BACKGROUND MyoD1 and myogenin are differentially expressed in early myogenesis and have been identified in rhabdomyosarcoma (RMS). This study evaluates reverse transcriptase-polymerase chain reaction (RT-PCR) for MyoD1 and myogenin mRNA as diagnostic markers of RMS, and the potential application of this method for the detection of small volume disease in bone marrow (BM) and peripheral blood (PB). PROCEDURE Expression of MyoD1 and myogenin mRNA was examined by RT-PCR in RMSs (9 alveolar RMS, 10 embryonal RMS, 1 pleomorphic RMS), and 21 other paediatric tumor samples (10 neuroblastoma, 10 Ewing sarcomas, and 1 Sarcoma (not otherwise specified) (S(NOS)). BM (n = 19) and PB (n = 22) samples from the same RMS study population were also examined for MyoD1 and myogenin mRNA expression. RESULTS Positive expression of both markers was demonstrated in adult muscle, but not in normal PB. Myogenin mRNA was expressed in 16/18 and MyoD1 mRNA in 12/12 RMSs studied. Myogenin was not expressed in 10/10

Extracellular microRNAs (miRNAs) are promising biomarkers of the inherited muscle wasting condition Duchenne muscular dystrophy, as they allow non-invasive monitoring of either disease progression or response to therapy. In this study, serum miRNA profiling reveals a distinct extracellular miRNA signature in dystrophin-deficient mdx mice, which shows profound dose-responsive restoration following dystrophin rescue. Extracellular dystrophy-associated miRNAs (dystromiRs) show dynamic patterns of expression that mirror the progression of muscle pathology in mdx mice. Expression of the myogenic miRNA, miR-206 and the myogenic transcription factor myogenin in the tibialis anterior muscle were found to positively correlate with serum dystromiR levels, suggesting that extracellular miRNAs are indicators of the regenerative status of the musculature. Similarly, extracellular dystromiRs were elevated following experimentally-induced skeletal muscle injury and regeneration in non-dystrophic mice. Only a minority

Myogenin: A myogenic regulatory factor that controls myogenesis. Myogenin is induced during differentiation of every skeletal muscle cell line that has been investigated, in contrast to the other myogenic regulatory factors that only appear in certain cell types.

Myogenin is a muscle-specific transcription factor that can induce myogenesis in a variety of cell types in tissue;culture. It is a member of a large family of proteins related by sequence homology, the helix-loop-helix (HLH);proteins. It is essential for the development of functional skeletal muscle.

(2011) Meadows et al. PLoS ONE. Duchenne muscular dystrophy (DMD) is the most prevalent inherited childhood muscle disorder in humans. mdx mice exhibit a similar pathophysiology to the human disorder allowing for an in-depth investigation of DMD. Myogenin, a myogenic regulatory factor, is best kn...

View Notes - Lecture_4Paper_31 from BCH 4122 at University of Ottawa. Bch 4122 Paper # 3: Skeletal Muscle Specification by myogenin and Mef2D via the SWI/SNF ATPase Brg1 Ohkawa Y., Marfella C.,

CiteSeerX - Scientific documents that cite the following paper: Cyclic amplification and selection of targets (CASTing) for the myogenin consensus binding site

Sigma-Aldrich offers abstracts and full-text articles by [Antonis Antoniou, Nikolaos P Mastroyiannopoulos, James B Uney, Leonidas A Phylactou].

Transcription factor that is thought to be involved in regulation of organogenesis. May be involved in determination and maintenance of retina formation. Binds a 5-GGTGTCAG-3 motif present in the ARE regulatory element of ATP1A1. Binds a 5-TCA[AG][AG]TTNC-3 motif present in the MEF3 element in the myogenin promoter, and in the IGFBP5 promoter (By similarity). Thought to be regulated by association with Dach and Eya proteins, and seems to be coactivated by EYA1, EYA2 and EYA3 (By similarity).

