ライフサイエンスコーパス: SMA

1 SMA at 6.25 parts per million harvested proteins from ce

2 SMA exhibited multiple response features that were absen

3 SMA exhibits premovement activity across a variety of co

4 SMA is caused by the loss of survival motor neuron 1 (SM

5 SMA is characterised by haemolysis and inadequate erythr

6 SMA is characterized by motoneuron death, skeletal muscl

7 al parameters were: RRA: L1 vertebrae (45%), SMA: L1 vertebrae (66%), CT: T12 vertebrae (46%), AB: L4

8 y, suffering from a genetically confirmed 5q-SMA under treatment with nusinersen in accordance with t

9 easured by the FSS in adult patients with 5q-SMA transiently after initiation of treatment.

10 tion of central and peripheral synapses in a SMA mouse model, resulting in an improvement of the sens

11 om cell membranes using styrene maleic acid (SMA) copolymer, elucidating structures of ASIC1 channels

12 In contrast, styrene maleic acid (SMA) copolymers offer a detergent-free method for biolog

13 Styrene maleic acid (SMA) is a polymer that extracts nanodiscs of biological

14 full-length receptor in styrene-maleic acid (SMA) lipid particles.

15 A set of styrene-maleic acid (SMA) polymers including a methylamine derivative facilit

16 uced TGFbeta1 and alpha-smooth muscle actin (SMA) protein expression in PLFs.

17 8% of childhood SMA cases and 48.5% of adult SMA cases in the study areas would have been averted if

18 cal improvement with the severe and advanced SMA type 1 variant.

19 Age, SMA type, and ambulatory status were significantly assoc

20 get for therapeutic intervention because all SMA patients retain SMN2.

21 ividuals, helps to develop a therapy for all SMA-affected individuals.

22 atically changing the natural history of all SMA subtypes, including substantial clinical improvement

23 ive materials including shape memory alloys (SMAs), piezoelectrics, dielectric elastomer actuators (D

24 Shape memory alloys (SMAs), such as Nitinol (i.e., NiTi), are of great import

25 applications including shape memory alloys (SMAs), switches based on metal-insulator transitions (MI

26 aining with alpha-smooth muscle actin (alpha SMA) revealed a significant reduction in hepatic stellat

27 nd FGF2), and higher muscle numbers of alpha SMA and pERK immunopositive cells, compared to control r

28 ontractile markers CNN-1 (calponin 1), alpha-SMA (alpha-smooth muscle actin), and SM22-alpha (smooth

29 to regulate alpha-smooth muscle actin (alpha-SMA) and collagen type I expression in Ang II-exposed ca

30 r levels of alpha-smooth muscle actin (alpha-SMA) expression, and exerted larger traction forces.

31 e levels of alpha smooth muscle actin (alpha-SMA) expression.

32 n of mature alpha-smooth muscle actin (alpha-SMA)+ myofibroblasts (verified by immunocytochemistry fo

33 pression of alpha-smooth muscle actin (alpha-SMA), an established marker for MF differentiation, is d

34 alpha1) and alpha-smooth muscle actin (alpha-SMA), and cell migration/wound healing.

35 pression of alpha-smooth muscle actin (alpha-SMA), and differential upregulation of aforementioned EC

36 pression of alpha-smooth muscle actin (alpha-SMA), fibronectin, and collagen 1.

37 ere performed for smooth muscle actin (alpha-SMA), pancytokeratin, and CK7.

38 s including alpha smooth muscle actin (alpha-SMA).

39 ich encodes alpha-smooth muscle actin (alpha-SMA).

40 Similarly, alpha-smooth muscle actin(alpha-SMA) expression, aortic collagen deposition was elevated

41 In addition, alpha-SMA (alpha-smooth muscle actin)-positive cells were redu

42 ation and migration as well as MMP and alpha-SMA expression.

43 pressing CD31(+) endothelial cells and alpha-SMA(+) vascular smooth muscle cells were detected within

44 to increased alpha-SMA expression and alpha-SMA-containing stress fibers.

