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1 e correction via homologous recombination in myogenic cells.
2 ive better under oxidative stress than CD56+ myogenic cells.
3 ion of miR-206 during differentiation of rat myogenic cells.
4 er and repressed FGFR1 gene transcription in myogenic cells.
5  of differentiating into both angiogenic and myogenic cells.
6 entiation of these cells into angiogenic and myogenic cells.
7 ntiation and retrospective identification of myogenic cells.
8 sitive satellite cells and other later stage myogenic cells.
9 initial activation of XmyoD transcription in myogenic cells.
10 ly morphological differentiation of cultured myogenic cells.
11  muscle tissues ('myobundles') using primary myogenic cells.
12 hibition in mouse myoblasts but not in avian myogenic cells.
13 s from the chicken fetus for the presence of myogenic cells.
14 unction to actively assemble and maintain in myogenic cells.
15 PTPRQ in non-myogenic cells and MYF5/MYF6 in myogenic cells.
16 populations that can self-renew and generate myogenic cells.
17  were also seen in PTPRQ mRNA-expressing non-myogenic cells.
18 ter day 14.5, the promoter becomes active in myogenic cells.
19 e withdrawal and differentiation of skeletal myogenic cells.
20 ng that neurons promote the proliferation of myogenic cells.
21 st in part by enhancing the proliferation of myogenic cells.
22  and are critical for differentiation of the myogenic cells.
23  genes and glucose metabolism in mouse C2C12 myogenic cells.
24 muscle eRMS arises from Hh/Gli quiescent non-myogenic cells.
25 d during differentiation and fusion of human myogenic cells.
26 nts the adhesive and fusogenic properties of myogenic cells.
27 arise from the uncontrolled proliferation of myogenic cells.
28 m myotubes without requiring co-culture with myogenic cells.
29 aling negatively regulates MEF2D function in myogenic cells.
30 X2 expression was lost in the differentiated myogenic cells.
31 liferation and reduced apoptosis in cultured myogenic cells.
32 ts both proliferation and differentiation of myogenic cells.
33 ed Bax translocation and cell death in mouse myogenic cells.
34 ite cells and are induced in quiescent C2C12 myogenic cells after ectopic expression of either Pax3 o
35 a plays an important role in the survival of myogenic cells after ischemia/reperfusion injury.
36 essed by PAX3/FOXO1A or PAX7/FOXO1A in C2C12 myogenic cells again as seen with Pax3/7DN.
37 these two stress proteins is able to protect myogenic cells against ischemia/reperfusion injury.
38  unmethylated at all the CpG sites tested in myogenic cells and a subpopulation of somite cells.
39 ast some ARMSs and the PAX3-FOXO1-expressing myogenic cells and demonstrate that fusion RNA profiling
40 e partially reprogrammed from differentiated myogenic cells and display a pluripotent-like state.
41 ted exclusively in regions that give rise to myogenic cells and dorsal spinal cord components reveali
42 g to isolate transcripts that are present in myogenic cells and in the embryo prior to MRF expression
43   Previous studies have shown that in rodent myogenic cells and in the hearts of transgenic mice in w
44  is transcribed from an intergenic region of myogenic cells and its expression is upregulated during
45 in expression in a much larger collection of myogenic cells and muscle biopsies derived from biceps a
46 ected in FSHD, but not in unaffected control myogenic cells and muscle tissue.
47 e DUX4-fl mRNA and protein were expressed in myogenic cells and muscle tissues derived from FSHD affe
48 s that upregulate expression of PTPRQ in non-myogenic cells and MYF5/MYF6 in myogenic cells.
49 ed fibro/adipogenic progenitors, can support myogenic cells and remodel the extracellular matrix.
50 both the number of terminally differentiated myogenic cells and the intricate slow/fast patterning of
51  perturb localization of Golgi components in myogenic cells, and myofibrillogenesis is normal.
