ライフサイエンスコーパス: desmin

1 cular endothelial growth factor receptor and desmin).

2 capacities for nebulin relative to wild-type desmin.

3 ocated within the nebulin-binding regions of desmin.

4 us status in living cells lacking endogenous desmin.

5 acts with the type III intermediate filament desmin.

6 sgenic overexpression of a DRC-linked mutant desmin.

7 ricular myocytes (NRVMs) expressing a mutant desmin.

8 myosin heavy chain, smooth muscle actin, and desmin.

9 lations and was significantly larger without desmin.

10 eloped to investigate the mechanical role of desmin.

11 d laterally by elastic elements representing desmin.

12 otein, or alphaB-crystallin, a chaperone for desmin.

13 lteration of the pericyte structural protein desmin.

14 (CK14) and DeltaN-p63 and another expressing desmin.

15 , tropomyosin, myosin-binding protein C, and desmin.

16 s in transfected cells expressing the mutant desmin.

17 which did not contain detectable amounts of desmin.

18 , expressing E-cadherin, cytokeratin 18, and desmin.

19 sion levels of podocyte markers, podocin and desmin.

20 of CD31, vascular endothelial cadherin, and desmin.

21 s of nesprin 1, desmin or both nesprin 1 and desmin.

22 rophils, decreased, and fewer HSCs expressed desmin.

23 s, Mip-1a and alphaB-crystallin; the mRNA of desmin, a regeneration-associated molecule, increased.

24 disease caused by dysfunctional mutations in desmin, a type III intermediate filament protein, or alp

25 We focus here on desmin, a type III intermediate filament, which is speci

26 )-mediated DRM is characterized by CryAB and desmin accumulations within cardiac muscle, mitochondria

27 asts induces desmin network disorganization, desmin aggregate formation, and a small decrease in the

28 ss that are characterized by the presence of desmin aggregates and a disorganization of sarcomeres.

29 min aggregates were located, indicating that desmin aggregates are rigid.

30 d some other membrane proteins, as well, and desmin aggregates in transfected cells expressing the mu

31 at higher Young's moduli were measured where desmin aggregates were located, indicating that desmin a

32 This variant produces desmin aggregates, the main pathological symptom of myof

33 ajor interaction site has been mapped to the desmin alpha-helical rod domain, indicating that the fil

34 derate accumulations together with myotilin, desmin alphaB-crystallin and alpha-actinin.

35 taining protein and filamin C, as well as in desmin, alphaB-crystallin and myotilin, result in simila

36 The identified disease proteins (desmin, alphaB-crystallin, myotilin, Zasp, filamin C, an

37 Our data suggest that mutated desmin already markedly impedes myocyte structure and fu

38 onstrate that expression of the E413K mutant desmin also alters the traction forces generation of sin

39 We demonstrate that mutant desmin alters myofibrillar cytoarchitecture, markedly di

40 oteins involved with cytoskeletal structure (desmin and alpha actinin-2 both decreased), chaperone fu

41 zed by changes in gene expression, including desmin and alpha-smooth muscle actin, matrix proteases a

42 ZASP or filamin C, besides previously known desmin and alphaB-crystallin.

43 type IV IF protein that forms filaments with desmin and also binds alpha-actinin and vinculin.

44 Overall, our data provide a new link between desmin and Ankrd1 regulation, which may be important for

45 y characterized by cytoplasmic aggregates of desmin and associated proteins at the cellular level.

46 245D mutant in myocytes displaces endogenous desmin and C-terminal nebulin from the Z-discs with a co

47 logenesis with disruption of alpha-actinin2, desmin and cardiac ankyrin repeat protein (CARP) was evi

48 ased the expression of podocin but increased desmin and ceramide levels in glomeruli from Asm(+/+) mi

49 le fluorescent proteins genetically fused to desmin and characterized the heterozygous status in livi

50 ve investigated the impact of overexpressing desmin and expressing a mutant desmin on the passive and

51 ified using dual immunofluorescence (IF) for desmin and GFAP.

52 ression of the intermediate filament protein desmin and interstitial matrix components fibronectin an

53 rim32 down-regulation attenuated the loss of desmin and myofibrillar proteins and reduced atrophy.

54 ted with mutations in titin, dysferlin, GNE, desmin and myosin.

55 etal liver mesenchymal cells expressing both desmin and p75 neurotrophin receptor (p75NTR): HSCs in t

56 ical cells, which also express collagen 1a1, desmin and platelet-derived growth factor (alpha polypep

57 rkers CD45 and F4/80 or the pericyte markers desmin and smooth muscle actin.

