Annexin A2 Mediates Dysferlin Accumulation and Muscle Cell Membrane Repair

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چکیده

منابع مشابه

Dysferlin and muscle membrane repair.

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 les...

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An actin-dependent annexin complex mediates plasma membrane repair in muscle

Disruption of the plasma membrane often accompanies cellular injury, and in muscle, plasma membrane resealing is essential for efficient recovery from injury. Muscle contraction, especially of lengthened muscle, disrupts the sarcolemma. To define the molecular machinery that directs repair, we applied laser wounding to live mammalian myofibers and assessed translocation of fluorescently tagged ...

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Dysferlin and the plasma membrane repair in muscular dystrophy.

Muscular dystrophy covers a group of genetically determined disorders that cause progressive weakness and wasting of the skeletal muscles. Dysferlin was identified as a gene mutated in limb-girdle muscular dystrophy (type 2B) and Miyoshi myopathy. The discovery of dysferlin revealed a new family of proteins, known as the ferlin family, which includes four different genes. Recent work suggests t...

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The S100A10-Annexin A2 Complex Provides a Novel Asymmetric Platform for Membrane Repair*

Membrane repair is mediated by multiprotein complexes, such as that formed between the dimeric EF-hand protein S100A10, the calcium- and phospholipid-binding protein annexin A2, the enlargeosome protein AHNAK, and members of the transmembrane ferlin family. Although interactions between these proteins have been shown, little is known about their structural arrangement and mechanisms of formatio...

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Annexin A2-dependent polymerization of actin mediates endosome biogenesis.

Early endosomes give rise to multivesicular intermediates during transport toward late endosomes. Much progress has been made in understanding the sorting of receptors into these intermediates, but the mechanisms responsible for their biogenesis remain unclear. Here, we report that F-actin is necessary for transport beyond early endosomes and endosome formation. We found that endosomes captured...

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ژورنال

عنوان ژورنال: Cells

سال: 2020

ISSN: 2073-4409

DOI: 10.3390/cells9091919