed-meshheading:18268005-Mice, Knockout,
pubmed-meshheading:18268005-Muscle Contraction,
pubmed-meshheading:18268005-Muscular Dystrophies,
pubmed-meshheading:18268005-Protein Binding,
pubmed-meshheading:18268005-TRPC Cation Channels
|
|
pubmed:year |
2008
|
|
pubmed:articleTitle |
Mice lacking Homer 1 exhibit a skeletal myopathy characterized by abnormal transient receptor potential channel activity.
|
|
pubmed:affiliation |
Department of Medicine, Duke University Medical Center, 4321 Medical Park Drive, Suite 200, Durham, NC 27704, USA.
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|