52                                   When mouse myogenic cells are implanted at the growing tip of early
53  remain distal to endogenous differentiating myogenic cells are more likely to remain undifferentiate
54 -PCR and cell culture analyses indicate that myogenic cells are present in the embryo before somite f
55 ICAM-1-ICAM-1 interactions was restricted to myogenic cells, as forced expression of ICAM-1 by fibrob
56          S1PR3 levels were high in quiescent myogenic cells before falling during entry into cell cyc
57 w that MIBP is abundantly expressed by C2C12 myogenic cells before fusion, and the expression of MIBP
58 tion at key developmental stages in Emd null myogenic cells, both in vivo and in vitro.
59                                     Cultured myogenic cells (C(2)C(12)) expressed beta-amyloid-42 (Ab
60 erefore to act as universal mediators of the myogenic cell-cell fusion mechanism underlying formation
61       Here, we show that in mouse muscle and myogenic cells, compensatory regulation of the histone d
62                                              Myogenic cells cotransduced with RCAS(A)-Raf BXB and RCA
63 ies suggest that elevating MBNL3 activity in myogenic cells could lead to muscle degeneration disorde
64          These vectors are able to transduce myogenic cell cultures and express dystrophin in myotube
65 o the expression of muscle-specific genes in myogenic cell cultures.
66 ild-type (WT) littermates, and the number of myogenic cells decreases with age.
67 r, we provide evidence that Cripto modulates myogenic cell determination and promotes proliferation b
68 es demonstrate that limb embryonic and fetal myogenic cells develop from distinct, but related progen
69 lar mechanisms of relaxin in regulating both myogenic cell differentiation and muscle healing process
70                    This novel perspective on myogenic cell differentiation revealed previously unreco
71 play multiple functions, including promoting myogenic cell differentiation, cytoskeletal rearrangemen
72 n of Six1 specifically in adult SCs impaired myogenic cell differentiation, impaired myofiber repair
73 f the HDAC6-dysferlin protein complex during myogenic cell differentiation.
74 ed from mouse fibroblasts, hematopoietic and myogenic cells exhibit distinct transcriptional and epig
75 tch signaling pathways are also essential to myogenic cell fate decisions during development and tiss
76 f6 signaling cascade plays a crucial role in myogenic cell fate determination and lineage progression
77 f Notch activity is crucial for specifying a myogenic cell fate only in asymmetric lineages.
78  balance and promotes the endothelial versus myogenic cell fate, before migration to the limb, in mul
79 reprogramming of muscle stem cells modulates myogenic cell fate.
80 s ligand Serrate apportions myogenic and non-myogenic cell fates within the early Xenopus heart field
81                          Satellite cells are myogenic cells found between the basal lamina and the sa
82                          Furthermore, though myogenic cells from genetically Bcl-2-null mice formed m
83 nd protein expression in muscle biopsies and myogenic cells from genetically unaffected relatives of
84          Here we detail a protocol to derive myogenic cells from human embryonic stem (ES) and induce
85  the "In-Out" mechanism whereby migration of myogenic cells from the somites into the limb bud is fol
86                                              Myogenic cells fused normally in vitro, but lacked well-
87 own to interfere with the differentiation of myogenic cells, genetically interacts with PAX7-FKHR: co
88              p21ras is a potent regulator of myogenic cell growth and differentiation.
89 sue; therefore, an unlimited availability of myogenic cells has applications in regenerative medicine
90 investigate whether embryonic and fetal limb myogenic cells have different genetic requirements we co
91 e long been recognized as the main source of myogenic cells in adult muscle, most of the knowledge ab
92 hanced BrdU incorporation into the nuclei of myogenic cells in both the presence and the absence of n
93 tion and polymerase chain reaction analyses, myogenic cells in the constructs were shown to survive i
94     We hypothesized that the early-appearing myogenic cells in the injured area differentiate into my
95  developmental origin of embryonic and fetal myogenic cells in the limb, we genetically labeled and a
96 aB by impairing the regenerative capacity of myogenic cells in the muscle microenvironment to drive m
97 of-function of Pitx2 decreases the number of myogenic cells in the somite, whereas overexpression inc
98 e independent of Smad4-mediated signaling in myogenic cells in the tongue.
99  sparing, but very little is known about the myogenic cells in this muscle group.
