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Plasma membrane repair

About: Plasma membrane repair is a research topic. Over the lifetime, 254 publications have been published within this topic receiving 22475 citations.


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Journal ArticleDOI
TL;DR: Lysosomes are dynamic organelles that receive and degrade macromolecules from the secretory, endocytic, autophagic and phagocytic membrane-trafficking pathways, as well as having more specialized secretory functions in some cell types.
Abstract: Far from being a static organelle at the end of the endocytic pathway, the lysosome is capable of dynamically fusing with many organelles as well as the plasma membrane. The lysosome provides hydrolytic enzymes for the degradation of macromolecules, has secretory functions and is important for plasma membrane repair. Lysosomes are dynamic organelles that receive and degrade macromolecules from the secretory, endocytic, autophagic and phagocytic membrane-trafficking pathways. Live-cell imaging has shown that fusion with lysosomes occurs by both transient and full fusion events, and yeast genetics and mammalian cell-free systems have identified much of the protein machinery that coordinates these fusion events. Many pathogens that hijack the endocytic pathways to enter cells have evolved mechanisms to avoid being degraded by the lysosome. However, the function of lysosomes is not restricted to protein degradation: they also fuse with the plasma membrane during cell injury, as well as having more specialized secretory functions in some cell types.

1,477 citations

Journal ArticleDOI
TL;DR: The identification of a master regulator, transcription factor EB (TFEB), that regulates lysosomal biogenesis and autophagy has revealed how the lyssome adapts to environmental cues, such as starvation, and targeting TFEB may provide a novel therapeutic strategy for modulating lysOSomal function in human disease.
Abstract: For a long time, lysosomes were considered merely to be cellular 'incinerators' involved in the degradation and recycling of cellular waste. However, now there is compelling evidence indicating that lysosomes have a much broader function and that they are involved in fundamental processes such as secretion, plasma membrane repair, signalling and energy metabolism. Furthermore, the essential role of lysosomes in autophagic pathways puts these organelles at the crossroads of several cellular processes, with significant implications for health and disease. The identification of a master regulator, transcription factor EB (TFEB), that regulates lysosomal biogenesis and autophagy has revealed how the lysosome adapts to environmental cues, such as starvation, and targeting TFEB may provide a novel therapeutic strategy for modulating lysosomal function in human disease.

1,311 citations

Journal ArticleDOI
TL;DR: Eukaryotic cells contain various Ca2-effector proteins that mediate cellular responses to changes in intracellular Ca2+ levels, and a unique class of these proteins — annexins — can bind to certain membrane phospholipids in a Ca2+.
Abstract: Eukaryotic cells contain various Ca(2+)-effector proteins that mediate cellular responses to changes in intracellular Ca(2+) levels. A unique class of these proteins - annexins - can bind to certain membrane phospholipids in a Ca(2+)-dependent manner, providing a link between Ca(2+) signalling and membrane functions. By forming networks on the membrane surface, annexins can function as organizers of membrane domains and membrane-recruitment platforms for proteins with which they interact. These and related properties enable annexins to participate in several otherwise unrelated events that range from membrane dynamics to cell differentiation and migration.

1,290 citations

Journal ArticleDOI
27 Jul 2001-Cell
TL;DR: It is shown that Ca(2+)-regulated exocytosis of lysosomes is required for the repair of plasma membrane disruptions and mediates the resealing of primary skin fibroblasts wounded during the contraction of collagen matrices.

931 citations

Journal ArticleDOI
08 May 2003-Nature
TL;DR: It is shown that disruption of the muscle membrane repair machinery is responsible for dysferlin-deficient muscle degeneration, and the importance of this basic cellular mechanism of membrane resealing in human disease is highlighted.
Abstract: Muscular dystrophy includes a diverse group of inherited muscle diseases characterized by wasting and weakness of skeletal muscle. Mutations in dysferlin are linked to two clinically distinct muscle diseases, limb-girdle muscular dystrophy type 2B and Miyoshi myopathy, but the mechanism that leads to muscle degeneration is unknown. Dysferlin is a homologue of the Caenorhabditis elegans fer-1 gene, which mediates vesicle fusion to the plasma membrane in spermatids. Here we show that dysferlin-null mice maintain a functional dystrophin-glycoprotein complex but nevertheless develop a progressive muscular dystrophy. In normal muscle, membrane patches enriched in dysferlin can be detected in response to sarcolemma injuries. In contrast, there are sub-sarcolemmal accumulations of vesicles in dysferlin-null muscle. Membrane repair assays with a two-photon laser-scanning microscope demonstrated that wild-type muscle fibres efficiently reseal their sarcolemma in the presence of Ca2+. Interestingly, dysferlin-deficient muscle fibres are defective in Ca2+-dependent sarcolemma resealing. Membrane repair is therefore an active process in skeletal muscle fibres, and dysferlin has an essential role in this process. Our findings show that disruption of the muscle membrane repair machinery is responsible for dysferlin-deficient muscle degeneration, and highlight the importance of this basic cellular mechanism of membrane resealing in human disease.

927 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20221
202128
202023
201921
201816
201720