45 Moreover, S100a4-lineage cells become alpha-SMA(+) myofibroblasts, via loss of S100a4 expression.

46 Colon expression of COL1A1, CTGF, alpha-SMA and COX-2 did not differ between TNBS rats and contr

47 y, we found that MPS peptide decreases alpha-SMA expression and synergistically interacts with ninted

48 Paired cornea-derived and BM-derived alpha-SMA+ myofibroblast primary cultures were generated from

49 Further, SCAP cells were positive for alpha-SMA while they completely lacked NG2 positive cells.

50 ve for pancytokeratin and positive for alpha-SMA, vimentin, CK7, N-cadherin, ZEB1, Snail, ROCK1, and

51 DPSC had alpha-SMA positive cells but showed very few NG2 positive cell

52 Asn117 also plays an important role in alpha-SMA function within the cerebrovascular smooth muscle ce

53 no stiffness-dependent differences in alpha-SMA immunofluorescence, suggesting that a stiff microenv

54 s and induces DR-mediated apoptosis in alpha-SMA(+ )MFBs through upregulated DR5 during its activatio

55 eling and targeting upregulated DR5 in alpha-SMA(+) MFBs is a viable therapy for fibrosis in sclerode

56 vation of airway remodelling including alpha-SMA, HSP-47, extracellular matrix (MMP7, 9 and TIMP-1),

57 A interference (RNAi) led to increased alpha-SMA expression and alpha-SMA-containing stress fibers.

58 inant TGF-beta1 (rTGF-beta1) to induce alpha-SMA expression.

59 ransforming growth factor-beta-induced alpha-SMA expression.

60 he induction of myofibroblast markers; alpha-SMA and Col-1 and reduced morphological changes of myofi

61 pha-actin isoforms from smooth muscle (alpha-SMA) and cardiac (alpha-CAA) to skeletal muscle alpha-ac

62 mpaired TGF-beta1 and TCM induction of alpha-SMA and calponin 1, but not of COL1A1.

63 nd/or TGFbeta2-induced upregulation of alpha-SMA and CTGF.

64 SC was greater with high expression of alpha-SMA and NG2 positive cells.

65 on factor (MRTF), a known regulator of alpha-SMA transcription and itself regulated by G-actin bindin

66 Colon expression of alpha-SMA was significantly lower in the MODULEN group versus

67 obstruction reversed the expression of alpha-SMA, fibronectin, and collagen 1 and increased expressio

68 ition of HA synthesis had no effect on alpha-SMA levels, suggesting a dispensable role for HA.

69 -positive endothelial cells and reduce alpha-SMA-positive cancer-associated fibroblasts at pharmacolo

70 increased RXFP1 expression and reduced alpha-SMA expression.

71 We concluded that CD44 regulates alpha-SMA gene expression through cooperation between two inte

72 f mechanisms linking CD44 knockdown to alpha-SMA induction, using RNAi and chemical inhibitors, revea

73 collagen receptor cross-talk underlies alpha-SMA-dependent collagen type I expression in cardiac fibr

74 d by immunocytochemistry for vimentin, alpha-SMA, desmin, and vinculin) generated from rabbit corneal

75 n of functional SMN significantly ameliorate SMA phenotypes in mouse models of severe SMA.

76 al NCALD reduction significantly ameliorated SMA pathology including electrophysiological and histolo

77 l accessibility for severe malarial anaemia (SMA) and cerebral malaria (CM).

78 of presenting with severe malarial anaemia (SMA) in children, with an OR of 2.79 (95% CI:1.92-4.06;

79 Severe malarial anaemia (SMA) is the most common life-threatening complication of

80 brotic genes, including TGFbeta2, BAMBI, and SMA.

81 Both CM and SMA demonstrated predominantly upregulated enrichment of

82 enable to interventions to ameliorate CM and SMA.

83 ted at relatively low levels in controls and SMA patients after 3 months of life.

84 In both controls and SMA, ~50% of alpha-MN nuclei express p-c-Jun with decrea

85 x, 78% received projections from both M1 and SMA (regardless of hemisphere); 83% of reticulospinal ce

86 significant deficits remain in both mice and SMA patients following treatment.

87 aria (CM; n = 79) or severe malarial anemia (SMA; n = 77).

88 In this study, we applied SMA at low concentration to human primary cardiovascular

89 or cortex (M1) and supplementary motor area (SMA) bilaterally were assessed.

90 Activity in the supplementary motor area (SMA) has been associated with tics in Tourette syndrome

91 NT The role of the supplementary motor area (SMA) in initiating movement remains unclear.

92 The supplementary motor area (SMA) is believed to contribute to higher order aspects o

93 ontribution of the supplementary motor area (SMA) to movement initiation remains unclear.