58 abnormalities in staining patterns for both desmin and SPEG.

59 thin the coil IB (nebulin-binding) region of desmin and that has been reported to cause human cardiom

60 ing Trim32 levels prevented the loss of both desmin and thin filament proteins.

61 ulin binding has on the assembly kinetics of desmin and three desminopathy-causing mutant desmin vari

62 persisted whereas cytoskeletal proteins (eg, desmin and vimentin) normalized.

63 o a reduction in the foot-process fusion and desmin, and a recovery of synaptopodin and podocin.

64 muscle gene promoters (Skeletal alpha-actin, Desmin, and alpha-Myosin heavy chain) in skeletal and ca

65 myosin heavy chain, smooth muscle actin, and desmin, and increased markers of dedifferentiation, cell

66 In addition, desmin, and intercalar disc-related proteins expression

67 muscle differentiation including pRB, MyoD, desmin, and M-cadherin; up-regulated Myf5; but no change

68 AE1/AE3, alpha actin, desmin, and myosin antibodies confirmed the presence of

69 myosin heavy chain, smooth muscle actin, and desmin, and negatively with cellular retinol-binding pro

70 ule, intercellular adhesion molecule, CD105, desmin, and neural growth proteoglycan 2 was similar bet

71 nce of three mesenchymal markers - vimentin, desmin, and PDGFbeta receptor, which indicates their mes

72 ti-collagen IV, rat anti-ICAM-2, rabbit anti-desmin, and rat anti-MECA 32; and intravital injection o

73 er (CD133) and mural cell markers (calponin, desmin, and smooth muscle alpha actin), suggesting dedif

74 ltures developed the expression of runx2 and desmin, and the cocultures that were stimulated with EMD

75 Expression of nephrin, podocin, desmin, and transient receptor potential channel C6 in t

76 enchymal markers including alpha-SMA, FSP-1, desmin, and vimentin.

77 yofibroblast markers, including alphaSMA and desmin, and were not myofibroblast precursors in injured

78 , which is characterized by the formation of desmin- and CryAB-containing aggregates within muscle fi

79 composed almost entirely of rhabdomyoblasts (desmin- and myogenin-positive) was discovered along with

80 conditions in which both healthy and mutant desmin are expressed at equimolar levels mimicking an in

81 In skeletal muscle, nesprin 1 and desmin are thought to link the nucleus to the cytoskelet

82 Although some misfolded proteins, such as desmin, are associated with mutations in the genes encod

83 ecessary for ASMC homeostasis and identifies desmin as a novel regulator of microRNA.

84 erall, our data demonstrate a novel role for desmin as an anti-hypertrophic protein necessary for ASM

85 sions, and identified through bioinformatics desmin as their major constituent.

86 Detyrosinated MTs associated with desmin at force-generating sarcomeres.

87 We show that the coil IB region of desmin binds to C-terminal nebulin (modules 160-164) wit

88 epatic stellate cells consistently expressed desmin but never elastin.

89 ar interface and in the parenchyma coexpress desmin but not alpha-SMA, i.e., they are not resident my

90 in synthesis of structural components (e.g., desmin) but maintenance of normal function; stage 4, "de

91 tenderisation protein markers troponin T and desmin by the four proteases was detected by western blo

92 el of alpha smooth muscle actin (alpha-SMA), desmin, calponin, and smoothelin in SMhAFSCs when compar

93 pulations and that staining with elastin and desmin can differentiate between them.

94 rupted the fine intracytoplasmic staining of desmin, causing clumping of the desmin protein.

95 dered specific for activated stellate cells (desmin, collagen I-a2, Mmp2, Mmp14) and myofibroblasts (

96 fixed-end stress increased as a function of desmin concentration and this relationship was influence

97 utation (Val459Ile) showed milder effects on desmin cytoplasmic network formation and appears to be a

98 ular and functional relationship between the desmin cytoskeleton and nebulette-containing sarcomeres

99 rapid muscle atrophy induced by fasting, the desmin cytoskeleton and the attached Z-band-bound thin f

100 enhances Trim32-mediated degradation of the desmin cytoskeleton, which appears to facilitate the bre

101 TNF-alpha in a genetic heart failure model, desmin-deficient mice.

102 Western blots indicated that postmortem desmin degradation was more rapid in GG than in DG sampl

103 al muscle disease caused by mutations in the desmin (DES) gene.