Skeletal muscle collection includes over 185 mAbs against myosin isoforms for myofiber typing, MyoD and myogenin TFs, and Troponin complex I and T

Skeletal muscle collection includes over 185 mAbs against myosin isoforms for myofiber typing, MyoD and myogenin TFs, and Troponin complex I and T

Since changes in ceramide content accompany myogenic differentiation of L6 cells, we asked whether drugs able to modify ceramide levels could influence the differentiative response of myoblasts. The effects of FB1 and myriocin were studied on the expression and nuclear accumulation of the muscle-specific transcription factor myogenin, which constitute one of the early crucial steps of the myogenic program (Perry and Rudnick, 2000). The synthesis of this transcription factor is maximal at day 2 after the induction of differentiation in several myogenic cell models (Nervi et al., 1995; Andres and Walsh, 1996). FB1 and myriocin both markedly increased the amount of myogenin expressed in cells induced to differentiate by a 48-hour AVP treatment, as evaluated by immunoblotting. Conversely, the cell-permeant short-chain C6-ceramide (N-hexanoylsphingosine) and C8-ceramide (N-octanoylsphingosine) significantly inhibited myogenin expression (Fig. 2A). FB1 and myriocin also potentiated the AVP-induced ...

Reprinted with permission from Elsevier from doi:10.1016/j.ydbio.2007.08.014 Dev Biol 311: 650-64, Davie JK; Cho JH; Meadows E; Flynn JM; Knapp JR; Klein WH, Target gene selectivity of the myogenic basic helix-loop-helix transcription factor myogenin in embryonic muscle. Copyright 2007 ...

Skeletal muscle differentiation is crucially dependent on four basic-helix-loop-helix (bHLH) transcription factors, Myf5, MyoD (also known as Myod1), Myogenin and Mrf4 (also known as Myf6), which are named the myogenic regulatory factors (MRFs) (Weintraub et al., 1991). Null mutations in mice have revealed hierarchical relationships and apparent functional overlap among the MRFs. The primary MRFs, Myf5 and MyoD, are required for the determination of skeletal myoblasts, whereas the secondary MRFs, Myogenin and MRF4, act later in the program as differentiation factors (reviewed by Tajbakhsh and Buckingham, 2000; Arnold and Braun, 2000; Bergstrom and Tapscott, 2001). Although Myf5 and MyoD can compensate for the absence of each other (Braun et al., 1992; Rudnicki et al., 1992; Rudnicki et al., 1993), they probably have distinct functions in the embryo. Myf5 transcripts are consistently detected prior those of MyoD in somites and limbs of mouse and chick embryos (Ontell et al., 1995; Tajbakhsh and ...

The Pax3 transcription factor regulates myogenesis during embryonic and foetal development by controlling the expression of Myf5, myogenin and other canonical myogenic regulatory factors - but what is its role in postnatal myogenesis? On page 2632, Arthur Young and Amy Wagers report that Pax3 induces the differentiation of postnatal, juvenile mouse skeletal-muscle stem cells via an apparently distinct myogenic regulatory pathway. The authors isolate primary myogenic cells from young mice and show that constitutive expression of Pax3 in these cells potently induces myogenic differentiation. By contrast, Pax3 expression in the mouse adult myoblast cell line C2C12 inhibits myogenic differentiation. Surprisingly, the authors show that ectopic Pax3 expression in early postnatal muscle stem cells does not induce expression of any of the canonical myogenic regulatory factors. Indeed, Myf5 or myogenin overexpression fails to induce the differentiation of these cells and Myf5 knockdown promotes their ...

TY - JOUR. T1 - Hypoxia Inhibits Myogenic Differentiation through Accelerated MyoD Degradation. AU - Di Carlo, Anna. AU - De Mori, Roberta. AU - Martelli, Fabio. AU - Pompilio, Giulio. AU - Capogrossi, Maurizio C.. AU - Germani, Antonia. PY - 2004/4/16. Y1 - 2004/4/16. N2 - Cells undergo a variety of biological responses when placed in hypoxic conditions, including alterations in metabolic state and growth rate. Here we investigated the effect of hypoxia on the ability of myogenic cells to differentiate in culture. Exposure of myoblasts to hypoxia strongly inhibited multinucleated myotube formation and the expression of differentiation markers. We showed that hypoxia reversibly inhibited MyoD, Myf5, and myogenin expression. One key step in skeletal muscle differentiation involves the up-regulation of the cell cycle-dependent kinase inhibitors p21 and p27 as well as the product of the retinoblastoma gene (pRb). Myoblasts cultured under hypoxic conditions in differentiation medium failed to ...

Tytuł projektu: Rozbudowa i przekształcenie bibliograficznej bazy danych AGRO w bazę bibliograficzno-abstraktową z wykorzystaniem oprogramowania YADDA. Nr umowy: POIG 02.03.02-00-031/09 (okres realizacji 2009-2013 ...

