https://transhumanist.ru/index.php?action=history&feed=atom&title=SIX1 2026-04-06T10:04:01Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=SIX1&diff=4014&oldid=prev 2021-04-29T18:56:25Z

<p>Новая страница: «Homeobox protein SIX1 (Sine oculis homeobox homolog 1) ==Publications== {{medline-entry |title=Low Six4 and Six5 gene dosage improves dystrophic phenotype and p...»</p> <p><b>Новая страница</b></p><div>Homeobox protein SIX1 (Sine oculis homeobox homolog 1)<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Low Six4 and Six5 gene dosage improves dystrophic phenotype and prolongs life span of mdx mice.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27224259<br /> |abstract=Muscle regeneration is an important process for skeletal muscle growth and recovery. Repair of muscle damage is exquisitely programmed by cellular mechanisms inherent in myogenic stem cells, also known as muscle satellite cells. We demonstrated previously the involvement of homeobox transcription factors, [[SIX1]], [[SIX4]] and [[SIX5]], in the coordinated proliferation and differentiation of isolated satellite cells in vitro. However, their roles in adult muscle regeneration in vivo remain elusive. To investigate [[SIX4]] and [[SIX5]] functions during muscle regeneration, we introduced knockout alleles of Six4 and Six5 into an animal model of Duchenne Muscular Dystrophy ([[DMD]]), mdx (Dmd(mdx) /Y) mice, characterized by frequent degeneration-regeneration cycles in muscles. A lower number of small myofibers, higher number of thick ones and lower serum creatine kinase and lactate dehydrogenase activities were noted in 50-week-old Six4( /-) 5( /-) Dmd(mdx) /Y mice than Dmd(mdx) /Y mice, indicating improvement of dystrophic phenotypes of Dmd(mdx) /Y mice. Higher proportions of cells positive for [[MYOD1]] and [[MYOG]] (markers of regenerating myonuclei) and [[SIX1]] (a marker of regenerating myoblasts and newly regenerated myofibers) in 12-week-old Six4( /-) 5( /-) Dmd(mdx) /Y mice suggested enhanced regeneration, compared with Dmd(mdx) /Y mice. Although grip strength was comparable in Six4( /-) 5( /-) Dmd(mdx) /Y and Dmd(mdx) /Y mice, treadmill exercise did not induce muscle weakness in Six4( /-) 5( /-) Dmd(mdx) /Y mice, suggesting higher regeneration capacity. In addition, Six4( /-) 5( /-) Dmd(mdx) /Y mice showed 33.8% extension of life span. The results indicated that low Six4 and Six5 gene dosage improved dystrophic phenotypes of Dmd(mdx) /Y mice by enhancing muscle regeneration, and suggested that [[SIX4]] and [[SIX5]] are potentially useful de novo targets in therapeutic applications against muscle disorders, including [[DMD]]. <br /> |mesh-terms=* Animals<br /> * Gene Dosage<br /> * Homeodomain Proteins<br /> * Longevity<br /> * Mice<br /> * Mice, Inbred mdx<br /> * Mice, Knockout<br /> * Muscle, Skeletal<br /> * MyoD Protein<br /> * Myogenin<br /> * Regeneration<br /> * Trans-Activators<br /> |keywords=* Six4<br /> * Six5<br /> * mdx<br /> * muscle satellite cell<br /> * skeletal muscle regeneration<br /> |full-text-url=https://sci-hub.do/10.1111/dgd.12290<br /> }}</div>

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