104 Desmin (DES) mutations cause severe skeletal and cardiac

105 rcalated discs, with disturbed expression of desmin, desmoplakin, connexin43 and vinculin being evide

106 ism probably corresponds to an alteration in desmin dimer and oligomer assembly and its connection wi

107 ed mice demonstrated increased apoptosis and desmin disruption, which was attenuated in the sildenafi

108 Desmin distribution was determined via immunofluorescenc

109 s, whereas the expression of a mutated E413K desmin does not.

110 Herein, we have created the nesprin-desmin double-knockout (DKO) mouse, eliminating a major

111 We demonstrate that desmin down-regulation by WFA via targeting the conserve

112 Collectively, these data suggest that the desmin E245D mutation interferes with the ability of neb

113 ignificantly delayed dynamics for the mutant desmin E245D relative to wild-type desmin in fluorescenc

114 ikingly perturbed in myocytes expressing the desmin-E245D mutant because most sarcomeres contained el

115 Expression of the desmin-E245D mutant in myocytes displaces endogenous des

116 cells transdifferentiated into NG2/PDGFRbeta/desmin-expressing cerebrovascular pericytes, enwrapping

117 t-related transcription factor 2 (runx2) and desmin expression by real-time polymerase chain reaction

118 thmatic patients show a negative correlation desmin expression in airway smooth muscle cell (ASMC) an

119 alization pattern for nebulette and impaired desmin expression were noted in the proband and chimeric

120 kidneys showed de novo cyclin D1, Ki-67, and desmin expression with loss of synaptopodin and WT-1 exp

121 SMCs, which stably suppresses 90% endogenous desmin expression.

122 on of p63, and low to undetectable levels of desmin expression.

123 runx2 and desmin expressions were increased in stimulated cocultur

124 ula occludens-1, mesenchymal markers such as desmin, fibroblast-specific protein-1, and matrix metall

125 scle cells, vascular smooth muscle cells and desmin(+) fibroblasts by lineage tagging.

126 duced alpha-smooth muscle actin (alpha-SMA), desmin, fibronectin, and collagen I expression, suggesti

127 of this disease, it is essential to analyze desmin filament structures under conditions in which bot

128 desmin polymerization induced disassembly of desmin filaments and destruction of thin filament compon

129 process involving the initial disassembly of desmin filaments by Trim32, which leads to the later myo

130 er denervation, inducing the dissociation of desmin filaments caused an accumulation of ubiquitinated

131 ation and Trim32-dependent ubiquitination of desmin filaments increased rapidly and stimulated their

132 lette extends outward from Z-disk-associated desmin filaments toward the center of the sarcomere.

133 Although myofibrils and desmin filaments were intact at 7 d after denervation, i

134 Desmin filaments were proposed to maintain the integrity

135 enervation required not only dissociation of desmin filaments, but also gene induction by PAX4.

136 accompanied by increased phosphorylation of desmin filaments, which promoted desmin ubiquitylation b

137 s influenced by the cellular location of the desmin filaments.

138 y to cardiac malfunction or to disruption of desmin filaments.

139 y in vitro interaction between nebulette and desmin filaments.

140 Unusual accumulations of desmin found in the cardiac muscle of the propositus pro

141 l-specific LCR, which is linked to the human desmin gene (DES).

142 ytes is evident since mutations in the human desmin gene cause severe myopathies and cardiomyopathies

143 In cultured human podocytes, CB1R and desmin gene expression were increased and podocin and ne

144 nterfering (si)RNA-mediated knockdown of the desmin gene in HASMCs, recombinant HASMCs (reHASMCs), up

145 of the propositus prompted us to examine the desmin gene in this patient, and in so doing, we identif

146 This mutation in the desmin gene is one of those leading to desminopathies, a

147 plice donor site mutation (IVS3+3A>G) of the desmin gene located on chromosome 2q35.

148 that proteasomal malfunction observed in MT-desmin hearts is not secondary to cardiac malfunction or

149 othelial cells, stimulating proliferation of desmin(+) hepatic stellate-like cells and enforcing a pr

150 ate that by interacting with desmoplakin and desmin, iASPP is an important regulator of desmosomal fu

151 Our study demonstrates that linkage to desmin IF networks via plectin is crucial for formation

152 ly for diseases, the related muscle-specific desmin IF networks.