94 r cortex (PM), the supplementary motor area (SMA), cortex on the medial wall, and from posterior pari

95 oth trial types in supplementary motor area (SMA), middle temporal gyrus and cerebellum in EP, but no

96 ng activity in the supplementary motor area (SMA), orchestrated and sequenced by activity in the dors

97 by clamping the superior mesenteric artery (SMA) for 45 minutes followed by 120 minutes reperfusion.

98 (CT), orifice of superior mesenteric artery (SMA), vena cava inferior confluence (CVC), abdominal aor

99 croelectrodes and surface-mediated assembly (SMA) of the NCs/NPs as chemically sensitive interfaces,

100 Spinal muscular atrophy (SMA) is a devastating infantile genetic disorder caused

101 Spinal Muscular Atrophy (SMA) is a monogenic neurodegenerative disorder and the l

102 Spinal muscular atrophy (SMA) is a motor neuron disease.

103 Spinal muscular atrophy (SMA) is a neurodegenerative disease caused by a deficien

104 NIFICANCE STATEMENT Spinal muscular atrophy (SMA) is a neurodegenerative disease, characterized by sy

105 Spinal muscular atrophy (SMA) is a neuromuscular disease caused by deletions or m

106 Spinal muscular atrophy (SMA) is a neuromuscular disease caused by mutations in s

107 Spinal muscular atrophy (SMA) is a neuromuscular disease causing the most frequen

108 Spinal muscular atrophy (SMA) is a neuromuscular disease characterized by loss of

109 Spinal muscular atrophy (SMA) is a neuromuscular disorder caused by homozygous mu

110 Spinal muscular atrophy (SMA) is an autosomal recessive motor neuron disease caus

111 BACKGROUNDSpinal muscular atrophy (SMA) is caused by deficient expression of survival motor

112 Spinal muscular atrophy (SMA) is caused by loss-of-function mutations in the surv

113 Spinal muscular atrophy (SMA) is caused by mutation or deletion of survival motor

114 logical hallmark of spinal muscular atrophy (SMA) is severe motor neuron (MN) loss, which results in

115 Spinal muscular atrophy (SMA) occurs as a result of cell-ubiquitous depletion of

116 exon 7 splicing in spinal muscular atrophy (SMA) patient fibroblasts, suggesting a potential applica

117 MN2 copy numbers in spinal muscular atrophy (SMA) samples has not been reported.

118 Spinal muscular atrophy (SMA) type 0 is the most severe form of SMA, associated w

119 f 199 patients with spinal muscular atrophy (SMA) type III assessed using the Hammersmith Functional

120 teral sclerosis and spinal muscular atrophy (SMA), and 3 mutations of the ASC-1 gene TRIP4 have been

121 systemic feature of spinal muscular atrophy (SMA), but little is known about the underlying molecular

122 ction at the NMJ in spinal muscular atrophy (SMA), X-linked spinal and bulbar muscular atrophy (SBMA)

123 uromuscular disease spinal muscular atrophy (SMA)-binds to ribosomes and that this interaction is tis

124 or neuron disorder, spinal muscular atrophy (SMA).

125 ve diseases such as spinal muscular atrophy (SMA).

126 n diseases, ALS and spinal muscular atrophy (SMA).

127 The dPCR-based SMA copy number determination was accomplished in 90 min

128 HFMSE score significantly decrease for both SMA IIIA (beta = -1.15, p < 0.0001) and IIIB (beta = -0.

129 the highest expression in children with both SMA and sickle cell disease (HbSS), corresponding with e

130 hemistry, PCSK6 was localized to fibrous cap SMA+ cells and neovessels in plaques.

131 f survival motor neuron (SMN) protein causes SMA, the molecular pathways that execute MN cell death a

132 sed disease severity in a well-characterized SMA mouse model.

133 We estimate that 42.8% of childhood SMA cases and 48.5% of adult SMA cases in the study area

134 method using styrene-maleic acid copolymers (SMA-PSI) have been investigated by pump-to-probe femtose

135 th blood-stage Plasmodium coatneyi developed SMA within 2 weeks, with no other severe outcomes, where

136 Does SMA influence initiation across contexts or does it play

137 full end manifestation of an already extreme SMA phenotype caused by substantial reduction of the SMN

138 nd increases the lifespan of male and female SMA mice.

139 7 years was set for the whole cohort and for SMA IIIA and IIIB.

