ライフサイエンスコーパス: sarcomeric

1 pics include strain-sensing via titin in the sarcomeric A-band as the basis for length-dependent acti

2 t the function of UNC-89 is to help organize sarcomeric A-bands, especially M-lines.

3 ouble staining for cardiomyocytes with alpha sarcomeric actin and caspase-3 or 3-NT confirmed the car

4 In wild-type muscles, dSMN colocalizes with sarcomeric actin and forms a complex with alpha-actinin,

5 ering of myonuclei and an altered pattern of sarcomeric actin and the Z-band-associated actin crossli

6 ic proteins including alpha-actinin-2, alpha-sarcomeric actin and tropomyosin were also present.

7 onic stages due to severe disorganization of sarcomeric actin filaments in body wall muscle.

8 egans, is required for organized assembly of sarcomeric actin filaments in the body wall muscle.

9 ent of the proper length and organization of sarcomeric actin filaments.

10 Fhod potently nucleates both cytoplasmic and sarcomeric actin isoforms.

11 sh caused stunted tail formation and altered sarcomeric actin organization, which phenocopies the los

12 tterns in muscle tissue, where they regulate sarcomeric actin organization.

13 elated myopathy (DRM), results in an altered sarcomeric actin pattern, in affected myofibrillar integ

14 hat expressed cardiomyocytic proteins (alpha-sarcomeric actin) but did not have a mature cardiomyocyt

15 al microscopy showed clusters of small alpha-sarcomeric actin-positive cells expressing Ki67 in the s

16 e stress results in the glutathionylation of sarcomeric actin.

17 -localization with GATA-4, Nkx2.5, and alpha-sarcomeric actin.

18 However, it is not completely understood how sarcomeric actin/thin filaments attain their stereotyped

19 ell observations of various modes of dynamic sarcomeric addition (and how these real-time images comp

20 onfocal microscope was used to study dynamic sarcomeric addition in single neonatal CMs in a 3D cultu

21 ogical hypertrophy is the dynamic process of sarcomeric addition, and it has not been observed.

22 ession changes, additional calcium-handling, sarcomeric, adrenergic signaling, and metabolic genes we

23 entification and characterization of a novel sarcomeric AKAP (A-kinase anchoring protein), cardiac tr

24 a novel role for cTnT as a dual-specificity sarcomeric AKAP.

25 beta-synemin was soluble and interacted with sarcomeric alpha-actinin by coimmunoprecipitation, while

26 alignment of actin cytoskeleton, bundle-like sarcomeric alpha-actinin expression, higher pacing beat

27 Sarcomeric alpha-actinin was equally abundant in the EOM

28 MyHC compared with other myosin isoforms and sarcomeric alpha-actinin.

29 In addition, we have demonstrated that the sarcomeric alpha-actinins play a role in the regulation

30 Our results suggest that the disruption of sarcomeric anchoring structures and sarcolemma integrity

31 e crucial role for dystrophin in stabilizing sarcomeric anchoring structures and the sarcolemma.

32 oes not cause wholesale proteolysis of other sarcomeric and actin cytoskeletal proteins in dystrophic

33 regulation of myofiber-specific isoforms of sarcomeric and calcium regulatory proteins that couple a

34 Mutations in sarcomeric and cytoskeletal proteins are a major cause o

35 nization with loss of adult CM rod-shape and sarcomeric and intercalated disk structural disorganizat

36 myopathy (DCM) can be caused by mutations in sarcomeric and non-sarcomeric genes.

37 iated with increased human-specific nuclear, sarcomeric, and gap junction content along with inductio

38 andidate gene that modulates the contractile sarcomeric apparatus.

39 Quantitative analysis of sarcomeric architecture revealed that the change of cont

40 How proteins assemble into sarcomeric arrays to form myofibrils is controversial.

41 on, as it supports the formation of extended sarcomeric arrays, or myofibrils, within a large volume

42 iated at around E8.0 and was associated with sarcomeric assembly and rapid Ca(2+) transients, underpi

43 We show that sarcomeric assembly is blocked at an early stage in fro

44 lignment and enhances myofibrillogenesis and sarcomeric banding.