The development of skeletal muscle is a multistep process in which pluripotent mesodermal cells give rise to myoblasts that subsequently withdraw from the cell cycle and differentiate into myotubes.2,13 These stages are controlled by the MyoD and myocyte enhancer factor 2 (MEF2) families of transcription factors, which interact with one another to establish a unique transcriptional code for activation of skeletal muscle-specific genes.14 It has been shown that such muscle differentiation-specific gene expression occurs in a stereotype pattern. Within 24 hours of switching to differentiation medium or serum withdrawal, proliferating myoblasts initiate the expression of myogenin, followed by the expression of MEF2 family of transcription factors, including MEF2D.15 Consistent with these observations, we showed in the present study that cell cycle withdrawal induced myogenin and MEF2D protein expression, peaking at 48 and 72 hours after medium switch, respectively. Furthermore, we demonstrated, for ...

Mouse Monoclonal Anti-Myogenin Antibody (MGN185) [Alexa Fluor® 647]. Skeletal Muscle Marker. Validated: WB, ELISA, Flow, ICC/IF, IHC-Fr, IHC-P, IP. Tested Reactivity: Human, Mouse, Rat, and more. 100% Guaranteed.

Mutation in the Myogenic Factor 6 Gene Symptom Checker: Possible causes include Congenital Myopathy with Excess of Thin Filaments. Check the full list of possible causes and conditions now! Talk to our Chatbot to narrow down your search.

The following probes were used in this study: MyoD, clone CMD9 1.5-kb full-length fragment (a gift from Professor Bruce Patterson); Pax-3, a 645-bp fragment corresponding to nucleotides 468-1,113 (a gift from Dr. Martin Goulding); Myf-5, a 1.1-kb fragment and Myogenin, a 1.2-kb fragment (both kind gifts from Professor Antony Graham); Pax-7 a 582-bp fragment (a kind gift from Dr. Susanne Dietrich ...

We report the cloning of two new quail myogenic cDNAs, quail myogenic factor 2 (qmf2) and qmf3, which encode helix-loop-helix proteins homologous to mammalian myogenic factors myogenin and myf-5. In situ hybridization has been used to investigate the developmental expression of qmf2 and qmf3, as wel …

The muscle-specific transcription factors Myf5 and Mrf4 are two of the four myogenic regulatory factors involved in the transcriptional cascade responsible for skeletal myogenesis in the vertebrate embryo. Myf5 is the first of these four genes to be expressed in the mouse. We have previously described discrete enhancers that drive Myf5 expression in epaxial and hypaxial somites, branchial arches and central nervous system, and argued that additional elements are required for proper expression (Summerbell, D., Ashby, P. R., Coutelle, O., Cox, D., Yee, S. P. and Rigby, P. W. J. (2000) Development 127, 3745-3757). We have now investigated the transcriptional regulation of both Myf5 and Mrf4 using bacterial artificial chromosome transgenesis. We show that a clone containing Myf5 and 140 kb of upstream sequences is sufficient to recapitulate the known expression patterns of both genes. Our results confirm and reinforce the conclusion of our earlier studies, that Myf5 expression is regulated ...

Transcription factors Myf5 and MyoD play critical roles in controlling myoblast identity and differentiation. In the myogenic cell line C2, we have found that

An analysis of a series of cell lines has indicated that the expression of myoD, myogenin and desmin can be detected inbona fide RMS. With the exception of the American Type Culture Collection lines A204, A673 and Hs729T and the St. Jude-derived cell line Rh1, expression of all three markers was readily apparent by Western analysis. We suspect that the extended time in culture of the former cell lines may have resulted in the down-regulation of these myogenic genes. Rh1 was originally diagnosed as an embryonal RMS, but it is now thought to be a tumor of primitive neuroectodermal origin (PNET). Because Rh1 was isolated from the patient in 1985 beforemyoD and myogenin antibodies were available, the primary diagnosis was determined from histopathology using conventional reagents. A recent immunohistochemical study of tumor samples using frozen sections essentially confirmed that all RMS expressedmyoD and that this gene product was undetectable in normal tissues, including both adult and fetal ...

