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Gomes et al., "Mrf4 determines skeletal muscle identity in Myf5:Myod double-mutant mice," Nature, vol.
Alway, "Stretch-induced myogenin, MyoD, and MRF4 expression and acute hypertrophy in quail slowtonic muscle are not dependent upon satellite cell proliferation," Cell and Tissue Research, vol.
Although MyoD converts undifferentiated myoblasts into myotubes, muscle development is not dramatically altered in MyoD mutant mice, suggesting that functional redundancy of other myogenic factors such as Myf5 and Mrf4 may compensate for dysfunctional activity of MyoD [19,20].
These corrected iPSCs will be used for myogenic progenitor cell induction followed by in utero injection into animal embryos carrying a defect of myogenic master genes such as MyoD, Myf5, and MRF4, allowing chimeric animal to develop human skeletal muscle.
Millert, "Regeneration of transgenic skeletal muscles with altered timing of expression of the basic helix-loop-helix muscle regulatory factor MRF4," American Journal of Pathology, vol.
Acute injections of rhEPO (15,000 IU) did not change mRNA levels of VEGF, hypoxia-inducible factor 1[alpha] (HIF-1[alpha]), insulin-like growth factor, ferroportin, myogenic differentiation 1 (MyoD), and myogen in biopsies obtained 2, 4, 6, and 10 h after injection of rhEPO, while small inductions of myoglobin, EPO-R, transferrin receptor, and myogenic regulatory factor (MRF4) were observed (39).
Alway, "Stretch-induced myogenin, MyoD, and MRF4 expression and acute hypertrophy in quail slow-tonic muscle are not dependent upon satellite cell proliferation," Cell and Tissue Research, vol.
MYOGENIN gene-knockout mice display deficiency of differentiated skeletal myofibers, while there are residual myofibers in the mutant mice possibly due to functional compensation by MYOD1 and/or MRF4. Interestingly, in the paper, the authors found that human iPSCs can differentiate into skeletal muscle without MYOGENIN activity in vitro, indicating similar compensation mechanisms by MYOD1 and/or MRF4 for myogenic differentiation of human iPSCs.
As terminal differentiation genes, MyoG and MRF4 are necessary to myocytes and fusion into myotubes.
It increases proliferative potential of satellite cells and differentiation capacity of myoblasts concomitantly with upregulation of myogenic regulatory factors including Myf5, MyoD, myogenin, and MRF4, promoting muscle regeneration with the recovery of muscle contractility .
In vertebrate embryos, skeletal muscles of the trunk and limbs are derived from the somites, from the dermomyotome which gives rise to myogenic progenitor cells that are directed into the skeletal muscle programme by four myogenic bHLH transcription factors, Myf5, Myod1, Mrf4, and Myogenin (Myog) [1-3].
These include MyoD, Myf5, myogenin, and MRF4 (Weintraub, 1993).
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- Mrevlishvili, Aleksandr
- Mrevlishvili, Aleksandr Romanovich
- Mrevlishvili, Mikhail
- Mrevlishvili, Mikhail Nikolaevich
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- MRF1-like protein