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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])
16              Stroke injury acutely increased myostatin (3-fold) and lowered brain-derived neurotrophi
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
19      We previously showed that expression of myostatin, a master negative regulator of skeletal muscl
20                                              Myostatin, a member of the TGF-beta family of ligands, i
21          To this end, we focused on blocking myostatin, a member of the transforming growth factor-be
22 own that AONs can also be used to knock down myostatin, a negative regulator of muscle growth and dif
23                                Inhibition of myostatin, a negative regulator of muscle mass, offers a
24  and pig components, against the backdrop of myostatin, a universal sequence commonly found in mammal
25           Thus, the controlled inhibition of myostatin action could potentially help repair damaged c
26          These data indicate that preventing myostatin activation has therapeutic potential in addres
27 oclonal antibody which specifically inhibits myostatin activation, effectively increases muscle mass
28 m of antibody-mediated neutralization of pro-myostatin activation.
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
31                            Here we show that myostatin/activin A inhibition can cause muscle hypertro
32  receptor (ACVR2B/Fc) to test the effects of myostatin/activin A inhibition in the R6/2 mouse model o
33                                Inhibition of myostatin/activin A signaling activated transcriptional
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
36                          New function of the myostatin/activin type I receptor (ALK4) as a mediator o
37                            Interference with myostatin activity improves insulin sensitivity that was
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.
40                                              Myostatin and activin A are structurally related secrete
41                     The cellular targets for myostatin and activin A in muscle and the role of satell
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
45 action is likely due to its ability to block myostatin and enhance neovacularization.
46                                         Both myostatin and GDF11 affected synapse formation in isolat
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
49                       However, expression of myostatin and its cognate receptors in other tissues, in
50                       We also show that both myostatin and its receptor were abundantly expressed in
51 ergoes conformational rearrangements to bind myostatin and likely acts as a site of specificity for t
52       Here, we aimed to decipher the role of myostatin and myostatin-dependent signaling pathways for
53 ype II receptors, preventing the activity of myostatin and other negative skeletal muscle regulators.
54 2/3, and thus presents a means of regulating myostatin and potentiating muscle growth.
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
57                                              Myostatin and the activins are capable of binding to bot
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
60 ss development, including the ligands GDF-8 (myostatin) and GDF-11 (BMP-11).
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
63  markers and protein expression of PI3K/Akt, myostatin, and autophagy signaling were measured.
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
67                                              Myostatin antagonism might become a therapeutic strategy
68 e regulator of muscle regeneration, with the myostatin antagonist follistatin.
69 and activin receptor, and an increase of the myostatin antagonist, follistatin.
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
76                      Finally, to investigate myostatin as a potential therapeutic target for the trea
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
79                                Regulators of myostatin at the protein (AKT1) and miRNA (miR-539 and m
80 uous electropositive surface is created when myostatin binds Fst288, which significantly increases th
81 y favorable phenotype can be reproduced when myostatin blockade begins at an adult age.
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.
85 ion solution structure of myostatin-free and myostatin-bound states of GASP-1 and GASP-2.
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
90         Foxa2 transcriptionally up-regulated Myostatin, contributing to exaggerated oxidative stress
91                                     Parental myostatin deficiency (Mstn(tm1Sjl/+)) increases muscle m
92             In wild-type offspring, maternal myostatin deficiency altered fetal growth and calvarial
93                   This large rodent model of myostatin deficiency did not have the negative consequen
94                                              Myostatin deficiency has been well studied in mice, but
95          Second, we sought to apply maternal myostatin deficiency to a mouse model with osteogenesis
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
100                       However, the effect of myostatin depends on the genetic and pathophysiological
101    In support to this argument, we show that myostatin directly up-regulated lipogenic genes and incr
102 muscle growth that operates independently of myostatin-driven mechanisms.
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.
107  the effect of AgRP neuron activation on BAT-myostatin expression and insulin sensitivity.
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.
111 ith CKD, we found a 2- to 3-fold increase in myostatin expression in muscle.
112 hole-body muscle-to-fat ratio with increased myostatin expression in muscle.
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,
116                                              Myostatin expression was decreased in atrial appendages
117 iation with Bbaa1 arthritis development, and myostatin expression was linked to IFN-beta production.
118                                Additionally, myostatin expression was upregulated in Smad7(-/-) muscl
119        The BCAA/LEU supplement did not alter myostatin expression, but mTOR signaling, autophagy meas
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
123                The increased skeletal muscle myostatin expression, reduced mammalian target of rapamy
124 ression of Numb in satellite cells inhibited Myostatin expression.
125 intaining Akt phosphorylation and inhibiting myostatin expression.C
126 lation of growth-inhibitory genes, including myostatin, Fbxo32 (MAFbx), and Trim63 (MuRF1).
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
129                  The TGF-beta family ligands myostatin, GDF11, and activins are negative regulators o
130 mpared with other TGFbeta superfamily member myostatin (GDF8).