140 PCR platform to meet the growing demand for SMA genotyping and prognostics.

141 projections from M1 in both hemispheres; for SMA, the equivalent figure was even higher (70%).

142 point of age 7 years is significant only for SMA IIIA (beta = 1.79, p < 0.0001).

143 N protein stability have great potential for SMA therapeutics.

144 e disease, which was particularly strong for SMA.

145 g the advent of this and other therapies for SMA, it is unclear whether the paralysis associated with

146 of an antisense oligonucleotide therapy for SMA was an important milestone in SMA research; however,

147 ation was highest at <1-hour travel time for SMA and CM although this was lower outside the predicted

148 The majority of treatments for SMA, approved or in clinic trials, focus on addressing t

149 Quite surprisingly, the detergent-free SMA-PSI complexes upon excitation by these long-wave pul

150 red primary spinal cord neurons derived from SMA mice.

151 ient fibroblast cells and other tissues from SMA mice.

152 liver, and spleen in a population of Gli1(+)SMA(+)PDGFRbeta(+) cells, a signature shared with vascul

153 yer in Epo induction and perivascular Gli1(+)SMA(+)PDGFRbeta(+) cells as a previously unrecognized EP

154 Hitherto it has been used to harvest SMA-lipid-membrane protein particles (SMALP) for biochem

155 Anisomycin treatment of human SMA fibroblasts and sciatic nerve ligation in SMA mice p

156 ts show that scAAV9-STMN1 treatment improves SMA pathology possibly by increasing microtubule turnove

157 between negative symptoms and activation in SMA and precentral gyrus was observed in EP patients and

158 We examined neural activity in SMA and primary motor cortex (M1) as monkeys cycled vari

159 We examined JNK-c-Jun activity in SMA mouse and human cultured cells and tissues.

160 s were cued to increase/decrease activity in SMA without receiving feedback.

161 lamin A/C dysregulation is also apparent in SMA patient fibroblast cells and other tissues from SMA

162 pathology and enhanced phenotypic benefit in SMA mice.

163 cial effects on the sensory-motor circuit in SMA.

164 -loop accumulation and rescues DNA damage in SMA mice, motor neurons and patient cells.

165 n addressing muscle and bone deficiencies in SMA patients.

166 isms underlying motor neuron degeneration in SMA remain elusive, as global cellular dysfunction obscu

167 cantly reduced at early stages of disease in SMA mice.

168 ls and rescues severe to moderate disease in SMA mice.

169 her characterization of miRNA dysfunction in SMA.

170 SMN locus and upregulates SMN2 expression in SMA mice and patient cells.

171 Reintroduction of miR-23a expression in SMA patient iPSC-derived motor neurons protected against

172 Motor function in SMA patients may be additionally improved by targeting s

173 sing approach to increase muscle function in SMA patients.

174 DNA damage leading to genomic instability in SMA mice and patient cells.

175 erved no basal increase of p-c-Jun levels in SMA compared to control cultured cells, human or mouse s

176 egulated in SMA, we profiled miRNA levels in SMA induced pluripotent stem cell (iPSC)-derived motor n

177 tes and influences SMN2 expression levels in SMA patient cells.

178 MA fibroblasts and sciatic nerve ligation in SMA mice provoked robust phosphorylated-c-Jun (p-c-Jun)

179 ajectory divergence, which was much lower in SMA versus M1.

180 contributor to the pathological mechanism in SMA.

181 herapy for SMA was an important milestone in SMA research; however, effective next-generation therape

182 for a direct contributing role of muscle in SMA and argue that an optimal therapy for the disease mu

183 ZPR1 reduces neurodegeneration in SMA mice and prevents degeneration of cultured primary s

184 genomic instability and neurodegeneration in SMA.

185 genomic instability and neurodegeneration in SMA.

186 files of neuronal and non-neuronal organs in SMA mouse embryos.

187 R-23a significantly reduced the pathology in SMA mice, including increased motor neuron size, reduced

188 new approach to target cardiac pathology in SMA.

189 ue-specific prenatal molecular phenotypes in SMA.

190 ggest that renal pathology may be present in SMA.

191 miRNAs that are differentially regulated in SMA, we profiled miRNA levels in SMA induced pluripotent

192 ncreased JNK-c-Jun signaling was reported in SMA raising the possibility that JNK inhibitors could be

193 elf a limited terminal sprouting response in SMA and wild-type normally-innervated endplates.