45 Phosphorylation of sarcomeric cardiac RLC and cytoplasmic nonmuscle RLC inc

46 XD1 localizes to the nucleus and to striated sarcomeric compartments.

47 n 1 (Ankrd1), a transcriptional cofactor and sarcomeric component, is strongly elevated by wounding a

48 e images obtained from fluorescently labeled sarcomeric components do not contain such illusory struc

49 ntext by other modules of the protein and/or sarcomeric components for its proper functioning.

50 Overall, ACTN3 influences sarcomeric composition in a dose-dependent fashion in mo

51 nical cardiomyopathies with abnormalities in sarcomeric contractile and biochemical parameters.

52 These genes seem generally to encode sarcomeric (contractile apparatus) or cytoskeletal prote

53 iomyopathy generally encode cytoskeletal and sarcomeric (contractile apparatus) proteins, although di

54 y-two genotyped individuals in families with sarcomeric DCM underwent clinical evaluation including s

55 type of AF due to a primary, atrial-specific sarcomeric defect.

56 le cardiomyocyte level, we demonstrated that sarcomeric disarray and accumulation of the physical agg

57 during diastole resulting in hypertrophy and sarcomeric disarray.

58 ine demonstrated increased susceptibility to sarcomeric disorganization (RBM20: 86 +/- 10.5% versus c

59 MEF2C, and MEF2-VP16 overexpression induced sarcomeric disorganization and focal elongation.

60 capitulate features of PYROXD1 myopathy with sarcomeric disorganization, myofibrillar aggregates, and

61 retinoblastoma protein (Rb), where Rb causes sarcomeric disorganization.

62 but by Day 7, skeletal muscles showed severe sarcomeric disruptions starting at the Z-line, along wit

63 and Ca2+ sparks could be observed spaced at sarcomeric distances throughout the entire cell, suggest

64 Because apoptosis and Ca(2+)-related sarcomeric dysfunction are molecular hallmarks of ICM in

65 lized cardiomyocytes demonstrated comparable sarcomeric dysfunction in both patient groups characteri

66 Using this segment, we estimated sarcomeric force development with a worm-like chain mode

67 hypertrophic-restrictive cardiomyopathies as sarcomeric, force generation disease; and arrhythmogenic

68 tivation of p38alpha MAPK directly depresses sarcomeric function in association with decreased phosph

69 To investigate the role of TPM1kappa in sarcomeric function, we generated transgenic mice overex

70 of PKC-dependent phosphorylation of cTnI on sarcomeric function, we measured contractile regulation

71 t activation of p38 MAPK directly influences sarcomeric function, we used transgenic mouse models wit

72 bands; most of the identified proteins were sarcomeric function-related proteins.

73 kx2.5+ cardiomyoblasts showed the absence of sarcomeric gene and the presence of cardiac transcriptio

74 found that Yin Yang 1 (YY1), a repressor of sarcomeric gene expression, is present in CPCs in vivo.

75 n ; also known as the p.K210del) and the non-sarcomeric gene mutation encoding lamin A/C (LMNAp.R331Q

76 y (DCM) is a highly heterogeneous trait with sarcomeric gene mutations predominating.

77 The presence of sarcomeric gene mutations was associated with increased

78 hies in mice associated with essentially any sarcomeric gene mutations, but also accurately predicts

79 Truncating mutations in the giant sarcomeric gene Titin are the most common type of geneti

80 To map the putative candidate sarcomeric gene, we perforbold locus-specific haplotypin

81 results in a dramatic loss of expression of sarcomeric genes and myocardial markers such as bmp4, np

82 ene-positive patients had 2 rare variants in sarcomeric genes but only in 1 case (0.4%) were both var

83 eds of mutations scattered among at least 10 sarcomeric genes confer the pathogenetic substrate for t

84 to the lack of systematic genetic studies of sarcomeric genes in an in vivo model.

