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1 ssues made from genetically modified primary skeletal myoblasts.
2 ucose uptake by L6 myotubes and neonatal rat skeletal myoblasts.
3 trisphosphate (IP3) response to BK in L8 rat skeletal myoblasts.
4 lso repressed the myogenic capacity of human skeletal myoblasts.
5  chain (ETC) complexes in mouse immortalized skeletal myoblasts.
6 imary cell line derived from mammalian (rat) skeletal myoblasts.
7 xocytosis and glucose uptake in cultured rat skeletal myoblasts.
8 y derive from direct conversion of committed skeletal myoblasts.
9 ed for leucine-induced activation of S6K1 in skeletal myoblasts.
10 d PDGF-BB, induces a fate switch in adjacent skeletal myoblasts.
11 in that promotes myogenic gene expression in skeletal myoblasts.
12 that EGLN3 promotes differentiation of C2C12 skeletal myoblasts.
13 ad a modulator of optimal differentiation of skeletal myoblasts.
14  in insulin receptor knock-out mouse-derived skeletal myoblasts.
15 elded multipotent mesenchymal precursors and skeletal myoblasts.
16 ncluding 3T3E1 osteoblasts and human primary skeletal myoblasts.
17 ival functions in terminally differentiating skeletal myoblasts.
18 re it proved to be more active than in C2C12 skeletal myoblasts.
19 ter myocardial injury to a similar degree as skeletal myoblasts.
20 , and many aspects of the differentiation of skeletal myoblasts.
21 myoblasts, whereas hTra2beta increases it in skeletal myoblasts.
22 ferentiation and the coincident apoptosis of skeletal myoblasts.
23 icted genes, and cellular differentiation of skeletal myoblasts.
24 licated previously in the differentiation of skeletal myoblasts.
25 apidly, and clinical trials using autologous skeletal myoblasts and bone marrow cells are under way.
26 l of several cell types, and both autologous skeletal myoblasts and bone marrow progenitor cells have
27 ols a bidirectional cell fate switch between skeletal myoblasts and brown fat cells.
28  miR-1, miR-206 and miR-133 is restricted to skeletal myoblasts and cardiac tissue during embryo deve
29 be an in vitro model of hypertrophy in C2C12 skeletal myoblasts and demonstrate that induction of hyp
30 nking region was an active promoter in C2C12 skeletal myoblasts and exhibited increased expression up
31 so shown to be necessary for the survival of skeletal myoblasts and for the efficient formation of in
32 we used two differentiated cell types, C2C12 skeletal myoblasts and LLC-PK1 kidney epithelial cells,
33 R-1a-2 are induced during differentiation of skeletal myoblasts and promote myogenesis in vitro.
34                          Cocultures of human skeletal myoblasts and rat cardiomyocytes resulted in re
35                             In animals, both skeletal myoblasts and stem cells partially restore myoc
36 restriction (GR) impaired differentiation of skeletal myoblasts and was associated with activation of
37                  Rem is expressed in primary skeletal myoblasts and, when overexpressed in C2C12 myob
38 stics of endothelial, neural, smooth muscle, skeletal myoblasts, and cardiac myocyte cells.
39 entiates BK-induced IP3 production in L8 rat skeletal myoblasts, and this action of insulin involves
40                                              Skeletal myoblasts are an attractive cell type for trans
41                   Using differentiated C2C12 skeletal myoblasts as a model system, we observe that ca
42  chondrocytes, adipocytes, stroma cells, and skeletal myoblasts) as well as visceral mesoderm (endoth
43 on of the dominant negative protein in C2C12 skeletal myoblasts blocked the differentiation-induced e
44                     These cell types include skeletal myoblasts, bone-marrow derived cells, endotheli
45 ) pathway is required for differentiation of skeletal myoblasts, but how the pathway is activated dur
46      Work began with committed cells such as skeletal myoblasts, but recently the field has expanded
47 es nuclear entry of NFAT in undifferentiated skeletal myoblasts, but the IP3R Ca(+2) pool in differen
48 osarcoma SVR cells) and control cells (mouse skeletal myoblast C2C12 cells).
