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1 growth by altering the binding capacity for myostatin.
2 ng the interactions of GASP antagonists with myostatin.
3 ntibody LY2495655 (LY) binds and neutralises myostatin.
4 unique in that they specifically antagonize myostatin.
5 fibers can be negatively regulated by bovine myostatin.
6 he heat shock response and the antagonism of myostatin.
7 ar proteolytic activation of pro- and latent myostatin.
8 olding and regulating biological activity of myostatin.
9 at has been identified in the serum bound to myostatin.
10 feration by antagonizing the TGF-beta ligand myostatin.
11 regions that harbor loci that interact with myostatin.
12 achexia by secreting peptide factors such as myostatin.
13 s accompanied by increased protein levels of myostatin.
14 signature, including increased expression of myostatin.
15 1 Nm/kg, P=0.04), elevated levels of MSTN-2 (myostatin-2), FBXO-32 (F-box only protein 32 [Atrogin1])
17 dependently of overexpression or knockout of myostatin, a key repressor of muscle development that ca
18 from cirrhotics had increased expression of myostatin, a known inhibitor of skeletal muscle accretio
22 own that AONs can also be used to knock down myostatin, a negative regulator of muscle growth and dif
24 and pig components, against the backdrop of myostatin, a universal sequence commonly found in mammal
27 oclonal antibody which specifically inhibits myostatin activation, effectively increases muscle mass
29 that ACE-083 binds and potently neutralizes myostatin, activin A, activin B and growth differentiati
30 least partially due to its ability to block myostatin, activin A, and transforming growth factor-bet
32 receptor (ACVR2B/Fc) to test the effects of myostatin/activin A inhibition in the R6/2 mouse model o
34 satellite cells playing little or no role in myostatin/activin A signaling in vivo and render support
35 ains in a competitive manner at the critical myostatin/activin binding site, hence preventing signal
38 statin interaction and significantly reduced myostatin activity upon L165041-mediated activation of P
39 hich functions through negatively modulating myostatin activity via a mechanism involving Gasp-1.
42 , which encodes a high-affinity receptor for myostatin and activin A specifically in myofibers is suf
43 g or atrophying diseases, with a decrease of myostatin and activin receptor, and an increase of the m
44 ActRIIA in addition to ActRIIB in mediating myostatin and activin signaling and highlight the need f
47 Myoglianin (MYO), the Drosophila homolog of myostatin and GDF11, regulates not only body weight and
48 MT attenuated the stroke-induced increase in myostatin and increased BDNF expression in skeletal musc
51 ergoes conformational rearrangements to bind myostatin and likely acts as a site of specificity for t
53 ype II receptors, preventing the activity of myostatin and other negative skeletal muscle regulators.
55 lammatory gene expression in muscle, such as myostatin and protein tyrosine phosphatase receptor-gamm
56 HPA-responsive transcripts such as Fkbp5 and Myostatin and reveals novel HPA-responsive pathways such
58 cuss the biochemical regulation of GDF11 and myostatin and their functions in the heart, skeletal mus
59 that multiple pathways, including decreased myostatin and up-regulated miRNAs, alpha-dystroglycan/li
61 ifferentiation factor 8 (GDF8; also known as myostatin) and GDF11 are closely related members of the
62 WEAK/Fn14 axis; FOXO-1, Atrogin-1 and MuRF1; Myostatin) and increased anabolic intracellular pathways
64 , it specifically induces IGF1 and represses myostatin, and expression of PGC-1alpha4 in vitro and in
65 Circulating insulin-like growth factor-1, myostatin, and growth and differentiation factor-15 were
66 f muscle mass--insulin-like growth factor-1, myostatin, and growth and differentiation factor-15--wer
70 treatment of young and old mice with an anti-myostatin antibody (ATA 842) for 4 wk increased muscle m
71 gical inhibition of myostatin, using an anti-myostatin antibody, resulted in statistically significan
72 sults in mice regarding the efficacy of anti-myostatin approaches and may inform patient selection an
73 y explain the poor clinical efficacy of anti-myostatin approaches in several of the clinical studies
74 al Bbaa1 congenic mice, formally implicating myostatin as a novel downstream mediator of the joint-sp
75 de support for pharmacological inhibition of myostatin as a potential therapeutic approach for age-re
77 domain (ND) of Fstl3 interacts uniquely with myostatin as compared with activin A, because it utilize
78 ecific recombinant congenic lines identified myostatin as uniquely upregulated in association with Bb
80 uous electropositive surface is created when myostatin binds Fst288, which significantly increases th
82 ease context, inducing muscle hypertrophy by myostatin blockade may have detrimental effects, which n
83 uscle wasting in heart failure, we infused a myostatin blocking antibody (JA-16), which promoted grea
84 ed highly up-regulated expression of p21 and Myostatin, both inhibitors of myoblast proliferation.