100 fited from the study of normal and malignant myogenic cells in vitro, facilitating the identification
101 ain whether migration and differentiation of myogenic cells in vivo are directly regulated by such gr
102 uscle injury triggers the differentiation of myogenic cells (including MC13 cells) into fibrotic cell
103 eta1 into skeletal muscle in vivo stimulated myogenic cells, including myofibers, to express TGF-beta
104 he local expression of this growth factor by myogenic cells, including regenerating myofibers, in inj
105 Expression of SRF-N, the 32-kDa fragment, in myogenic cells inhibited the transcriptional activity of
106 nopathy, we investigated in vitro macrophage-myogenic cell interactions and found that Dysf-deficient
107 t the amount of muscle formed from implanted myogenic cells is greatly augmented by prior irradiation
108 uble mutant, whereas excessive production of myogenic cells is observed in the trunk.
109                                       In the myogenic cell line C2, we have found that Myf5 expressio
110 isms of IGF action in muscle, we developed a myogenic cell line that overexpresses IGF-binding protei
111                During differentiation of the myogenic cell line, C2C12, muscle-specific MAP4 transcri
112    In this investigation we use a "dyspedic" myogenic cell line, which does not express any ryanodine
113 s prepared from myotubes produced by a mouse myogenic cell line.
114 acterized in vitro using the mammalian C2C12 myogenic cell line.
115 ased during the differentiation of the C2C12 myogenic cell line.
116 D and Myf-5 are critical to establishing the myogenic cell lineage and producing committed, undiffere
117                      Whereas ablation of the myogenic cell lineage facilitated adipogenic differentia
118 uscle satellite cells as a model and through myogenic cell lineage-specific NICD(OE) (overexpression
119 tinction between periocular myogenic and non-myogenic cell lineages according to their mutually exclu
120 e that previous support for Myf5-independent myogenic cell lineages was confounded by inefficiencies
121  p38 prevents the differentiation program in myogenic cell lines and human primary myocytes.
122 erences for outgrowth on membranes of clonal myogenic cell lines derived from specific rostral and ca
123           A variety of cell types, including myogenic cell lines, adult skeletal myoblasts, immoratal
124                                           In myogenic cell lines, phosphorylation of p38beta residue
125 l expression caused aberrant localization of myogenic cells marked with alpha-actin promoter-driven e
126      We have observed that the origin of the myogenic cells may influence their survival in the injec
127       At the forelimb level, endothelial and myogenic cells migrate from adjacent somites into the li
128                                       Nai;ve myogenic cells migrate from the somites into the develop
129 sed in this abnormal domain, indicating that myogenic cell migration and differentiation are occurrin
130 n de novo FSHD, we have established a clonal myogenic cell model from a mosaic patient.
131 lineage tracers into single identified adult myogenic cells (muscle or noncontractile muscle-derived
132      These results suggest that, at least in myogenic cells, nuclear Tmod may be involved in the diff
133 tudies demonstrate specific abnormalities in myogenic cell number and behavior that may relate to the
134 lpha2-deficient muscles and cells, including myogenic cells obtained from patients with a clinical di
135 erative capacity, and in vivo engraftment of myogenic cells obtained from severely symptomatic (Mtm1d
136 expressed exclusively and transiently in the myogenic cells of the differentiating chicken heart was
137    pCMF1 is transiently expressed within the myogenic cells of the primitive heart tube from stages 9
138 minantly expressed by macrophages but not by myogenic cells or capillary endothelia cells in injured
139                     CCR2 was not detected in myogenic cells or capillary endothelial cells in injured
140                                        Fetal myogenic cells originating from transgenic mice carrying
141                                              Myogenic cells overexpressing activated Raf and kinase-d
142 ip between expression and phenotype in human myogenic cells, PAX3-FKHR was introduced into immortaliz
143 dentified in addition to the expected GFP(+) myogenic cells (presumably satellite cells), a second do
144 induction of growth factors and reduction of myogenic cell proliferation and differentiation activiti
145                                              Myogenic cell proliferation and differentiation are regu
146  regeneration and reveals highly coordinated myogenic cell proliferation and differentiation programs
147 lly controlled transcriptional regulation of myogenic cell proliferation and differentiation via expr
148 is and Fgf10 expression as well as decreased myogenic cell proliferation, reduced cell number and dis
149 thesis that TRIM32 is involved in control of myogenic cells proliferation and differentiation.