85 ent of key nutrient sensing, ion channel and sarcomeric genes in cardiac ageing.

86 thy (HCM) are caused by mutations in cardiac sarcomeric genes, but environmental factors are believed

87 ve mutations have been identified in several sarcomeric genes, including the cardiac myosin binding p

88 be caused by mutations in sarcomeric and non-sarcomeric genes.

89 The patient tested negative for six other sarcomeric genes.

90 rdiomyopathy is often caused by mutations in sarcomeric genes.

91 adolinium enhancement were more extensive in sarcomeric HCM than sarcomere-negative HCM.

92 of discordant variant classifications in the Sarcomeric Human Cardiomyopathy Registry (SHaRe), a cons

93 Elucidation of the molecular genetics of sarcomeric hypertrophic cardiomyopathy and many of the p

94 H7-directed beta-MyHC protein expression and sarcomeric incorporation was observed as soon as 1 day a

95 Finally, we suggest that sarcomeric inhomogeneity, caused by asymmetric thick fil

96 f BTB-Kelch family members in maintenance of sarcomeric integrity in NM.

97 re t-tubules were absent, junctophilin 2 had sarcomeric intracellular distribution.

98 Morpholino-based knockdown of the sarcomeric isoform, actn2, leads to skeletal muscle, car

99 t cofilin-1 serves as an early developmental sarcomeric isoform.

100 ntify functional differences in vivo between sarcomeric isoforms, we employed computational and molec

101 ensitive cytoskeletal and Ca(2+)-insensitive sarcomeric isoforms.

102 ogenesis-the terminal differentiation of the sarcomeric lattice.

103 Indeed, RBM20 hiPSC-CMs exhibited increased sarcomeric length (RBM20: 1.747 +/- 0.238 microm versus

104 Reduced diastolic sarcomeric length, increased shortening, and prolonged C

105 sly interpreted as aggregates may be in part sarcomeric lesions.

106 l Ca imaging to measure CaT alternans at the sarcomeric level within individual myocytes in the intac

107 Our results show how heterogeneity at the sarcomeric level, in conjunction with the dynamics of Ca

108 , network contraction is dominated by either sarcomeric-like or buckling mechanisms.

109 The effects of sarcomere length (SL) on sarcomeric loaded shortening velocity, power output and

110 The sarcomeric localization of Smn is conserved in mouse myo

111 ons in mouse skeletal muscle revealed robust sarcomeric localization.

112 hrough sequestration of sAnk1.5/KCTD6 at the sarcomeric M-band, away from the Z-disk-associated culli

113 UNC-89 is a giant polypeptide located at the sarcomeric M-line of Caenorhabditis elegans muscle.

114 MEL-26 and UNC-89 partially colocalize at sarcomeric M-lines.

115 nd LIM-9 also bind to UNC-96, a component of sarcomeric M-lines.

116 The organization of other sarcomeric markers, including alpha-actinin, was not aff

117 ed the consequences of tafazzin knockdown on sarcomeric mitochondria and cardiac function in mice.

118 cytosolic M-CK (M-CK(-/-)) or both M-CK and sarcomeric mitochondrial CK (M-CK/ScCKmit(-/-)) isoforms

119 Hearts lacking both M-CK and sarcomeric mitochondrial CK have diminished PCr turnover

120 tal and heart muscle diseases rely on direct sarcomeric modulators, which are molecules that can dire

121 In fact, ttna is the earliest sarcomeric mRNA that is expressed in the heart, which ma

122 this study, we used mice bearing a knock-in sarcomeric mutation, which is exhibited in human hypertr

123 Current paradigms propose that sarcomeric mutations associated with DCM decrease the my

124 the cardiac sarcomere, the pathways by which sarcomeric mutations engender myocyte hypertrophy and el

125 effects of three DCM-causing mutations: the sarcomeric mutations in genes encoding cardiac troponin

126 nderlying mechanisms of SCD in patients with sarcomeric mutations will also allow us to design new an

127 han being a direct consequence of the causal sarcomeric mutations.

