ライフサイエンスコーパス: M protein

1 trophoresis for monoclonal gammopathy (MG or M-protein).

2 D30 (sCD30), and monoclonal immunoglobulins (M-proteins).

3 NP protein is incompatible with mumps virus M protein.

4 s normal brain cells than VSV with wild-type M protein.

5 virus harboring an S369A mutation within the M protein.

6 red mutations that mainly affected the viral M protein.

7 inal tetracysteine tag (Mtc) in place of the M protein.

8 in trans both L and M proteins but not just M protein.

9 oviruses encoding and incorporating a tagged M protein.

10 s as well as in transfected cells expressing M protein.

11 respiratory syndrome coronavirus (MERS-CoV) M protein.

12 onserved but hidden sequence patterns in the M protein.

13 ecessary and sufficient for interaction with M protein.

14 the retention time of each patient-specific M-protein.

15 al M-protein (PAM) as its major cell surface M-protein.

16 e a vast amount of an immunoglobulin-derived M-protein.

17 ed-coil structure and thermal instability of M proteins.

18 ntial disease through deposition of secreted M proteins.

19 furin protease into pr peptide and membrane (M) protein.

20 (SYNV) SIE is mediated by the viral matrix (M) protein.

21 emain more polymerogenic than the wild-type (M) protein.

22 n of cellular gene expression by the matrix (M) protein.

23 S1 is a structural paralogue of hRSV matrix (M) protein.

24 those elicited by virus expressing wild-type MS protein.

25 nt heavy (NF-H) and neurofilament medium (NF-M) proteins.

26 budding process coordinated by viral matrix (M) proteins.

27 rsons with a normal FLC ratio and without an M-protein, 17 had elevated kappa and/or lambda FLC level

28 rs: myomesin 1 (185kDa isoform 1), myomesin (M-protein) 2, 165kDa, and myomesin family member 3, were

29 presence of an immunoglobulin G lambda serum M protein (4,784 mg/dL) and confirmed by the findings of

30 irus (SYNV) is mediated by the viral matrix (M) protein, a multifunctional protein involved in transc

31 From these data, we propose that M protein accumulating in nuclei with primary SYNV infec

32 ifferences in age, plasma cell infiltration, M protein, albumin, beta2-microglobulin, performance sta

33 We show that SK and M-protein alterations influenced the virulence of GAS an

34 Group A streptococcus (Strep A) surface M protein, an alpha-helical coiled-coil dimer, is a vacc

35 to reduce the time required to perform LC/MS/MS protein analyses to within a single day.

36 MALDI-ISD MS protein analysis involves only minimal sample prepara

37 of T cells crossreactive with streptococcal M protein and cardiac myosin.

38 of fibrils formed by the full-length beta(2)m protein and compare spectra of fibrils prepared under

39 mulated, as judged by a greater abundance of M protein and greater association of the M mRNA with pol

40 In this study, we focus on M protein and identify a key phosphorylation site (Thr20

41 M protein and nsp13, the helicase, of JHM.WU are require

42 o form at a low rate and contained the viral M protein and nucleoprotein (N).

43 In contrast, M protein and other Mga-regulated proteins contribute to

44 port, leading to nuclear accumulation of RSV M protein and reduction in RSV levels.

45 Here we show that M protein and SfbI are anchored simultaneously throughou

46 g of the interaction between the coronavirus M protein and the nucleocapsid protein.

47 host factors that interact with henipavirus M proteins and contribute to viral particle assembly.

48 to peptide sequences common to streptococcal M proteins and skin keratins have been detected in patie

49 nificant neurological consequences with high M-protein and EBV-R.

50 method was able to differentiate between the M-protein and elotuzumab mass signatures in 91 out of 92

51 In an additional case, an IgM kappa M-protein and excess kappa FLCs were both detected in pl

52 a cells assessed by iFISH and combination of M-protein and plasma cell infiltration as surrogates of

53 The M-protein and the related increase in blood viscosity co

54 The deconvoluted peak heights of M-protein and therapeutic antibody light chain are conve

55 M-proteins and abnormal FLC ratios were detected up to 9

56 bicinchoninic acid (BCA) and targeted LC/MS/MS protein and peptide assays.

