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1 trisphosphate (IP3) response to BK in L8 rat skeletal myoblasts.
2 ed for leucine-induced activation of S6K1 in skeletal myoblasts.
3 d PDGF-BB, induces a fate switch in adjacent skeletal myoblasts.
4 in that promotes myogenic gene expression in skeletal myoblasts.
5 that EGLN3 promotes differentiation of C2C12 skeletal myoblasts.
6 ucose uptake by L6 myotubes and neonatal rat skeletal myoblasts.
7  in insulin receptor knock-out mouse-derived skeletal myoblasts.
8 lso repressed the myogenic capacity of human skeletal myoblasts.
9 elded multipotent mesenchymal precursors and skeletal myoblasts.
10 ncluding 3T3E1 osteoblasts and human primary skeletal myoblasts.
11 ival functions in terminally differentiating skeletal myoblasts.
12 re it proved to be more active than in C2C12 skeletal myoblasts.
13 imary cell line derived from mammalian (rat) skeletal myoblasts.
14 y derive from direct conversion of committed skeletal myoblasts.
15 ter myocardial injury to a similar degree as skeletal myoblasts.
16 , and many aspects of the differentiation of skeletal myoblasts.
17 myoblasts, whereas hTra2beta increases it in skeletal myoblasts.
18 ferentiation and the coincident apoptosis of skeletal myoblasts.
19 icted genes, and cellular differentiation of skeletal myoblasts.
20 licated previously in the differentiation of skeletal myoblasts.
21 ssues made from genetically modified primary skeletal myoblasts.
22 apidly, and clinical trials using autologous skeletal myoblasts and bone marrow cells are under way.
23 l of several cell types, and both autologous skeletal myoblasts and bone marrow progenitor cells have
24 ols a bidirectional cell fate switch between skeletal myoblasts and brown fat cells.
25  miR-1, miR-206 and miR-133 is restricted to skeletal myoblasts and cardiac tissue during embryo deve
26 be an in vitro model of hypertrophy in C2C12 skeletal myoblasts and demonstrate that induction of hyp
27 nking region was an active promoter in C2C12 skeletal myoblasts and exhibited increased expression up
28 so shown to be necessary for the survival of skeletal myoblasts and for the efficient formation of in
29 we used two differentiated cell types, C2C12 skeletal myoblasts and LLC-PK1 kidney epithelial cells,
30                          Cocultures of human skeletal myoblasts and rat cardiomyocytes resulted in re
31                             In animals, both skeletal myoblasts and stem cells partially restore myoc
32 restriction (GR) impaired differentiation of skeletal myoblasts and was associated with activation of
33                  Rem is expressed in primary skeletal myoblasts and, when overexpressed in C2C12 myob
34 stics of endothelial, neural, smooth muscle, skeletal myoblasts, and cardiac myocyte cells.
35 entiates BK-induced IP3 production in L8 rat skeletal myoblasts, and this action of insulin involves
36                                              Skeletal myoblasts are an attractive cell type for trans
37                   Using differentiated C2C12 skeletal myoblasts as a model system, we observe that ca
38  chondrocytes, adipocytes, stroma cells, and skeletal myoblasts) as well as visceral mesoderm (endoth
39 on of the dominant negative protein in C2C12 skeletal myoblasts blocked the differentiation-induced e
40                     These cell types include skeletal myoblasts, bone-marrow derived cells, endotheli
41 ) pathway is required for differentiation of skeletal myoblasts, but how the pathway is activated dur
42      Work began with committed cells such as skeletal myoblasts, but recently the field has expanded
43 es nuclear entry of NFAT in undifferentiated skeletal myoblasts, but the IP3R Ca(+2) pool in differen
44 osarcoma SVR cells) and control cells (mouse skeletal myoblast C2C12 cells).
45    To accomplish this goal, we determined if skeletal myoblasts can distinguish among differences in
46                                        Thus, skeletal myoblasts can establish new muscle tissue when
47 he Raf kinase signal transduction pathway in skeletal myoblasts causes a complete cessation of myofib
48                                              Skeletal myoblast cell proliferation and subsequent diff
49           During terminal differentiation of skeletal myoblasts, cells fuse to form postmitotic multi
50  induced during the differentiation of C2C12 skeletal myoblasts, coincident with myoblast fusion.
51 isease who were transplanted with autologous skeletal myoblasts concurrent with left ventricular assi
52      Based on these results, we propose that skeletal myoblasts contain multiple mechanosensory eleme
53                              To determine if skeletal myoblasts could establish new contractile tissu
54                  In this study, neonatal rat skeletal myoblasts cultured within 3-dimensional enginee
55 volved in it, a parallel study on normal rat skeletal myoblast cultures was conducted.
56                                 Heat-shocked skeletal myoblasts demonstrated improved tolerance to hy
57                                              Skeletal myoblasts derived from SIRT1+/- heterozygous mi
58 ith the functional benefits of newly formed, skeletal myoblast-derived muscle in the later phase.
59           Expression of MURF is required for skeletal myoblast differentiation and myotube fusion.
60 nduces the secretion of a novel inhibitor of skeletal myoblast differentiation.
61 port that EGLN3 levels increase during C2C12 skeletal myoblast differentiation.
62 rom a genome-wide transcriptional dataset of skeletal myoblast differentiation.
63 tion of the i-proteasome also impaired human skeletal myoblast differentiation.
64 sin heavy chain and myogenin, two markers of skeletal myoblast differentiation.
65                              Bone marrow and skeletal myoblasts do not promote true tissue regenerati
66 n exposed to Dll4 and PDGF-BB, but not Dll1, skeletal myoblasts downregulate myogenic genes, except M
67  and specifically expressed in proliferating skeletal myoblasts during myogenesis was identified.