150 ulators of fiber type, low levels of Tcf4 in myogenic cells promote both slow and fast myogenesis, th
151                   shRNA knockdown of CD82 in myogenic cells reduces myoblast proliferation, suggestin
152   Constitutive PKD activation in mouse C2C12 myogenic cells regulated metabolic genes and glucose met
153 blastoma subtype containing muscle elements, myogenic cells share cytogenetic signatures with the pri
154              Under coculture conditions with myogenic cells, some cells within the SP cell population
155                            A wide variety of myogenic cell sources have been used for repair of injur
156                   The 10T1/2-MRF4 fibroblast/myogenic cell system was used to address the following i
157 ofibers from HFrD rats gave rise to 20% less myogenic cells than the Ang 1-7-treated rats.
158             Mtm1delta4 muscle contains fewer myogenic cells than wild-type (WT) littermates, and the
159                                              Myogenic cells that are able both to carry full-length g
160                    Pax3 was not expressed by myogenic cells that migrate into the branchial arches de
161 initiate regeneration promptly by activating myogenic cells that proliferate and differentiate into m
162          As myod expression is restricted to myogenic cells, the data show that myogenesis is essenti
163  In contrast to the other two populations of myogenic cells, the transplantation of the long-time pro
164 n response to muscle injury, and the derived myogenic cells then fuse to repair damaged muscle fibers
165 ades in skeletal muscle and the induction of myogenic cells to differentiate into myofibroblastic cel
166 dbrain and branchial arches act on migrating myogenic cells to influence their gene expression and de
167 ization characteristics of these kinesins in myogenic cells to others previously identified in muscle
168 r the first time the susceptibility of human myogenic cells to SINV infection.
169 iding a positive feedback loop that switches myogenic cells to terminal differentiation.
170        We conclude that the vast majority of myogenic cells transit through a MyoD+ state, and that M
171                                              Myogenic cell transplantation (MT), a potential therapy
172 an be exploited to potentiate the outcome of myogenic cell transplantation into dystrophic muscles.
173                                              Myogenic cell transplantation survival was decreased whe
174 rentiation was reversible and independent of myogenic cell type.
175             A surprisingly wide range of non-myogenic cell types improves ventricular function, sugge
176 scle-specific gene expression in these three myogenic cell types.
177 d arrow M(264)) by caspase-6 in vitro and in myogenic cells undergoing apoptosis.
178 a-1 expression is upregulated in a subset of myogenic cells upon muscle injury.
179         Transient energy deprivation of H9c2 myogenic cells, used as an in vitro model of myocardial
180  To examine the role of FAK in the fusion of myogenic cells, we examined the expression of FAK and th
181                                     In mouse myogenic cells, we found that, as in non-muscle cells, B
182            To clarify the origin(s) of adult myogenic cells, we used phenotypic, morphological, and f
183 ofibers in the nonlacerated muscle and these myogenic cells were gradually replaced by myofibroblasti
184                         Three populations of myogenic cells were isolated from normal mouse skeletal
185 through embryoid body method and MYF5-GFP(+) myogenic cells were sorted and characterized.
186                       Because tumor cells or myogenic cells were used for those studies, it is not cl
187 ficient mouse muscle and primary human MDC1A myogenic cells, which indicates a conserved mechanism of
188                                 Treatment of myogenic cells with pan-HDAC or HDAC6-specific inhibitor
189 bition of PRC2 permits MyoD re-expression in myogenic cells with reduced Spt6.
190 mportant in electromechanical integration of myogenic cells with surrounding re-cipient rat cardiomyo
191 mental relationships between endothelial and myogenic cells within human skeletal muscle.
192 aling (1) blocks terminal differentiation of myogenic cells within the somite and (2) sustains myobla
193 ed for the normal mediolateral patterning of myogenic cells within the somite.

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