In our studies, we explored a model of myoblasts, i.e. activated satellite cells that are located on the surface of myofiber. At the time of muscle injury, these cell are activated, undergoing the changes supervised by transcription factors (Myf5, MyoD) when myoblasts multiply and transform into myotube by myogenin and then as the muscle fiber (Mrf4). We have performed two clinical trials of I/II phase studying the role of myoblasts in regeneration of post-infarction heart. Each trial contained 10 patients. The first attempt included delivery of autologous myoblasts directly to myocardium at the opportunity of bypass surgery (CABG) on the open heart. Myoblasts were then implanted to post-infarction scar. We have obtained the improvement of basic hemodynamic heart parameter, which is ejection fraction (EF) in the all studied patients, however, it was impossible to say which factor was primarily responsible for the observed improvement - CABG or myoblast delivery, and in which proportion? We ...

MyoD is a master regulatory gene for myogenesis. Under the control of a retroviral long terminal repeat, MyoD was expressed in a variety of differentiated cell types by using either a DNA transfection vector or a retrovirus. Expression of muscle-specific proteins was observed in chicken, human, and …

Mouse monoclonal Myogenin antibody [F5D] validated for WB, IHC, Flow Cyt, ICC/IF and tested in Human, Mouse and Rat. Referenced in 29 publications and 7…

Anti-Myod sera was raised in rabbits against a fragment of the zebrafish Myod ... Anti-Myod sera was raised in rabbits against a fragment of the zebrafish Myod protein corresponding to amino acid 170-275 fused to glutathione S-transferase (GST), which was expressed in and purified from E. coli. ...

Gentaur molecular products has all kinds of products like :search , Signosis 2011 \ MyoD EMSA Kit \ GS-0064 for more molecular products just contact us

TY - JOUR. T1 - Electrical activity-dependent regulation of the acetylcholine receptor δ- subunit gene, MyoD, and myogenin in primary myotubes. AU - Dutton, E. K.. AU - Simon, A. M.. AU - Burden, S. J.. N1 - Copyright: Copyright 2018 Elsevier B.V., All rights reserved.. PY - 1993. Y1 - 1993. N2 - Expression of the skeletal muscle acetylcholine receptor (AChR) is regulated by nerve-evoked muscle activity. Studies using transgenic mice have shown that this regulation is controlled largely by transcriptional mechanisms because responsiveness to electrical activity can be conferred by transgenes containing cis-acting sequences from the AChR subunit genes. The lack of a convenient muscle cell culture system for studying electrical activity-dependent gene regulation, however, has made it difficult to identify the important cis-acting sequences and to characterize an electrical activity-dependent signaling pathway. We developed a muscle culture system to study the mechanisms of electrical ...

Acts as a transcriptional activator that promotes transcription of muscle-specific target genes and plays a role in muscle differentiation, cell cycle exit and muscle atrophy. Essential for the development of functional embryonic skeletal fiber muscle differentiation. However is dispensable for postnatal skeletal muscle growth; phosphorylation by CAMK2G inhibits its transcriptional activity in respons to muscle activity. Required for the recruitment of the FACT complex to muscle-specific promoter regions, thus promoting gene expression initiation. During terminal myoblast differentiation, plays a role as a strong activator of transcription at loci with an open chromatin structure previously initiated by MYOD1. Together with MYF5 and MYOD1, co-occupies muscle-specific gene promoter core regions during myogenesis. Cooperates also with myocyte-specific enhancer factor MEF2D and BRG1-dependent recruitment of SWI/SNF chromatin-remodeling enzymes to alter chromatin structure at myogenic late gene promoters.

Rhabdomyosarcoma is a soft tissue sarcoma mainly seen in children. Despite considerable progress within the last few years, therapeutic approaches for this type of tumor are still limited. The respective tumor cells originate from myogenic precursor

Interferon-related developmental regulator 1 is a protein that in humans is encoded by the IFRD1 gene. The gene is expressed mostly in neutrophils, skeletal and cardiac muscle, brain, pancreas. The rat and the mouse homolog genes of interferon-related developmental regulator 1 gene (and their proteins) are also known with the name PC4 and Tis21, respectively. IFRD1 is member of a gene family that comprises a second gene, IFRD2, also known as SKmc15. IFRD1 has been identified as a modifier gene for cystic fibrosis lung disease. In humans, neutrophil effector function is dependent on the type of IRFD1 polymorphism present in the individual. Human and mouse data both indicate that IFRD1 has a sizable impact on cystic fibrosis pathogenesis by regulating neutrophil effector function. IFRD1(also known as PC4 or Tis7, see above) participates to the process of skeletal muscle cell differentiation. In fact, inhibition of IFRD1 function in C2C12 myoblasts, by antisense IFRD1 cDNA transfection or ...

