Редактирование: ADAM12

Disintegrin and metalloproteinase domain-containing protein 12 precursor (EC 3.4.24.-) (ADAM 12) (Meltrin-alpha) [MLTN] [UNQ346/PRO545]

==Publications==

{{medline-entry
|title=Transgenic overexpression of [[ADAM12]] suppresses muscle regeneration and aggravates dystrophy in aged mdx mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/17982130
|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.
|mesh-terms=* ADAM Proteins
* ADAM12 Protein
* Aging
* Animals
* Antigens, CD
* Cell Differentiation
* Dystrophin
* Fibrosis
* Integrin alpha Chains
* Mice
* Mice, Inbred mdx
* Mice, Transgenic
* Muscular Dystrophy, Animal
* Muscular Dystrophy, Duchenne
* Myoblasts
* Regeneration
* Satellite Cells, Skeletal Muscle
* Utrophin

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2043520
}}