128 sis on hypertrophic cardiomyopathy caused by sarcomeric mutations.

129 pe of cardiomyopathy, but many patients lack sarcomeric/myofilament mutations.

130 ssed in striated muscle and brain, encodes a sarcomeric myosin and the intronic microRNA miR-499.

131 The sarcomeric myosin gene, Myh7b, encodes an intronic micro

132 network at the perimembrane region, whereas sarcomeric myosin is independently assembled into thick

133 In muscle, the assembly of sarcomeric myosin is regulated to produce stable, unifor

134 accounted for approximately 18% of the total sarcomeric myosin, the amplitude of sarcomere-length sho

135 The rod of sarcomeric myosins directs thick filament assembly and i

136 The sarcomeric network also provides a well-defined target t

137 Thus, preventing sarcomeric OGT and OGA displacement represents a new pos

138 of VOIs and whether mutations are present in sarcomeric or nonsarcomeric genes.

139 me iPSCs are larger, have a higher degree of sarcomeric organization and preferential localization of

140 is time correlate with a progressive loss of sarcomeric organization and suggest that the unaffected

141 r maintenance of cardiomyocyte structure and sarcomeric organization and that cell-autonomous loss of

142 e structural information suggesting periodic sarcomeric organization similar to striated muscle.

143 expression of mature cardiomyocyte markers, sarcomeric organization, and exhibition of spontaneous c

144 reveals that cholesterol depletion abrogates sarcomeric organization, changing spacing and alignment

145 ne ablation is accompanied by dissolution of sarcomeric organization, disruption of the intercalated

146 (+) cells expressed cardiac myocyte markers, sarcomeric organization, excitation-contraction coupling

147 es induced a loss of actin and alpha-actinin sarcomeric organization, whereas CHC depletion in vivo i

148 This mechanism is not based on an ordered sarcomeric organization.

149 (NES)-fused form of Rb caused disruption of sarcomeric organization.

150 mechanism of TNF-alpha-induced disruption of sarcomeric organization.

151 upted cell-cell junctions, with no effect on sarcomeric organization.

152 eir skeletal muscle, indicative of disrupted sarcomeric organization.

153 ed cardiomyocytes revealed indistinguishable sarcomeric organizations.

154 lysis of immunolabelled lysosomes suggests a sarcomeric pattern (dominant wavelength 1.80 mum).

155 yocardin; cardiac proteins 24 h later; and a sarcomeric pattern 4-6 days later.

156 elop an in vivo-like morphology with regular sarcomeric patterns.

157 c attenuation of cheerio leads to CryAB-like sarcomeric phenotypes.

158 We studied if changes in sarcomeric properties in HCM depend on the underlying pr

159 Small molecules binding to the mutant sarcomeric protein complex should be able to mitigate th

160 n, triggers changes in energy metabolism and sarcomeric protein composition, loss of cardiomyocytes,

161 Encoded MYPN is a sarcomeric protein exclusively localized in striated mus

162 ated muscle Activator of Rho Signaling) is a sarcomeric protein expressed early in cardiac developmen

163 Titin, a sarcomeric protein expressed primarily in striated muscl

164 generate beating PM cells due to inadequate sarcomeric protein expression and organization.

165 We assessed sarcomeric protein expression and phosphorylation and co

166 Embryos that lack Tm2 also showed reduced sarcomeric protein expression, and embryos that expresse

167 We, therefore, assessed sarcomeric protein expression, modification, titin isofo

168 lly separable events: myotube elongation and sarcomeric protein expression.

169 tic due to defects in myotube elongation and sarcomeric protein expression.