The MyoD gene is part of the core regulatory network that governs skeletal myogenesis and acts as an essential determinant of the myogenic cell fate. Although generic regulatory networks converging on this gene have been described, the specific mechanisms leading to MyoD expression in muscles of different ontology remain misunderstood. We now show that the homeobox gene Pitx2 is required for initial activation of the MyoD gene in limb muscle precursors through direct binding of Pitx2 to the MyoD core enhancer. Whereas Myf5 and Mrf4 are dispensable for limb muscle progenitor fate, inactivation of Myf5 and Mrf4 in Pitx2 mutants results in a drastic decrease of limb MyoD expression. Thus, Pitx2 and Myf5 define parallel genetic pathways for limb myogenesis. We show a similar dependence on Pitx2 and Myf5(Mrf4) in myotome, where MyoD expression is initially activated by Myf5 and Mrf4 . In their absence, MyoD expression is eventually rescued by a Pax3 -dependent mechanism. We now provide evidence that ...

Species: Mouse Immunogen: N-terminal decapeptide of alpha smooth muscle isoform of actin and conjugated to KLH. Clone: 1A4 Isotype: IgG2a, kappa Species Reactivity: Human, Baboon, Monkey, Cow, Pig, Sheep, Goat, Cat, Dog, Rabbit, Mouse, Rat, Guinea Pig and Chicken. Others not known. Positive Control: Blood vessels in all tissues, smooth muscle or leiomyosarcoma. Specificity: This MAb is highly specific to actin from smooth muscles. Its epitope lies in the first four N-terminal amino acids. This MAb does not stain cardiac or skeletal muscle; however, it does stain myofibroblasts and myoepithelial cells. In most cases of rhabdomyosarcoma, this antibody yields negative results whereas anti-muscle specific actin and myogenin are positive. Leiomyosarcomas are positive only with anti-muscle specific actin and anti-smooth muscle actin and are negative with anti-myogenin. Status: ...

Species: Mouse Immunogen: N-terminal decapeptide of alpha smooth muscle isoform of actin and conjugated to KLH. Clone: 1A4 Isotype: IgG2a, kappa Species Reactivity: Human, Baboon, Monkey, Cow, Pig, Sheep, Goat, Cat, Dog, Rabbit, Mouse, Rat, Guinea Pig and Chicken. Others not known. Positive Control: Blood vessels in all tissues, smooth muscle or leiomyosarcoma. Specificity: This MAb is highly specific to actin from smooth muscles. Its epitope lies in the first four N-terminal amino acids. This MAb does not stain cardiac or skeletal muscle; however, it does stain myofibroblasts and myoepithelial cells. In most cases of rhabdomyosarcoma, this antibody yields negative results whereas anti-muscle specific actin and myogenin are positive. Leiomyosarcomas are positive only with anti-muscle specific actin and anti-smooth muscle actin and are negative with anti-myogenin. Status: ...

I am interested in elucidating the regulatory pathways that control eukaryotic cell proliferation, particularly in relation to embryogenesis and development. Current projects include: 1) understanding why and how the cells of the paraxial mesoderm stop dividing during convergent extension and somitogenesis, 2) the development of an in vivo system to search for G2 checkpoint abrogators-compounds that will be useful both in developmental biology studies and in cancer treatment, and 3) the discovery of myogenin as a differentiation factor in the primary myogenesis of the frog Xenopus.. ...

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MYF6山羊多克隆抗体(ab106253)可与人样本反应并经WB实验严格验证。中国75%以上现货，所有产品均提供质保服务，可通过电话、电邮或微信获得本地专属技术支持。

The molecular mechanisms underlying muscle atrophy during spaceflight are not well understood. We have analyzed the effects of a 10-day spaceflight on Caenorhabditis elegans muscle development. DNA microarray, real-time quantitative PCR, and quantitative western blot analyses revealed that the amount of MHC in both body-wall and pharyngeal muscle decrease in response to spaceflight. Decreased transcription of the body-wall myogenic transcription factor HLH-1 (CeMyoD) and of the three pharyngeal myogenic transcription factors, PEB-1, CEH-22 and PHA-4 were also observed. Upon return to Earth animals displayed reduced rates of movement, indicating a functional defect. These results demonstrate that C. elegans muscle development is altered in response to spaceflight. This altered development occurs at the level of gene transcription and was observed in the presence of innervation, not simply in isolated cells. This important finding coupled with past observations of decreased levels of the same ...