49    To accomplish this goal, we determined if skeletal myoblasts can distinguish among differences in
50                                        Thus, skeletal myoblasts can establish new muscle tissue when
51 he Raf kinase signal transduction pathway in skeletal myoblasts causes a complete cessation of myofib
52 nally modifies Cys184 of HRas in C2C12 mouse skeletal myoblasts, causing a reduction in the localizat
53 n during myodifferentiation of LHCN-M2 human skeletal myoblast cell line.
54  we show that hypomorphic mtFAS mutant mouse skeletal myoblast cell lines display a severe loss of el
55                                              Skeletal myoblast cell proliferation and subsequent diff
56           During terminal differentiation of skeletal myoblasts, cells fuse to form postmitotic multi
57  induced during the differentiation of C2C12 skeletal myoblasts, coincident with myoblast fusion.
58 isease who were transplanted with autologous skeletal myoblasts concurrent with left ventricular assi
59      Based on these results, we propose that skeletal myoblasts contain multiple mechanosensory eleme
60                              To determine if skeletal myoblasts could establish new contractile tissu
61                  In this study, neonatal rat skeletal myoblasts cultured within 3-dimensional enginee
62 volved in it, a parallel study on normal rat skeletal myoblast cultures was conducted.
63                                 Heat-shocked skeletal myoblasts demonstrated improved tolerance to hy
64                                              Skeletal myoblasts derived from SIRT1+/- heterozygous mi
65 ith the functional benefits of newly formed, skeletal myoblast-derived muscle in the later phase.
66           Expression of MURF is required for skeletal myoblast differentiation and myotube fusion.
67 zed to the nuclear envelope, such that C2C12 skeletal myoblast differentiation and neonatal rat ventr
68 nduces the secretion of a novel inhibitor of skeletal myoblast differentiation.
69 tion of the i-proteasome also impaired human skeletal myoblast differentiation.
70 port that EGLN3 levels increase during C2C12 skeletal myoblast differentiation.
71 rom a genome-wide transcriptional dataset of skeletal myoblast differentiation.
72 sin heavy chain and myogenin, two markers of skeletal myoblast differentiation.
73                              Bone marrow and skeletal myoblasts do not promote true tissue regenerati
74 n exposed to Dll4 and PDGF-BB, but not Dll1, skeletal myoblasts downregulate myogenic genes, except M
75  and specifically expressed in proliferating skeletal myoblasts during myogenesis was identified.
76    Here, we report that undifferentiated rat skeletal myoblasts expressed N-cadherin and connexin43,
77 and host myocytes following transplantation, skeletal myoblasts expressing an enhanced green fluoresc
78                                       L6 rat skeletal myoblasts expressing ss-galactosidase (ss-gal)
79 tal myotubes differentiated from C2C12 mouse skeletal myoblasts for three weeks by utilizing micromol
80                                              Skeletal myoblasts form grafts of mature muscle in injur
81                                    Implanted skeletal myoblasts form viable grafts in infarcted myoca
82                                The implanted skeletal myoblasts formed viable grafts in heavily scarr
83 alyzed GRalpha and 11beta-HSD1 expression in skeletal myoblasts from men (n = 14) with contrasting le
84                                              Skeletal myoblast fusion in vitro requires the expressio
85                          Thus engraftment of skeletal myoblasts generated spatial heterogeneity of [C
86                                              Skeletal myoblast grafts can form contractile tissue to
87                                              Skeletal myoblasts grown in vitro and induced to differe
88  infarcts by transplanting cardiomyocytes or skeletal myoblasts have failed to reconstitute healthy m
89  types, including myogenic cell lines, adult skeletal myoblasts, immoratalized atrial cells, embryoni
90 er, bovine serum albumin (BSA), fibrin glue, skeletal myoblasts in BSA, or skeletal myoblasts in fibr
91 s as an autocrine differentiation factor for skeletal myoblasts in culture.
92  induced during the differentiation of C2C12 skeletal myoblasts in culture.
93   After five weeks, the mean area covered by skeletal myoblasts in fibrin glue was significantly grea
94 , fibrin glue, skeletal myoblasts in BSA, or skeletal myoblasts in fibrin glue were injected into the
95 FAS impairment blocks the differentiation of skeletal myoblasts in vitro.
96    Since the initial report of cell therapy (skeletal myoblasts) in HF in 1998, research has proceede
97 to prevent this progression, we transplanted skeletal myoblasts into cryoinfarcted myocardium of the
98 lcium levels inhibits the differentiation of skeletal myoblasts into mature myotubes.
