https://transhumanist.ru/index.php?action=history&feed=atom&title=ADAM12 2026-06-14T00:11:26Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=ADAM12&diff=5168&oldid=prev 2021-05-12T13:32:14Z

<p>Новая страница: «Disintegrin and metalloproteinase domain-containing protein 12 precursor (EC 3.4.24.-) (ADAM 12) (Meltrin-alpha) [MLTN] [UNQ346/PRO545] ==Publications== {{medli...»</p> <p><b>Новая страница</b></p><div>Disintegrin and metalloproteinase domain-containing protein 12 precursor (EC 3.4.24.-) (ADAM 12) (Meltrin-alpha) [MLTN] [UNQ346/PRO545]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Transgenic overexpression of [[ADAM12]] suppresses muscle regeneration and aggravates dystrophy in aged mdx mice.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/17982130<br /> |abstract=Muscular dystrophies are characterized by insufficient restoration and gradual replacement of the skeletal muscle by fat and connective tissue. [[ADAM12]] has previously been shown to alleviate the pathology of young dystrophin-deficient mdx mice, a model for Duchenne muscular dystrophy. The observed effect of [[ADAM12]] was suggested to be mediated via a membrane-stabilizing up-regulation of utrophin, alpha7B integrin, and dystroglycans. Ectopic [[ADAM12]] expression in normal mouse skeletal muscle also improved regeneration after freeze injury, presumably by the same mechanism. Hence, it was suggested that [[ADAM12]] could be a candidate for nonreplacement gene therapy of Duchenne muscular dystrophy. We therefore evaluated the long-term effect of [[ADAM12]] overexpression in muscle. Surprisingly, we observed loss of skeletal muscle and accelerated fibrosis and adipogenesis in 1-year-old mdx mice transgenically overexpressing [[ADAM12]] ([[ADAM12]]( )/mdx mice), even though their utrophin levels were mildly elevated compared with age-matched controls. Thus, membrane stabilization was not sufficient to provide protection during prolonged disease. Consequently, we reinvestigated skeletal muscle regeneration in [[ADAM12]] transgenic mice ([[ADAM12]]( )) after a knife cut lesion and observed that the regeneration process was significantly impaired. [[ADAM12]] seemed to inhibit the satellite cell response and delay myoblast differentiation. These results discourage long-term therapeutic use of [[ADAM12]]. They also point to impaired regeneration as a possible factor in development of muscular dystrophy.<br /> |mesh-terms=* ADAM Proteins<br /> * ADAM12 Protein<br /> * Aging<br /> * Animals<br /> * Antigens, CD<br /> * Cell Differentiation<br /> * Dystrophin<br /> * Fibrosis<br /> * Integrin alpha Chains<br /> * Mice<br /> * Mice, Inbred mdx<br /> * Mice, Transgenic<br /> * Muscular Dystrophy, Animal<br /> * Muscular Dystrophy, Duchenne<br /> * Myoblasts<br /> * Regeneration<br /> * Satellite Cells, Skeletal Muscle<br /> * Utrophin<br /> <br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2043520<br /> }}</div>

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