Редактирование: MYOD1

Myoblast determination protein 1 (Class C basic helix-loop-helix protein 1) (bHLHc1) (Myogenic factor 3) (Myf-3) [BHLHC1] [MYF3] [MYOD]

==Publications==

{{medline-entry
|title=Low Six4 and Six5 gene dosage improves dystrophic phenotype and prolongs life span of mdx mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27224259
|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]]. 
|mesh-terms=* Animals
* Gene Dosage
* Homeodomain Proteins
* Longevity
* Mice
* Mice, Inbred mdx
* Mice, Knockout
* Muscle, Skeletal
* MyoD Protein
* Myogenin
* Regeneration
* Trans-Activators
|keywords=* Six4
* Six5
* mdx
* muscle satellite cell
* skeletal muscle regeneration
|full-text-url=https://sci-hub.do/10.1111/dgd.12290
}}
{{medline-entry
|title=Age-associated changes in DNA methylation across multiple tissues in an inbred mouse model.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26861500
|abstract=Epigenetic disruption has been implicated in many diseases of aging, and age-associated DNA methylation changes at specific genomic loci in humans are strongly correlated with chronological age. The aim of this study was to explore the specificity of selected age-associated differentially methylated positions (aDMPs) identified in human epidemiological studies by quantifying DNA methylation across multiple tissues in homologous regions of the murine genome. We selected four high-confidence aDMPs (located in the vicinity of the [[ELOVL2]], [[GLRA1]], [[MYOD1]] and [[PDE4C]] genes) and quantified DNA methylation across these regions in four tissues (blood, lung, cerebellum and hippocampus) from male and female C57BL/6J mice, ranging in age from fetal (embryonic day 17) to 630 days. We observed tissue-specific age-associated changes in DNA methylation that was directionally consistent with those observed in humans. These findings lend further support to the notion that changes in DNA methylation are associated with chronological age and suggest that these processes are often conserved across tissues and between mammalian species. Our data highlight the relevance of utilizing model systems, in which environmental and genetic influences can be carefully controlled, for the further study of these phenomena. 
|mesh-terms=* Aging
* Animals
* DNA Methylation
* Female
* Gene Expression Regulation
* Humans
* Male
* Mice
* Models, Biological
* Organ Specificity
|keywords=* Aging
* Cross-tissue
* DNA methylation
* Epigenetics
* Inbred mouse
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4798846
}}