153 hat beta-synemin mediates the association of desmin IFs with Z disks, whereas alpha-synemin stabilize

154 We show that the expression of this mutant desmin in C2C12 myoblasts induces desmin network disorga

155 iASPP interacts with desmoplakin and desmin in cardiomyocytes to maintain the integrity of de

156 This dissociates a direct role for desmin in corneal cell proliferation.

157 he mutant desmin E245D relative to wild-type desmin in fluorescence recovery after photobleaching in

158 Moreover, loss of desmin in HASMCs increases the phosphorylation of Akt, i

159 ession of either MyoD or, more surprisingly, desmin in Lmna(-/-) myoblasts resulted in increased diff

160 , significantly attenuated the expression of desmin in pericytes.

161 muscle had myofibrillar disorganization and desmin inclusions.

162 st show that the overexpression of wild-type-desmin increases the overall rigidity of the cells, wher

163 pression of nephrin, synaptopodin, WT-1, and desmin, indicating that PI3KC2alpha deficiency specifica

164 or NF-kappaB inhibitor inhibits the loss of desmin-induced Ankrd1 up-regulation, suggesting Akt/NF-k

165 hese mice also displayed interruption of DSP-desmin interaction at intercalated discs (IDs) and marke

166 Desmin interacts with nebulin establishing a direct link

167 ion in cardiomyocytes of the extrasarcomeric desmin intermediate filament system is frequently observ

168 Desmin intermediate filaments (DIFs) form an intricate m

169 ells to reach high indentation depths, where desmin intermediate filaments are typically located.

170 Our findings reveal a novel role for desmin intermediate filaments in modulating actin filame

171 In striated muscle, desmin intermediate filaments interlink the contractile

172 ssing a mutant form of the gene encoding for desmin intermediate filaments, p.D399Y.

173 Desmin is an intermediate filament protein in skeletal m

174 Our earlier study showed that desmin is an intracellular load-bearing protein that inf

175 We previously showed that desmin is an intracellular load-bearing protein, which i

176 Thus, during atrophy, the initial loss of desmin is critical for the subsequent myofibril destruct

177 The intermediate filament protein desmin is encoded by the gene DES and contributes to the

178 ylation of the intermediate filament protein desmin is significantly increased (5.7-fold, p < 0.005)

179 ated from young hetero- and homozygous R349P desmin knock-in mice, which carry the orthologue of the

180 ly subjected immortalized heterozygous R349P desmin knock-in myoblasts to magnetic tweezer experiment

181 ese cables (but not their size) increases in desmin knockout muscle (a fibrosis model).

182 on shared poor growth in culture and lack of desmin labelling, we believe that PTP dysregulation may

183 ired myogenesis is linked to reduced MyoD or desmin levels, these proteins were individually expresse

184 1B (lamin A/C), LGMD1C (caveolin-3), LGMD1D (desmin), LGMD1E (DNAJB6), and more recently for LGMD1F (

185 coding for the intermediate filament protein desmin may cause skeletal and cardiac myopathies, which

186 These results suggest that desmin may play an important role in ASMC homeostasis.

187 These results suggest that Ankrd1 and desmin may play important roles on ASMC homeostasis.

188 compared with wild-type, nesprin 1(-/-) and desmin(-/-) mice.

189 ry the orthologue of the most frequent human desmin missense mutation R350P.

190 a-acetylcholine (ACh) receptor (alpha-AChR), desmin, muscle creatine kinase (MCK), myosin heavy chain

191 nravel short distance structural patterns of desmin mutants in filaments.

192 e demonstrated filament formation defects of desmin mutants, associated with arrhythmogenic right ven

193 a, we suggest that for some filament-forming desmin mutants, the molecular etiology of desminopathy r

194 Here we show that desmin-mutated cells display a 39% increased median elas

195 Desmin-mutated cells required higher forces than wild-ty

196 N5A polymorphisms were identified in 2 and a desmin mutation in 1.

197 Here, we examined a desmin mutation, E245D, that is located within the coil

198 is patient, and in so doing, we identified a desmin mutation, in addition to the LMNA mutation in the

199 the structural effects of five heterozygous desmin mutations on filament formation in vitro and in l

200 of expression of certain disease-associated desmin mutations.

201 yte nuclear factor 4alpha(+) hepatocytes and desmin(+) myofibroblasts surrounding reactive ducts in D

202 ns showed the tumor cells to be positive for desmin, myogenin, and myogenic differentiation 1 (MyoD1)

203 Mutations in alphaB-crystallin, desmin, myotilin, Zasp, or filamin-C can cause MFMs and

204 ctin positive, weakly calponin positive, and desmin negative.