194 downregulation was identified selectively in SMA motor neurons, consistent with previous reports wher

195 ifically, cardiac ventricles were smaller in SMA hearts, whilst liver and brain remained unaffected.

196 changes at an early, presymptomatic stage in SMA mice, revealing a significant developmental componen

197 ully applied to minimizing the hysteresis in SMAs.

198 s different motor neuron diseases, including SMA.

199 ight mitigate neuromuscular symptoms in mild SMA.

200 ve served to generate mice that model milder SMA, referred to as pharmacological SMA mice, which surv

201 Described here is a rapid multiplex SMA dPCR genotyping assay run on a fully integrated dPCR

202 ons of microRNAs for clinical assessments of SMA disease progression and treatment.

203 e as splice-switching ASOs in the context of SMA and potentially other diseases, and discuss the adva

204 ophy (SMA) type 0 is the most severe form of SMA, associated with the SMN1 gene and manifesting at bi

205 a robust molecular phenotype in the heart of SMA mice and show that lamin A/C dysregulation is also a

206 increased lamin A/C levels in the hearts of SMA mice therefore provide a likely mechanism explaining

207 the understanding of the natural history of SMA type III and will be helpful in the interpretation o

208 ress-activated JNK-c-Jun signaling in MNs of SMA mice or human tissues, but do highlight the importan

209 riants of the pharmacological mouse model of SMA in which pharmacologic restoration of SMN has taken

210 tomatic changes in a prenatal mouse model of SMA.

211 ior in both sexes of a severe mouse model of SMA.

212 ically lowered by ~90-95% in mouse models of SMA.

213 ion is proven to be a protective modifier of SMA across species, including worm, zebrafish, and mice.

214 at miR-23a is a novel protective modifier of SMA, warranting further characterization of miRNA dysfun

215 ntial and temporal relationships to onset of SMA.

216 rstanding of the biology and pathogenesis of SMA.

217 lammatory responses with the pathogenesis of SMA.

218 nding movement is altered by perturbation of SMA activity.

219 as nusinersen-displayed efficient rescue of SMA mouse models.

220 ression and leads to SMN-dependent rescue of SMA.

221 we use microstimulation to probe the role of SMA across a range of behavioral contexts that vary in t

222 Severity of SMA disease correlates inversely with SMN levels.

223 ant implications for optimizing treatment of SMA patients and warrant further investigations to enhan

224 tly in clinical development for treatment of SMA.

225 ndependent therapeutics for the treatment of SMA.

226 developing a new method for the treatment of SMA.

227 m Ugandan children with acute CM (n = 17) or SMA (n = 17) and community children without Plasmodium f

228 All children with CM or SMA, and 35 (42.2%) CC, were iron-deficient and were ran

229 To address this question, we perturbed SMA activity via microstimulation at variable times befo

230 l milder SMA, referred to as pharmacological SMA mice, which survive into early adulthood.

231 Here, we show that pharmacological SMA mice are capable of terminal sprouting following rei

232 tas and plaques but also with overall plaque SMA+ cell content and pericyte fraction.

233 on in cell viability at 24 and 72 hours post-SMA (MTT assay).

234 Pre-SMA dysfunction is thought to be a critical factor in th

235 voxel pattern response of the dorsal ACC/pre-SMA.

236 (pre-SMA) stimulation by 10 or 4 ms and pre-SMA stimulation preceding IFC stimulation by 10 or 4 ms.

237 The pre-supplementary motor area (pre-SMA) plays a critical role in linking higher-level goals

238 eding right presupplementary motor area (pre-SMA) stimulation by 10 or 4 ms and pre-SMA stimulation p

239 (dACC) and pre-supplementary motor area (pre-SMA).

240 supplementary/supplementary motor areas (pre-SMA/SMA) in humans, regions important for movement prepa

241 e observations provide insights into how pre-SMA dysfunction might impact cognitive function.

242 sly recorded single neurons in the human pre-SMA and eye movements while subjects performed goal-dire

243 Together, our results show that human pre-SMA neurons carry abstract signals during visual search

244 error neuron responses appeared first in pre-SMA, and ~50 ms later in dACC.