86 tatin, which increased circulating levels of myostatin by 3- to 4-fold, caused a reduction in weight
87 or TGF-beta/activin family members including myostatin, can prevent or restore loss of lean body mass
88 orted to bind to and inhibit the activity of myostatin; consistent with this, we found that enhanced
89 e results demonstrate the mechanism by which Myostatin contributes to DNA damage in skeletal muscle o
96 ts demonstrated that the effects of maternal myostatin deficiency were conferred by the postimplantat
97 ent rats was markedly different from that of myostatin-deficient mice, which have impaired contractil
98 Overall, the muscle and tendon phenotype of myostatin-deficient rats was markedly different from tha
99 aimed to decipher the role of myostatin and myostatin-dependent signaling pathways for cardiac funct
101 In support to this argument, we show that myostatin directly up-regulated lipogenic genes and incr
103 y outstanding questions related to GDF11 and myostatin dynamics and signaling during development, gro
104 In young mdx mice, combined dystrophin and myostatin exon skipping therapy greatly improved DMD pat
105 Skeletal muscle autophagic proteolysis and myostatin expression (inhibitor of protein synthesis) ar
106 1R ablation enhanced AKT signaling, reducing myostatin expression and increasing IL-6 secretion.
108 unique insights into hyperammonemia-induced myostatin expression and suggests a mechanism by which s
109 ecific null mice, indicating that myocardial myostatin expression controls muscle atrophy in heart fa
110 e demonstrate that hyperammonemia stimulated myostatin expression in a NF-kappaB-dependent manner.
113 duced muscle mass and strength and increased myostatin expression in wild-type compared with postdeve
114 monstrated a higher interleukin-15 and lower myostatin expression relative to controls, indicating a
115 n cultured muscle cells, TNF-alpha increased myostatin expression via a NF-kappaB-dependent pathway,
117 iation with Bbaa1 arthritis development, and myostatin expression was linked to IFN-beta production.
120 le cannabinoid 1 receptor regulates Il-6 and myostatin expression, governing physical performance and
121 al muscle molecular markers showed increased myostatin expression, impaired mTOR signaling, and incre
122 conditions, expression of DN FoxO decreased myostatin expression, increased MyoD expression and sate
127 e First low resolution solution structure of myostatin-free and myostatin-bound states of GASP-1 and
128 more tight binding with the mature peptide, myostatin function is inhibited, resulting in the change
131 n with a naturally occurring mutation in the myostatin gene (Compact (Cmpt)) leading to a hypermuscul
132 ency of the C-variant (g.66493737C/T) at the myostatin gene (MSTN) in cohorts of the Thoroughbred hor
135 a variation in the 5' flanking region of the myostatin gene is associated with the genetic regulation
138 nt study, the coding region of bMSTN (bovine myostatin) gene was amplified and mutated (A224C and G93
141 n activating growth factors, such as BMP2/4, myostatin, growth differentiation factor 11, and transfo
142 tors of muscle mass (e.g., MAFbx, MURF1, and myostatin) had peaked on days 2-4 but normalized by day
143 egeneration, primarily through inhibition of myostatin, have shown promise in the laboratory and are
145 ions of the prodomain in the pro- and latent myostatin homodimers, suggesting a 1:1 (antibody:myostat
146 ore potent than GASP-2, preferentially binds myostatin in an asymmetrical 1:1 complex, whereas GASP-2
148 n dose-dependently inhibited the response to myostatin in cardiomyocytes and in perfused mouse hearts
152 Here, we present the crystal structure of myostatin in complex with the antagonist follistatin 288
154 Our results uncover an important role of myostatin in the heart for maintaining cardiac energy ho
156 er, our results reveal an essential role for myostatin in the pathogenesis of cancer cachexia and lin
157 ls, and suggests that the greatest impact of myostatin in the regulation of muscle mass may not be to
159 n of follistatin (an endogenous inhibitor of myostatin) in our LGMD R1 model (C3KO) resulted in 1.5-
161 achexia, combined inhibition of activins and myostatin increased mass or prevented muscle wasting, re
162 phy, M-p110alphaKO mice show decreased serum myostatin, increased mitochondrial mass, increased mitoc
168 suggest that muscle hypertrophy, induced by myostatin inhibition, leads to loss of oxidative capacit
169 rmine if induction of muscle growth, through myostatin inhibition, represents a viable therapeutic st
170 ficacy of both SMN2 splicing modifiers and a myostatin inhibitor in mice at later disease stages.
