Journal article
Dysferlin and muscle membrane repair
Current opinion in cell biology, Vol.19(4), pp.409-416
08/2007
DOI: 10.1016/j.ceb.2007.07.001
PMCID: PMC2144911
PMID: 17662592
Abstract
The ability to repair membrane damage is conserved across eukaryotic cells and is necessary for the cells to survive a variety of physiological and pathological membrane disruptions. Membrane repair is mediated by rapid Ca(2+)-triggered exocytosis of various intracellular vesicles, such as lysosomes and enlargeosomes, which lead to the formation of a membrane patch that reseals the membrane lesion. Recent findings suggest a crucial role for dysferlin in this repair process in muscle, possibly as a Ca(2+) sensor that triggers vesicle fusion. The importance of membrane repair is highlighted by the genetic disease, dysferlinopathy, in which the primary defect is the loss of Ca(2+)-regulated membrane repair due to dysferlin deficiency. Future research on dysferlin and its interacting partners will enhance the understanding of this important process and provide novel avenues to potential therapies.
Details
- Title: Subtitle
- Dysferlin and muscle membrane repair
- Creators
- Renzhi Han - Howard Hughes Medical Institute, Department of Molecular Physiology and Biophysics, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, IA 52242, USAKevin P Campbell
- Resource Type
- Journal article
- Publication Details
- Current opinion in cell biology, Vol.19(4), pp.409-416
- DOI
- 10.1016/j.ceb.2007.07.001
- PMID
- 17662592
- PMCID
- PMC2144911
- NLM abbreviation
- Curr Opin Cell Biol
- ISSN
- 0955-0674
- eISSN
- 1879-0410
- Publisher
- England
- Grant note
- R01 AR051199-04 / NIAMS NIH HHS\nU54 NS053672-03 / NINDS NIH HHS\nU54 NS053672 / NINDS NIH HHS\n1 U54 NS053672 / NINDS NIH HHS\nR01 AR051199 / NIAMS NIH HHS
- Language
- English
- Date published
- 08/2007
- Academic Unit
- Neurology; Molecular Physiology and Biophysics; Iowa Neuroscience Institute
- Record Identifier
- 9984068372602771
Metrics
13 Record Views