68    Here, we report that undifferentiated rat skeletal myoblasts expressed N-cadherin and connexin43,
69 and host myocytes following transplantation, skeletal myoblasts expressing an enhanced green fluoresc
70                                       L6 rat skeletal myoblasts expressing ss-galactosidase (ss-gal)
71 tal myotubes differentiated from C2C12 mouse skeletal myoblasts for three weeks by utilizing micromol
72                                              Skeletal myoblasts form grafts of mature muscle in injur
73                                    Implanted skeletal myoblasts form viable grafts in infarcted myoca
74                                The implanted skeletal myoblasts formed viable grafts in heavily scarr
75 alyzed GRalpha and 11beta-HSD1 expression in skeletal myoblasts from men (n = 14) with contrasting le
76                                              Skeletal myoblast fusion in vitro requires the expressio
77                          Thus engraftment of skeletal myoblasts generated spatial heterogeneity of [C
78                                              Skeletal myoblast grafts can form contractile tissue to
79                                              Skeletal myoblasts grown in vitro and induced to differe
80  infarcts by transplanting cardiomyocytes or skeletal myoblasts have failed to reconstitute healthy m
81  types, including myogenic cell lines, adult skeletal myoblasts, immoratalized atrial cells, embryoni
82 er, bovine serum albumin (BSA), fibrin glue, skeletal myoblasts in BSA, or skeletal myoblasts in fibr
83 s as an autocrine differentiation factor for skeletal myoblasts in culture.
84  induced during the differentiation of C2C12 skeletal myoblasts in culture.
85   After five weeks, the mean area covered by skeletal myoblasts in fibrin glue was significantly grea
86 , fibrin glue, skeletal myoblasts in BSA, or skeletal myoblasts in fibrin glue were injected into the
87    Since the initial report of cell therapy (skeletal myoblasts) in HF in 1998, research has proceede
88 to prevent this progression, we transplanted skeletal myoblasts into cryoinfarcted myocardium of the
89 lcium levels inhibits the differentiation of skeletal myoblasts into mature myotubes.
90                           Differentiation of skeletal myoblasts into multinucleated myotubes is a mul
91               Direct injection of autologous skeletal myoblasts into the peri-infarct area has been p
92  Raf on the differentiation and apoptosis of skeletal myoblasts is dictated by the level of Raf signa
93          Expression of oncogenic Ras in 23A2 skeletal myoblasts is sufficient to induce both a transf
94 lar, we find that the predominant isoform in skeletal myoblasts is Tbx5c, and we show that it is dram
95 initiation of differentiation of C2C12 mouse skeletal myoblasts, knockdown of USP9X increases mTORC2
96 d in endothelial cells, smooth muscle cells, skeletal myoblasts (L6, BC3H1, C2C12), fibroblasts, and
97                         Cardiomyoplasty with skeletal myoblasts may benefit cardiac function after in
98                                   In primary skeletal myoblasts pioglitazone also up-regulates PGC-1a
99 ver, when cocultured with endothelial cells, skeletal myoblasts, previously treated with Dll4 and PDG
100 ions of endogenous erythropoietin to promote skeletal myoblast proliferation and survival and wound h
101 cleus and thus control the fate of committed skeletal myoblasts remains poorly understood.
102                                              Skeletal myoblast (SkM) implantation improves cardiac fu
103                        Strategies to enhance skeletal myoblast (SkM) survival after transplantation i
104 tion of AdVEGF-165 to the transplantation of skeletal myoblasts (SKMB) transfected with AdVEGF-165 in
105 ar cells (MN), mesenchymal stem cells (MSC), skeletal myoblasts (SkMb), and fibroblasts (Fibro) expre
106 ion chronic heart failure model, we compared skeletal myoblast (SMB) with bone marrow cell (BMC) inje
107                      Cell transplantation of skeletal myoblasts (SMs) is one possible treatment for r
108 restricted, being 80-fold greater in primary skeletal myoblasts than in liver-derived HepG2 cells.
109 for SHP-2 as a nutrient-sensing regulator in skeletal myoblasts that is required for the activation o
110 aling system via a tyrosine kinase in L8 rat skeletal myoblasts that results in increased IP3 formati
111                 Exposure of undifferentiated skeletal myoblasts to DIs, followed by incubation in dif
112 mized, multicenter pilot study of autologous skeletal myoblast transplantation concurrent with CABG o
113                                              Skeletal myoblast transplantation has been shown to impr
114                        Successful autologous skeletal myoblast transplantation into infarcted myocard
115                                              Skeletal myoblast transplantation is a potential treatme
116                         Graft survival after skeletal myoblast transplantation is affected by various
117                                              Skeletal myoblast transplantation is promising for the t
118                                   Autologous skeletal myoblast transplantation is under investigation
119 monstrated the feasibility and efficiency of skeletal myoblast transplantation via the intracoronary
120                                      Primary skeletal myoblasts were stably transfected with a hFIX e
121                          One million primary skeletal myoblasts were then infused via the coronary ar
122                                  Primary rat skeletal myoblasts were transfected with the human VEGF(
123 ologous, unfractionated bone marrow cells or skeletal myoblasts were used in early clinical trails to
124                   We found that hESC-derived skeletal myoblasts were viable after transplantation int
125 losely resemble quiescent, stably programmed skeletal myoblasts with the capacity to differentiate wh
126                Survival and proliferation of skeletal myoblasts within the cardiac environment are cr
127 n documented survival and engraftment of the skeletal myoblasts within the infarcted myocardium.
128 ther supplementing infarcted myocardium with skeletal myoblasts would (1) result in viable myoblast i

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