During Xenopus laevis metamorphosis, larval-to-adult muscle conversion depends on the differential responses of adult and larval myogenic cells to thyroid hormone. Essential differences in cell growth, differentiation, and hormone-dependent life-or-death fate have been reported between cultured larval (tail) and adult (hindlimb) myogenic cells. A previous study revealed that tail notochord cells suppress terminal differentiation in adult (but not larval) myogenic cells. However, little is known about the differences in expression patterns of myogenic regulatory factors (MRF) and the satellite cell marker Pax7 between adult and larval myogenic cells. In the present study, we compared mRNA expression of these factors between the two types. At first, reverse transcription polymerase chain reaction analysis of hindlimb buds showed sequential upregulation of myf5, myogenin, myod, and mrf4 during stages 50-54, when limb buds elongate and muscles begin to form. By contrast, in the tail, there was no such

The aim of this study was to investigate the effects of a resistance training program with excessive training load and insufficient recovery time between bouts on muscle hypertrophy- and atrophy-related protein expression. Male Wistar rats were randomly assigned to either a trained (TR, N = 9) or a sedentary (SE, N = 9) group. The TR group was subjected to a 12-week resistance training program with excessive training load and insufficient recovery between bouts that was designed to induce plantaris muscle atrophy. After the 12-week experiment, the plantaris muscle was collected to analyze the cross-sectional area (CSA) of the muscle fibers, and MAFbx, MyoD, myogenin, and IGF-I protein expression (Western blot). The CSA was reduced significantly (-17%, p ≤ 0.05) in the TR group compared with the SE group. Reciprocally, there was a significant (p ≤ 0.05) 20% increase in MAFbx protein expression, whereas the MyoD (-27%), myogenin (-29%), and IGF-I (-43%) protein levels decreased significantly ...

Akirin is a recently discovered nuclear factor that plays an important role in innate immune responses. Beyond its role in innate immune responses, Akirin has recently been shown to play an important role in skeletal myogenesis. In this article, we will briefly review the structure and tissue distribution of Akirin and discuss recent advances in our understanding of its role and signal pathway in skeletal myogenesis.

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Webcat Plus: Development of membrane excitability during the in vitro differentiation of a clonal mouse myogenic cell line, 博士論文;博士論文

TPA Induced Sequence 7 acts as a transcriptional co-regulator controlling the expression of genes involved in differentiation of various cell types, including skeletal myoblasts. We and others have shown that TIS7 regulates adult myogenesis through MyoD, one of the essential myogenic regulatory factors. Here, we present data identifying ICln as the specific, novel protein downstream of TIS7 controlling myogenesis. We show that TIS7/ICln epigenetically regulate myoD expression controlling protein methyl transferase activity. In particular, ICln regulates MyoD expression via its interaction with PRMT5 by an epigenetic modification that utilizes symmetrical di-methylation of histone H3 on arginine 8. We provide multiple evidences that TIS7 directly binds DNA, which is a functional feature necessary for its role in transcriptional regulation. We present here a molecular insight into TIS7-specific control of MyoD gene expression and thereby skeletal muscle differentiation.

Myogenesis involves the stable commitment of progenitor cells followed by the execution of myogenic differentiation, processes that are coordinated by myogenic regulatory factors, microRNAs and BAF chromatin remodeling complexes. BAF60a, BAF60b and BAF60c are structural subunits of the BAF complex that bind to the core ATPase Brg1 to provide functional specificity. BAF60c is essential for myogenesis; however, the mechanisms regulating the subunit composition of BAF/Brg1 complexes, in particular the incorporation of different BAF60 variants, are not understood. Here we reveal their dynamic expression during embryo myogenesis and uncover the concerted negative regulation of BAF60a and BAF60b by the muscle-specific microRNAs (myomiRs) miR-133 and miR-1/206 during somite differentiation. MicroRNA inhibition in chick embryos leads to increased BAF60a or BAF60b levels, a concomitant switch in BAF/Brg1 subunit composition and delayed myogenesis. The phenotypes are mimicked by sustained BAF60a or BAF60b ...

basic helix-loop-helix (bHLH) transcription factor belonging to the class A family; acts as a general negative regulator of cell proliferation; binds specifically to oligomers of E-box motifs; forms heterodimers with other bHLH proteins of both class A and class B, e.g. E2A, TAL1, myogenin and MyoD; implicated in myogenesis, hematopoiesis and neurogenesis ...

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