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
133                       The first two exons of myostatin gene code for the N-propeptide and its third e
134                                              Myostatin gene inactivation prevented the severe loss of
135 a variation in the 5' flanking region of the myostatin gene is associated with the genetic regulation
136 n the myostatin promoter, and stimulation of myostatin gene transcription.
137  in % (w/w), a reference system based on the myostatin gene was used.
138 nt study, the coding region of bMSTN (bovine myostatin) gene was amplified and mutated (A224C and G93
139                    Previously, we found that Myostatin genotype, reciprocal cross, and sex interacted
140   A total of 12 of these QTL interacted with myostatin genotype.
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
144 tatin homodimers, suggesting a 1:1 (antibody:myostatin homodimer) binding stoichiometry.
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
147                       Targeted inhibition of myostatin in cardiac cachexia might be a therapeutic opt
148 n dose-dependently inhibited the response to myostatin in cardiomyocytes and in perfused mouse hearts
149  glycogen accumulation after inactivation of myostatin in cardiomyocytes.
150                 The crystal structure of pro-myostatin in complex with 29H4-16 Fab, a high-affinity v
151    Here, we present the crystal structure of myostatin in complex with Fstl3.
152    Here, we present the crystal structure of myostatin in complex with the antagonist follistatin 288
153 respect to a potential role for GDF11 and/or myostatin in humans with heart disease.
154     Our results uncover an important role of myostatin in the heart for maintaining cardiac energy ho
155                     However, the function of myostatin in the heart is barely understood, although it
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
158                                Inhibition of myostatin in vivo suppressed Lyme arthritis in the reduc
159 n of follistatin (an endogenous inhibitor of myostatin) in our LGMD R1 model (C3KO) resulted in 1.5-
160 ants, we generated a mouse model that allows myostatin inactivation in adult cardiomyocytes.
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
163                                   Inhibiting myostatin induced a more profound increase in muscle mas
164                                      Loss of myostatin induced eccentric hypertrophy and enhanced car
165                              Pharmacological myostatin inhibition also decreased the rate of protein
166                           Here, we show that myostatin inhibition by follistatin transgene expression
167      We therefore tested the hypothesis that myostatin inhibition would improve recovery of skeletal
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.
171                                              Myostatin inhibitors are currently being pursued as ther
172            New advances in the use of potent myostatin inhibitors have made this an attractive approa
173        Remarkably, codelivery of activin and myostatin inhibitors induced a synergistic response, res
174  truncations of GASP-1 result in less potent myostatin inhibitors that form a 2:1 complex, suggesting
175 s field to include more novel agents such as myostatin inhibitors.
176                                              Myostatin inhibits skeletal muscle growth.
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
179                                              Myostatin is a cytokine of the transforming growth facto
180                                              Myostatin is a major negative regulator of skeletal musc
181                                              Myostatin is a muscle-specific member of the TGF-beta su
182                                              Myostatin is a negative regulator of muscle growth, and
183                                              Myostatin is a negative regulator of muscle mass.
184                                              Myostatin is a negative regulator of skeletal muscle and
185 sarcopenia, but the antihypertrophic myokine myostatin is a potential therapeutic target.
186                                              Myostatin is a secreted signaling molecule that normally
187            For instance, the TGF-beta ligand myostatin is a staunch negative regulator of muscle grow
188                                              Myostatin is a transforming growth factor-beta family me
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
192                                              Myostatin is secreted as a latent configuration formed b
193                                              Myostatin is tightly controlled by Fst-like 3 (Fstl3), w
194                                     GDF8, or myostatin, is a member of the TGF-beta superfamily of se
195        In addition, a muscle atrophy marker, myostatin, is increased in UUO muscle; provision of miR-
196 in wild-type compared with postdevelopmental myostatin knockout mice.
197 nsulin-like growth factor-1 and unexpectedly myostatin, known mediators of muscle hypertrophy and atr
198                                      Indeed, myostatin levels in the plasma were significantly increa
199                                     Notably, myostatin loss also impeded the growth of LLC tumors, th
200                             Mechanistically, myostatin loss attenuated the activation of muscle fiber
201                         Muscle expression of myostatin, mammalian target of rapamycin (mTOR) targets,
202 her these results suggest that inhibition of myostatin may not be a promising therapeutic strategy in
203                                           In Myostatin(-/-) mice however, Streptozotocin treatment di
204 Moreover, Foxa2 levels remained unaltered in Myostatin(-/-) mice, while levels of p63/REDD1 were high
205 nd 8.5-fold (P < 0.001) higher expression of myostatin mRNA and protein in patients.
206 1) and miRNA (miR-539 and miR-208b targeting myostatin mRNA) levels were altered in GRMD CS, consiste
207          We used a Cre/loxP system to ablate myostatin (Mstn gene) expression in a cell type-specific
208 ucleases were used to genetically inactivate myostatin (MSTN(Delta/Delta) ) would exhibit an increase
209 egulated by the secreted signaling proteins, myostatin (MSTN) and activin A.