174 truncations of GASP-1 result in less potent myostatin inhibitors that form a 2:1 complex, suggesting
177 hanced secretion of Gasp-1, increased Gasp-1 myostatin interaction and significantly reduced myostati
178 owever, in contrast, the prodomain of GDF-8 (myostatin) interacts with the glycosaminoglycan side cha
189 regulate aging of multiple tissues, whereas myostatin is a well-described negative regulator of post
190 ested the hypothesis that the muscle protein myostatin is involved in mediating the pathogenesis of c
191 Similar to other TGF-beta family ligands, myostatin is neutralized by binding one of a number of s
197 nsulin-like growth factor-1 and unexpectedly myostatin, known mediators of muscle hypertrophy and atr
202 her these results suggest that inhibition of myostatin may not be a promising therapeutic strategy in
204 Moreover, Foxa2 levels remained unaltered in Myostatin(-/-) mice, while levels of p63/REDD1 were high
206 1) and miRNA (miR-539 and miR-208b targeting myostatin mRNA) levels were altered in GRMD CS, consiste
208 ucleases were used to genetically inactivate myostatin (MSTN(Delta/Delta) ) would exhibit an increase
225 ntagonist of another TGF-beta family member, myostatin (Mstn), for the promotion of muscle growth in
226 ily member, and a close homolog of mammalian Myostatin (Mstn), is a muscle-derived extrinsic factor t
227 gen-related receptor gamma (Errgamma) on the myostatin (Mtn) mouse null background (Mtn(-/-)/Errgamma
228 NA damage and muscle atrophy was observed in Myostatin(-/-) muscle in response to Streptozotocin trea
229 ccurring in constitutive and germ-line-based myostatin mutants, we generated a mouse model that allow
232 output and beta-adrenergic responsiveness of myostatin null mice was therefore due to increased SR Ca
234 F2 population of 1000 mice derived from the Myostatin-null C57BL/6 and M16i mouse lines, six imprint
236 atellite cell loss also persists with age in myostatin-null mice regardless of increased muscle mass.
237 o and liver regeneration via the analysis of myostatin-null mice, in which skeletal muscle is hypertr
239 needed to determine whether direct impact of myostatin on liver and aortic endothelium may contribute
240 ieves only a partial signaling blockade upon myostatin or activin A stimulation, and this leads to on
243 Growth differentiation factor 11 (GDF11) and myostatin (or GDF8) are closely related members of the t
246 effects of the age-dependent decline of the myostatin paralog growth and differentiation factor 11.
247 arin coding gene Mtm1) that a down-regulated myostatin pathway can be reactivated by correcting the u
249 lity, we examined the effect of blocking the myostatin pathway in dysferlin-deficient (Dysf(-/-)) mic
250 Use of a soluble ActRIIB-Fc "trap," to block myostatin pathway signaling in normal or cachectic mice
252 ional environment, and specifically prenatal myostatin pathways, provides a potential therapeutic win
253 bition by subcutaneous injections of an anti-myostatin peptibody into CKD mice (IC(50) approximately
254 cle (n = 15) and MCAO mice receiving an anti-myostatin PINTA745 (n = 12; subcutaneous injection of 7.
256 we reported that AAV-mediated delivery of a myostatin pro-peptide D76A mutant in adult mice attenuat
258 paB p65 subunit to specific sites within the myostatin promoter, and stimulation of myostatin gene tr
259 pQTL, tQTL and eQTL that interacted with Myostatin, reciprocal cross, and sex were detected as we
260 mice, but limited data are available on how myostatin regulates the structure and function of muscle
261 for the first time show the role of Foxa2 in Myostatin regulation in skeletal muscle in diabetic mice
268 ac MRI revealed that genetic inactivation of myostatin signaling in the adult murine heart caused car
271 how that the expression of components of the myostatin signaling pathway is downregulated in muscle w
272 IIB receptor (ActRIIB)-mFc (an inhibitor of myostatin signaling) to promote hypertrophy and increase
273 GRMD CS, consistent with down-regulation of myostatin signaling, CS hypertrophy, and functional resc
276 of genetic and pharmacological inhibition of myostatin signalling on the disease phenotype in a mouse
281 ent pathway, whereas muscle cells exposed to myostatin stimulated IL-6 production via p38 MAPK and ME
283 eEF2, ERK1/2 and UBF; gene expression of the myostatin target Mighty as well as c-Myc and its targets
285 es conformational changes in pro- and latent myostatin that span the arm region, the loops contiguous
286 h factor-beta superfamily members, including myostatin, that are involved in the negative regulation
287 in breakdown, we conclude that CKD increases myostatin through cytokine-activated pathways, leading t
289 re are loci in the genome that interact with myostatin to control backfat depth and other complex tra
292 ion or gene silencing of NF-kappaB abolished myostatin up-regulation under conditions of hyperammonem
298 Levels of FBXO32 (Atrogin-1), ActRIIB and myostatin were significantly changed in the irradiated c
299 Moreover, cardiac-specific overexpression of myostatin, which increased circulating levels of myostat
300 ltured aortic endothelial cells responded to myostatin with a reduction in eNOS phosphorylation and a