170 and proteomic approaches, we identified the sarcomeric protein filamin C (FLNc) as a binding partner

171 Previously, we showed that SMN is a sarcomeric protein in flies and mice.

172 Titin is the first sarcomeric protein linked to arrhythmogenic cardiomyopat

173 Sarcomeric protein missense mutations known to cause oth

174 reviously unavailable tool to study specific sarcomeric protein mutations in an intact mammalian musc

175 KCepsilon (PKCepsilon TG) displayed enhanced sarcomeric protein phosphorylation and dilated cardiomyo

176 gth-dependent activation, cooperativity, and sarcomeric protein phosphorylation status.

177 diac myosin-binding protein C (cMyBP-C) is a sarcomeric protein that dynamically regulates thick-fila

178 Nebulin is a giant modular sarcomeric protein that has been proposed to play critic

179 Nebulin is a sarcomeric protein that when absent (NEB KO mouse) or pr

180 The sarcomeric protein titin is a molecular spring responsib

181 Truncating mutations in the giant sarcomeric protein Titin result in dilated cardiomyopath

182 as exemplified by the isoform switch of the sarcomeric protein titin, which adjusts ventricular fill

183 nt regulator of sarcomeric stiffening is the sarcomeric protein titin.

184 ein complex containing Smyd2, Hsp90, and the sarcomeric protein titin.

185 d surprising developmental functions for the sarcomeric protein Tropomyosin 2 (Tm2).

186 we show that MEL-26 interacts with the giant sarcomeric protein UNC-89 (obscurin).

187 CM from patients with a mutation in TNNT2, a sarcomeric protein.

188 cardiomyopathy (HCM) is a disease of mutant sarcomeric proteins (except for phenocopy).

189 is a genetic disorder caused by mutations in sarcomeric proteins (excluding phenocopy).

190 hich are molecules that can directly bind to sarcomeric proteins and either inhibit or enhance their

191 netic disorder caused mainly by mutations in sarcomeric proteins and is characterized by maladaptive

192 iants in more than 30 genes, mostly encoding sarcomeric proteins and proteins of the cytoskeleton, ha

193 in ligases for the UPS-dependent turnover of sarcomeric proteins and reveal a potential basis for myo

194 eads to the downregulation of genes encoding sarcomeric proteins and upregulation of hsp90a and sever

195 ence microscopy shows that a number of known sarcomeric proteins are abnormal, but the most dramatic

196 Point mutations in genes encoding sarcomeric proteins are the leading cause of inherited p

197 Increased acetylation of sarcomeric proteins by HDAC inhibition (using class I an

198 Mutations in genes coding for sarcomeric proteins cause hypertrophic cardiomyopathy.

199 rent mutations in genes encoding a few dozen sarcomeric proteins cause two reciprocal human disease p

200 function requires a precise stoichiometry of sarcomeric proteins for proper assembly of the contracti

201 To potentially relate the genes encoding the sarcomeric proteins functionally, a hierarchical cluster

202 PKA-dependent phosphorylation of cardiac sarcomeric proteins has been the subject of intense inve

203 shing number of mutations affecting numerous sarcomeric proteins have been described.

204 ctional relationships and the roles of those sarcomeric proteins in animal behaviors remain unclear.

205 , the complex localization of SALS and other sarcomeric proteins in myofibrils reveals that the full

206 Increased amounts of other sarcomeric proteins including alpha-actinin-2, alpha-sar

207 rdiomyopathy (FHC) is caused by mutations in sarcomeric proteins including the myosin regulatory ligh

208 by single-point mutations in genes encoding sarcomeric proteins including ventricular myosin regulat

209 Myofibrillogenesis, the precise assembly of sarcomeric proteins into the highly organized sarcomeres

210 posed for MyBPC, its interactions with other sarcomeric proteins remain obscure.

211 genes encoding lineage-specific isoforms of sarcomeric proteins such as MyHC and troponin.