210     Muscle growth is negatively regulated by myostatin (MSTN) and activins.
211                                              Myostatin (MSTN) and growth and differentiation factor-1
212                            Null mutations of myostatin (Mstn) are associated with increased muscle ma
213                                              Myostatin (MSTN) belongs to the transforming growth fact
214 ac as well as skeletal muscle cells promotes myostatin (Mstn) expression.
215                                          The myostatin (MSTN) gene is important because of its role i
216         High doses of dexamethasone (Dex) or myostatin (Mstn) induce severe atrophy of skeletal muscl
217                                              Myostatin (Mstn) is a conserved negative regulator of sk
218                                              Myostatin (MSTN) is a dominant inhibitor of skeletal mus
219                                              Myostatin (MSTN) is a member of the transforming growth
220                                              Myostatin (MSTN) is a negative regulator of skeletal mus
221                                              Myostatin (MSTN) is a transforming growth factor-beta (T
222                                              Myostatin (Mstn) is predominantly expressed in skeletal
223                            The growth factor myostatin (MSTN) negatively regulates skeletal muscle gr
224                                     Ablating myostatin (Mstn) prevents obesity, so we investigated if
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
230                             A non-functional myostatin mutation leads to a double muscling phenotype
231                                     Although myostatin negatively regulates skeletal muscle growth, i
232 output and beta-adrenergic responsiveness of myostatin null mice was therefore due to increased SR Ca
233                              This was due to myostatin null ventricular myocytes having larger [Ca(2+
234  F2 population of 1000 mice derived from the Myostatin-null C57BL/6 and M16i mouse lines, six imprint
235  were collected on F2 progeny derived from a myostatin-null C57BL/6 strain by M16i cross.
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
238 tegrin-linked kinase are dysregulated in the myostatin-null mice.
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
241                        Genetic disruption of myostatin or its related signaling is known to cause str
242                                              Myostatin (or GDF8) and GDF11 are potent negative regula
243 Growth differentiation factor 11 (GDF11) and myostatin (or GDF8) are closely related members of the t
244                                              Myostatin (or growth/differentiation factor 8 (GDF8)) is
245                                              Myostatin, or GDF8, is an inhibitor of skeletal muscle g
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
248                  Several drugs targeting the myostatin pathway have been used in clinical trials to i
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
251  myonuclear degeneration and the role of the myostatin pathway.
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.
255                   AAV-mediated expression of myostatin pro-peptide D76A mutant in adult Ldlr null mic
256  we reported that AAV-mediated delivery of a myostatin pro-peptide D76A mutant in adult mice attenuat
257 ull mice resulted in sustained expression of myostatin pro-peptide in the liver.
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
262                                              Myostatin released from cardiomyocytes induces skeletal
263                                We found that myostatin represses AMP-activated kinase activation in t
264 re identified to significantly interact with myostatin, sex or reciprocal cross.
265                                              Myostatin showed an age-dependent decrease and an invers
266       An analysis of a Tcap binding protein, myostatin, showed that deletion of Tcap was accompanied
267                      Modalities that inhibit myostatin signaling are currently in clinical trials for
268 ac MRI revealed that genetic inactivation of myostatin signaling in the adult murine heart caused car
269                          Loss or blockade of myostatin signaling increases muscle mass and improves m
270                                Inhibition of myostatin signaling increases muscle mass, and therapeut
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
274                                Inhibition of myostatin signalling in C3KO muscles resulted in signifi
275                                Inhibition of myostatin signalling is unlikely to be a valid therapeut
276 of genetic and pharmacological inhibition of myostatin signalling on the disease phenotype in a mouse
277                 Smad7 inhibits intracellular myostatin signalling via Smad2/3, and thus presents a me
278                       In this study, we used myostatin small interfering (si)RNA (siGDF-8), a major i
279                            Transfection with Myostatin-specific siRNA rescued the proliferation defec
280                                 Furthermore, myostatin stimulated expression of regulator of G-protei
281 ent pathway, whereas muscle cells exposed to myostatin stimulated IL-6 production via p38 MAPK and ME
282                           Therefore, an anti-myostatin strategy can improve skeletal muscle recovery
283 eEF2, ERK1/2 and UBF; gene expression of the myostatin target Mighty as well as c-Myc and its targets
284  associated with higher muscle expression of myostatin than placebo.
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
288          We found that genetic inhibition of myostatin through overexpression of follistatin (an endo
289 re are loci in the genome that interact with myostatin to control backfat depth and other complex tra
290 designed to identify loci that interact with myostatin to impact growth traits in mice.
291 ted at developing drugs capable of targeting myostatin to treat patients with muscle loss.
292 ion or gene silencing of NF-kappaB abolished myostatin up-regulation under conditions of hyperammonem
293                      In addition, inhibiting myostatin using intramuscular injection of AAV1-follista
294                Pharmacological inhibition of myostatin, using an anti-myostatin antibody, resulted in
295          We find that the prehelix region of myostatin very closely resembles that of TGF-beta class
296                          Local inhibition of myostatin was also not affected by rapamycin and may con
297 ed medium (CM), but IL-6, OSM, TNFalpha, and myostatin were not.
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

 
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