205 ac myocytes, and the effects on cytoskeletal desmin network architecture were analyzed with confocal

206 his mutant desmin in C2C12 myoblasts induces desmin network disorganization, desmin aggregate formati

207 he lack of severe disruption of cytoskeletal desmin network formation seen with mutations in the 1A a

208 Our data suggest that a well-organized desmin network is required to accommodate an optimal con

209 The desmin network's pivotal role in myocytes is evident sin

210 uggests that dysfunction of seemingly intact desmin networks is sufficient to cause DCM.

211 of mature pericytes and immunoreactivity for desmin, NG-2, platelet-derived growth factor receptor be

212 ere misalignment and stress in wild-type and desmin null fibers.

213 Here, we report that ASMCs of desmin null mice (ASMCs(Des-/-)) show hypertrophy and up

214 During fixed-end contraction, desmin null simulations also demonstrated greater sarcom

215 arly with fiber strain in both wild-type and desmin null simulations and was significantly larger wit

216 verexpressing desmin and expressing a mutant desmin on the passive and active mechanical properties o

217 stained positive for smooth muscle actin and desmin; on typical epidermal grafts, abundant melanocyte

218 ed in the periportal region do not coexpress desmin or alpha smooth muscle actin (alpha-SMA).

219 global ablation murine models of nesprin 1, desmin or both nesprin 1 and desmin.

220 s by transgenic overexpression of the mutant desmin or CryAB(R120G) both in intact mice and in vitro.

221 ilaments, and Dys-ABD did not associate with desmin or K8/K18 filaments.

222 ytes, identified by PDGF receptor beta, NG2, desmin, or alpha-smooth muscle actin immunoreactivity, i

223 on of EMT markers alpha-smooth muscle actin, desmin, or FSP-1.

224 KIT expression without expression of actin, desmin, or S-100.

225 SPEG localizes in a double line, flanking desmin over the Z lines, and is apparently in alignment

226 orneal opacity, we identify a novel role for desmin overexpression in corneal haze.

227 the ability of a comparable level of mutant desmin overexpression to accumulate ubiquitinated protei

228 Presumably, the loss of the desmin-p.

229 The in vitro experiments of desmin-p.A120D reveal a severe intrinsic filament format

230 The functional experiments of desmin-p.H326R did not demonstrate any differences from

231 immature fibers including M-Cadherin, MyoD, desmin, Pax7 and Myf6 were elevated by western-blot anal

232 CD34, Ano1, NTPDase2, connexin 43, vimentin, desmin, PDGFbeta receptor and merlin/NF2.

233 and CD31(+) endothelial cells or LacZ(+) and desmin(+) pericytes confirmed that chimeric mice transpl

234 zed with either CD31(+) endothelial cells or desmin(+) pericytes.

235 d with disrupted co-localization of ECs with desmin(+) perivascular cells, and reduction of blood flo

236 Thus, during fasting, desmin phosphorylation increases and enhances Trim32-med

237 rthermore, overexpression of an inhibitor of desmin polymerization induced disassembly of desmin fila

238 n glomerular development as stromal-derived, desmin-positive cells fail to coalesce near forming neph

239 there was a significant decrease in GFAP and desmin-positive cells, compared to WT mice ( approximate

240 alized nuclei, myofibrillar disorganization, desmin-positive inclusions, and thickened Z-bands.

241 ution, mGFP expression was observed again in desmin-positive peri-sinusoidal HSCs; no mGFP expression

242 EBS-MD myofibers, including the presence of desmin-positive protein aggregates and a concurrent disa

243 ctin in skeletal muscle display pathological desmin-positive protein aggregation and misalignment of

244 phic rhabdomyosarcomas (MyoD-, Myogenin- and Desmin-positive), whereas introduction of the same oncog

245 imulations with only a fraction of wild-type desmin present, fixed-end stress increased as a function

246 staining of desmin, causing clumping of the desmin protein.

247 a drug or by expression of dominant-negative desmin reduces type I collagen expression, primarily due

248 with high affinity, whereas binding of this desmin region containing the E245D mutation appears to e

249 einaceous deposits are characteristic of the desmin-related cardiomyopathies and crystallin cardiomyo

250 erapeutic efficacy of doxycycline (Doxy) for desmin-related cardiomyopathy (DRC) and to elucidate the

251 expression or voluntary exercise ameliorated desmin-related cardiomyopathy (DRC).

252 allin (CryAB) gene triggers a severe form of desmin-related cardiomyopathy (DRCM) characterized by ac

253 art-failure patients and in animal models of desmin-related cardiomyopathy (DRM).