212 d mechanism controlling its interaction with sarcomeric proteins such as titin, lays a foundation for

213 parallel with cardiomyocytes expressing more sarcomeric proteins that increase the contractile stress

214 Finally, the phosphorylation level of sarcomeric proteins was reduced in PAH patients, which w

215 al abnormalities occur related to changes in sarcomeric proteins, abnormal calcium handling, and fibr

216 diac function in vivo, reduced expression of sarcomeric proteins, and increased tissue damage associa

217 disruption of expression and localisation of sarcomeric proteins, gross myofibril disarray and growth

218 In addition, a majority of sarcomeric proteins, including Myosin Heavy Chain (MHC)

219 CM) results from mutations in genes encoding sarcomeric proteins, most often MYBPC3, which encodes ca

220 the proteasome-dependent degradation of key sarcomeric proteins, such as alpha-actinin and filamin C

221 rdiomyopathy (HCM) is caused by mutations in sarcomeric proteins, the commonest being MYBPC3 encoding

222 in HCM caused by mutations in genes encoding sarcomeric proteins, which account for most of HCM cases

223 onse to familial mutations in genes encoding sarcomeric proteins, which are responsible for contracti

224 hondrial proteins, metabolic regulators, and sarcomeric proteins, with 80% of them also modified in w

225 f which are caused by mutations in genes for sarcomeric proteins.

226 ve mutations have been identified in various sarcomeric proteins.

227 trophy, frequently is caused by mutations in sarcomeric proteins.

228 is involved in degradation of old or damaged sarcomeric proteins.

229 hat is associated with reduced levels of all sarcomeric proteins.

230 er folding and assembly of newly synthesized sarcomeric proteins.

231 and hypertrophy and represses expression of sarcomeric proteins.

232 in mitochondrial, cytoskeletal, Z-line, and sarcomeric proteins.

233 horylation affected phosphorylation of other sarcomeric proteins.

234 DNA binding by GATA-4 and restored critical sarcomeric proteins.

235 ffecting paramyosin's interaction with other sarcomeric proteins.

236 ll affect its ability to interact with other sarcomeric proteins.

237 opathies are mutations in the genes encoding sarcomeric proteins.

238 e, by restoring the expression of additional sarcomeric RNAs, and by promoting myoblast fusion.

239 main, appears to be a critical aspect of its sarcomeric roles.

240 Furthermore, the polarization dependence of sarcomeric SHG is not affected by either the proportion

241 elocity of contraction (by motility assay or sarcomeric shortening) at different actin concentrations

242 thematical models to represent a subcellular sarcomeric space in a cardiac myocyte with varying detai

243 ters to reconstruct an in silico subcellular sarcomeric space with spatially distinct cAMP production

244 ty of the spatio-temporal characteristics of sarcomeric sparks and ultrastructural characteristics of

245 An important regulator of sarcomeric stiffening is the sarcomeric protein titin.

246 wo thick filament protein domains on passive sarcomeric stiffness, and to investigate their correlati

247 en attributed to truncating mutations in the sarcomeric structural protein titin (TTNtv).

248 Affected muscles have normal sarcomeric structure at the electron microscopy level bu

249 n minor disruption to indirect flight muscle sarcomeric structure compared with a transgenic control.

250 tical role for nebulin in the maintenance of sarcomeric structure in skeletal muscle.

251 All iPSC-CMs exhibited a reliable sarcomeric structure stained with antibodies against car

252 The sarcomeric structure was intact at birth, but by Day 7,

253 e when evaluated in terms of cell viability, sarcomeric structure, action potentials and conduction v

254 ebrafish, mutant MYL4 leads to disruption of sarcomeric structure, atrial enlargement and electrical

255 lture for 120 days to demonstrate definitive sarcomeric structure, cell and matrix deformation, contr

256 e have smaller muscle fibers, a disorganized sarcomeric structure, increased extracellular matrix, an

257 inclusion of MCs facilitated more mature CM sarcomeric structure, preferential alignment, and activa

258 -tropomyosin polymerization and with overall sarcomeric structure.