245 er with observations of hyperactivity in pre-SMA/SMA in both OCD and Tourette syndrome, and evidence

246 and Tourette syndrome, and evidence that pre-SMA is a potential target for repetitive transcranial ma

247 This suggests that the pre-SMA contributes to goal-directed behaviour by flexibly s

248 improved when the IFC pulse preceded the pre-SMA pulse by 4 ms.

249 airments in response inhibition when the pre-SMA pulse preceded the IFC pulse by 10 ms.

250 better mechanistic understanding of the pre-SMA's role in cognition.

251 aracterized two groups of neurons in the pre-SMA.

252 iological membrane solubilisation to produce SMA-lipid particles (SMALPs) containing membrane protein

253 plasia, PCSK6 was expressed by proliferating SMA+ cells and upregulated after 5 days in rat carotid b

254 h previous findings that the type I receptor SMA-6 is recycled via the retromer complex, our work dem

255 ng a novel treatment paradigm for ALS, SBMA, SMA, and related disorders.

256 presymptomatically administered in a severe SMA mouse model.

257 outing has been difficult to study in severe SMA mice due to their short lifespan.

258 e MNs during the period of MN loss in severe SMA model mice.

259 t renal pathology in a mouse model of severe SMA, further reinforcing the need to develop and adminis

260 ate SMA phenotypes in mouse models of severe SMA.

261 sue from the Taiwanese mouse model of severe SMA.

262 s using an established mouse model of severe SMA.

263 ctions and improves significantly the severe SMA phenotype.

264 This new SMI-SMA strategy has significant implications for manufactur

265 otype 9 (scAAV9) viral vector in the Smn2B/- SMA mouse model.

266 nusinersen in severe and/or post-symptomatic SMA-affected individuals is insufficient to counteract t

267 These results argue that SMA participates in the computations that lead to moveme

268 Quantitative muCT analyses revealed that SMA embryos were significantly smaller than littermate c

269 Lesion experiments suggest that SMA makes a critical contribution only for self-initiate

270 tic resonance imaging neurofeedback from the SMA-for reduction of tics in adolescents with TS.

271 in the sensory-motor circuit to improve the SMA motor phenotype.SIGNIFICANCE STATEMENT Spinal muscul

272 trafast pathway for charge separation in the SMA-PSI that may be disrupted during detergent isolation

273 and 6, which showed a partial rescue of the SMA phenotype.

274 The secondary outcome was control over the SMA assessed in neuroimaging scans, in which subjects we

275 found in terms of change in control over the SMA, the hypothesized mechanism of action.

276 on the secondary measure of control over the SMA.

277 rate that STMN1 can significantly reduce the SMA phenotype independent of restoring SMN protein and h

278 he boundary at which homologs can rescue the SMA phenotype.

279 We tested the SMA patient SMN1 missense mutation alleles A2G, D44V, A1

280 opic gradient in a mirror orientation to the SMA.

281 ngue gradient in a mirror orientation to the SMA.

282 ds result in a trimeric form of PSI, yet the SMA-PSI complexes display a heterogenous kinetic behavio

283 ing two sessions of neurofeedback from their SMA.

284 on of the infectivity of PrP(Sc) attached to SMA lipid particles in mice and hamsters indicated that

285 ing a significant developmental component to SMA pathogenesis.

286 ted with P. coatneyi has similar features to SMA in children.

287 Using AAV9 to deliver Smn homologs to SMA mice, we identified a conservation threshold that ma

288 es were markedly decreased in CM relative to SMA despite higher hemoglobin levels and appropriate inc

289 mRNAs encoding proteins that are relevant to SMA pathogenesis.

290 (ASO), was the first approved drug to treat SMA.

291 In tissues isolated from nusinersen-treated SMA patients, antisense oligonucleotide (ASO) concentrat

292 menting the protein is one means of treating SMA and recently led to FDA approval of an intrathecally

293 his raises a fundamental question of whether SMA has presymptomatic, developmental components to dise

294 e ASC-1 gene TRIP4 have been associated with SMA or congenital myopathy.

295 that the low levels of ZPR1 associated with SMA pathogenesis cause accumulation of co-transcriptiona

296 However, after 12 mo, children with SMA in the delayed compared with the immediate arm had a

297 ed genes were overexpressed in children with SMA relative to CM, with the highest expression in child

298 Compared with SMA, CM is associated with downregulation of Nrf2-relate

299 Ds, which are homologous to the small worms (SMA) and Drosophilia mothers against decapentaplegic (MA

300 Yet SMA is active before movements made under a range of con