99                           Differentiation of skeletal myoblasts into multinucleated myotubes is a mul
100               Direct injection of autologous skeletal myoblasts into the peri-infarct area has been p
101  Raf on the differentiation and apoptosis of skeletal myoblasts is dictated by the level of Raf signa
102          Expression of oncogenic Ras in 23A2 skeletal myoblasts is sufficient to induce both a transf
103 lar, we find that the predominant isoform in skeletal myoblasts is Tbx5c, and we show that it is dram
104 initiation of differentiation of C2C12 mouse skeletal myoblasts, knockdown of USP9X increases mTORC2
105 d in endothelial cells, smooth muscle cells, skeletal myoblasts (L6, BC3H1, C2C12), fibroblasts, and
106 dren and represents a high-grade neoplasm of skeletal myoblast-like cells.
107                         Cardiomyoplasty with skeletal myoblasts may benefit cardiac function after in
108                                   In primary skeletal myoblasts pioglitazone also up-regulates PGC-1a
109 ver, when cocultured with endothelial cells, skeletal myoblasts, previously treated with Dll4 and PDG
110 ions of endogenous erythropoietin to promote skeletal myoblast proliferation and survival and wound h
111 cleus and thus control the fate of committed skeletal myoblasts remains poorly understood.
112 ntriguingly, mammalian sperm could fuse with skeletal myoblasts, requiring PtdSer on sperm and BAI1/3
113                   Gene silencing of Fbxl2 in skeletal myoblasts resulted in increased proliferative r
114                                              Skeletal myoblast (SkM) implantation improves cardiac fu
115                        Strategies to enhance skeletal myoblast (SkM) survival after transplantation i
116 tion of AdVEGF-165 to the transplantation of skeletal myoblasts (SKMB) transfected with AdVEGF-165 in
117 ar cells (MN), mesenchymal stem cells (MSC), skeletal myoblasts (SkMb), and fibroblasts (Fibro) expre
118 ion chronic heart failure model, we compared skeletal myoblast (SMB) with bone marrow cell (BMC) inje
119                      Cell transplantation of skeletal myoblasts (SMs) is one possible treatment for r
120 restricted, being 80-fold greater in primary skeletal myoblasts than in liver-derived HepG2 cells.
121 for SHP-2 as a nutrient-sensing regulator in skeletal myoblasts that is required for the activation o
122 aling system via a tyrosine kinase in L8 rat skeletal myoblasts that results in increased IP3 formati
123                 Exposure of undifferentiated skeletal myoblasts to DIs, followed by incubation in dif
124 ion, we show that forcing immortalized human skeletal myoblasts to produce the 40p53 isoform, instead
125 mized, multicenter pilot study of autologous skeletal myoblast transplantation concurrent with CABG o
126                                              Skeletal myoblast transplantation has been shown to impr
127                        Successful autologous skeletal myoblast transplantation into infarcted myocard
128                                              Skeletal myoblast transplantation is a potential treatme
129                         Graft survival after skeletal myoblast transplantation is affected by various
130                                              Skeletal myoblast transplantation is promising for the t
131                                   Autologous skeletal myoblast transplantation is under investigation
132 monstrated the feasibility and efficiency of skeletal myoblast transplantation via the intracoronary
133  muscle cell ischemia in which primary human skeletal myoblasts were exposed to hypoxic conditions (1
134                                      Primary skeletal myoblasts were stably transfected with a hFIX e
135                          One million primary skeletal myoblasts were then infused via the coronary ar
136                                  Primary rat skeletal myoblasts were transfected with the human VEGF(
137 ologous, unfractionated bone marrow cells or skeletal myoblasts were used in early clinical trails to
138                   We found that hESC-derived skeletal myoblasts were viable after transplantation int
139 losely resemble quiescent, stably programmed skeletal myoblasts with the capacity to differentiate wh
140                Survival and proliferation of skeletal myoblasts within the cardiac environment are cr
141 n documented survival and engraftment of the skeletal myoblasts within the infarcted myocardium.
142 ther supplementing infarcted myocardium with skeletal myoblasts would (1) result in viable myoblast i

 
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