259 tural analysis was performed to evaluate EOM sarcomeric structure.

260 h an accelerated and severe fragmentation of sarcomeric structures compared with overexpression of wi

261 sarcolemmas were visualized, although normal sarcomeric structures were maintained.

262 )1.3 colocalized with ryanodine receptors in sarcomeric structures while Ca(v)1.2 was largely restric

263 into host myocardium and generated organized sarcomeric structures, and endothelial and smooth muscle

264 rin and obscurin-like-1 (Obsl1)-in different sarcomeric subregions.

265 shown that PKD also phosphorylates multiple sarcomeric substrates to regulate myofilament function.

266 onsist of the molecular motor myosin II, the sarcomeric template protein, titin, and the cardiac modu

267 models that permit the systematic tuning of sarcomeric tension generation and calcium fluxing, we id

268 e first mouse model in which a mutation in a sarcomeric thin filament protein, specifically TM, leads

269 ive NM genes, all encoding components of the sarcomeric thin filament, are known.

270 -tropomyosin gene encodes a component of the sarcomeric thin filament.

271 NM is thought to be a disease of sarcomeric thin filaments as six of eight known genes wh

272 These results indicate that sarcomeric thin filaments can accommodate substantial in

273 Absence of components of the sarcomeric thin filaments causes nemaline myopathy, a le

274 t LMOD3 is essential for the organization of sarcomeric thin filaments in skeletal muscle.

275 ric incorporation of gamma-(cyto) actin into sarcomeric thin filaments.

276 Thus, Tmod1 per se, rather than total sarcomeric Tmod levels, controls thin filament lengths i

277 muscle types, but the relative abundances of sarcomeric Tmods are muscle specific.

278 escribe the abrupt and marked evolution of a sarcomeric to infiltrative cardiomyopathy, leading to an

279 The sarcomeric tropomodulin (Tmod) isoforms Tmod1 and Tmod4

280 Here we identify the two sarcomeric tropomodulin (Tmod) isoforms, Tmod1 and Tmod4

281 for RBM20-dependent splice variants affected sarcomeric (TTN and LDB3) and calcium (Ca(2+)) handling

282 loss of myofibril organization and defective sarcomeric ultrastructure.

283 bations in the myosin rod can disturb normal sarcomeric uniformity and, like motor domain lesions, wo

284 nin to form a continuous belt of muscle-like sarcomeric units ( approximately 400-600 nm) around each

285 +/- 0.194 microm; P < 0.0001) and decreased sarcomeric width (RBM20: 0.791 +/- 0.609 microm versus c

286 dial dysfunctions with disintegration of the sarcomeric Z disk.

287 -infected mandarin fish develop disorganized sarcomeric Z disks in cardiomyocytes.

288 ted mandarin fish develop similar disordered sarcomeric Z disks in cardiomyocytes.

289 Of note, the sarcomeric z-disc also represents a nodal point in cardi

290 onserved, as the Tcap protein appears in the sarcomeric Z-disc and reduction of Tcap resulted in musc

291 ats, and SPRY domains and interacts with the sarcomeric Z-disc protein, alpha-actinin-2.

292 n-binding protein Xin and interacts with the sarcomeric Z-disc protein, alpha-actinin-2.

293 both proteins localized predominantly to the sarcomeric Z-disc, where they partially replaced endogen

294 as murine heart tissue located Fbxl22 to the sarcomeric z-disc.

295 he entire mouse Smn complex localizes to the sarcomeric Z-disc.

296 ical analysis of the heart revealed aberrant sarcomeric Z-disk and M-band structures, and misalignmen

297 plays a crucial role in maintaining cardiac sarcomeric Z-disks and endothelial/endocardial cell inte

298 roles of Tln1 in the maintenance of cardiac sarcomeric Z-disks and endothelial/endocardial cell inte

299 P is a cytoskeletal protein localized in the sarcomeric Z-line.

300 on of constructs such as actin filaments and sarcomeric Z-lines.