254 lation of the mutant protein associated with desmin-related cardiomyopathy in cultured cardiomyocytes

255 Desmin-related cardiomyopathy is characterized by the fo

256 ryAB (alphaB-crystallin) causative for human desmin-related cardiomyopathy were used for a total geno

257 rdiomyocytes in transgenic (TG) mice, causes desmin-related cardiomyopathy, a protein conformational

258 allin R120G mutation (CryAB(R120G)) model of desmin-related cardiomyopathy, accumulate cytotoxic misf

259 as been observed in proteinopathies, such as desmin-related cardiomyopathy, and implicated in many co

260 nction were tested in a proteotoxic model of desmin-related cardiomyopathy, caused by cardiomyocyte-s

261 ice representing a well-established model of desmin-related cardiomyopathy, we demonstrated that CR-P

262 n aggregates in mice with CryAB(R120G)-based desmin-related cardiomyopathy.

263 ck protein alpha-B-crystallin (CryAB) causes desmin-related cardiomyopathy.

264 Desmin-related myofibrillar myopathy (DRM) is a cardiac

265 iniscent of a major histological hallmark of desmin-related myopathies.

266 rders, such as neural degenerative diseases, desmin-related myopathy (DRM), and congestive heart fail

267 G), which carries a mutation associated with desmin-related myopathy (DRM), results in an altered sar

268 tein alphaB-crystallin (CryAB(R120G)) causes desmin-related myopathy (DRM), which is characterized by

269 n in alphaB-crystallin (CryAB(R120G)) causes desmin-related myopathy (DRM).

270 diomyopathy missense mutation, R157H, or the desmin-related myopathy mutation, R120G.

271 by cardiac-restricted expression of a human desmin-related myopathy-linked missense mutation of alph

272 ose a mechanism by which mutant desmin slows desmin remodeling in myocytes by retaining nebulin near

273 rowth pattern and cellular adhesion, reduced desmin RNA expression, and some other membrane proteins,

274 tations in the head, rod, or tail domains of desmin (S46F, E245D, and T453I).

275 th PKCzeta A119E and T410E mutants increased desmin Ser/Thr phosphorylation.

276 es in Z-bands of human cardiac myocytes with desmin, SERCA2, PLB, and AKAP18.

277 all, our data demonstrate that nesprin 1 and desmin serve redundant roles in nuclear anchorage and th

278 We propose a mechanism by which mutant desmin slows desmin remodeling in myocytes by retaining

279 This model suggests that desmin stabilizes Z-disks and enables greater stress pro

280 ineage were characterized morphologically by desmin staining and differentiated successfully into mul

281 ventricular tissue slices revealed a loss of desmin staining within the intercalated disk and severe

282 Levels of the pericyte structural protein, desmin, substantially increased after noise exposure in

283 Some of these cells express desmin, suggesting a contribution to the stellate cell p

284 (IFs) in cardiomyocytes consist primarily of desmin, surround myofibrils at Z disks, and transmit for

285 abundance in the LIF-null animals including desmin, tenascin, Cox-2, bone morphogenetic protein (BMP

286 hat, although nebulin M160-164 bound to both desmin tetrameric complexes and mature filaments, all th

287 ntracellular aggregates containing CryAB and desmin that are amyloid positive, and disease can be rec

288 myocytes by 70% and resulted in a failure of desmin to align with Z disks and disrupted cell-cell jun

289 mechanisms that regulate the association of desmin to sarcomeres and their role in desminopathy are

290 rylation of desmin filaments, which promoted desmin ubiquitylation by Trim32 and degradation.

291 desmin and three desminopathy-causing mutant desmin variants carrying mutations in the head, rod, or

292 The disease-mutant desmin variants E245D and T453I exhibited increased bind

293 latelet-derived growth factor receptor beta, desmin, vimentin, tissue inhibitor of metalloproteinase-

294 Increased expression levels of desmin were associated with the induction of hypoxia ind

295 immunoprecipitation, while alpha-synemin and desmin were insoluble.

296 that expressed alpha-smooth muscle actin or desmin were lost, along with expression of cyclooxygenas

297 Pericytes, cells that express both CD31 and desmin, were found both in the walls of tumor-associated

298 at all stages in culture but never expressed desmin, whereas hepatic stellate cells consistently expr

299 issues express alpha-smooth muscle actin and desmin, which are markers for uterine differentiation.

300 of alpha-SMA, type I collagen, vimentin, and desmin, with concurrent transition to a fibroblast-like