57 ng J8-DT (conserved peptide vaccine from the M protein) and a recombinant SpyCEP fragment protects ag

58 ion, disruption of the nuclear export of RSV M protein, and inactivation of the NF-kappaB signaling p

59 EBV-R with rising Epstein-Barr viral load, M-protein, and associated clinical sequelae were capture

60 The prevalence of an abnormal FLC ratio, M-protein, and hypogamma-globulinemia before CLL diagnos

61 Concordance of FLCs, M-proteins, and PTLD tumor light chain restriction was i

62 rm distribution of the number of acquired MS/MS, protein, and peptide identifications across all 126

63 orted by a lack of detectable Nra effects on M protein- and SpeB-dependent phenotypes.

64 Idealized M proteins appear to have promise as vaccine immunogens.

65 The M protein appears to facilitate core particle envelopmen

66 Antigenically variable M proteins are major virulence factors and immunogens of

67 artment (ERGIC), but the mechanisms by which M proteins are transported from their site of synthesis,

68 F) protein cytoplasmic tail (CT) and matrix (M) protein are key mediators of viral assembly, but the

69 containing wild-type (wt) or mutant matrix (M) proteins are being developed as candidate vaccine vec

70 For paramyxoviruses, viral matrix (M) proteins are key drivers of virus assembly and buddin

71 In traditional HDX-MS, proteins are incubated in D(2)O as a function of tim

72 able chimeras containing the entire SARS-CoV M protein as well as mutants with intramolecular substit

73 Currently available M-protein assays have several limitations, particularly

74 ts application to previously published LC/MS/MS protein assays from our laboratory for two cardiotoxi

75 ntramolecular substitutions that partitioned M protein at the boundaries between the ectodomain, tran

76 ns between proteins difficult, and hindering M protein-based vaccine development.

77 d cheminformatics to construct a recombinant M protein-based vaccine that included six Strep A M pept

78 Hinge-derived polypeptide was sufficient for M protein binding in coimmunoprecipitation assays.

79 The mechanism for hPg/M protein binding uncovered here may facilitate targetin

80 vaccinia Ankara (MVA) prime/intramuscular (i.m.) protein boost regimen induced functional IgG respons

81 ion regulator DivIVA also diminishes surface M protein but increases SfbI.

82 d peptidoglycan synthesis diminishes surface M protein but not SfbI.

83 most potential connections was not the viral M protein but the nonstructural protein 3 (nsp3), which

84 be reversed by providing in trans both L and M proteins but not just M protein.

85 The PIV5 M protein (but not the PIV5 nucleocapsid protein) was fo

86 Transient expression of the SYNV M protein, but not other viral proteins, interfered with

87 inuclear locations, and both copurified with M proteins, but E.T was entirely incompetent for VLP pro

88 to 38) within the N terminus of the matrix (M) protein, but the functions of this potential L-domain

89 The GAS M protein, by which strains are differentiated into >220

90 M proteins coalesce at sites underlying infected cell me

91 wn that IgA-binding regions of streptococcal M proteins colocalize with IgA in mesangial immune depos

92 ane outside the virus budding sites, nor was M protein colocalized with microdomains containing the h

93 Notably, the M protein competed for in vitro binding of various oligo

94 In a subanalysis, monoclonal (M)-protein concentration and type were used as exposure.

95 r study confirms that abnormal FLC ratio and M-protein concentration >1.5 g/dL, factors previously co

96 ee light-chain (FLC) ratio (<0.26 or >1.65), M-protein concentration (>/=1.5 g/dL), and reduction of

97 M patients with prior knowledge of MGUS, low M-protein concentration (<0.5 g/dL) at MGUS diagnosis wa

98 approximately half the study population, the M-protein concentration and involved FLC-ratio levels sh

99 The observation that a low M-protein concentration at MGUS diagnosis was associated

100 ) MGUS, and the highest risk associated with M-protein concentrations > 1.5 g/dL, support a role for

101 d AML/MDS; patients with monoclonal-protein (M-protein) concentrations > 1.5 g/dL (SIR = 11.12; 3.61-

102 We found that the M protein contacts the Rae1*Nup98 heterodimer principall

103 nerated a recombinant VSV encoding a matrix (M) protein containing a C-terminal tetracysteine Lumio t

104 ne these subjects, isogenic chimeric SK- and M-protein-containing GAS strains were generated, and the

105 e, share the common C-terminal S region; the M protein contains an additional preS2 sequence N-termin

106 e sequence-variable N-terminal region of the M protein defines the M type and also contains epitopes

107 in complex, are present between neighbouring M-protein densities on the same helical turn and between

108 uses was also dependent on the viral capsid (M) protein-directed assembly and budding from GSL-enrich

109 Of 21 patients with MG, M protein disappeared in 12 patients (58%) over 5 years

110 -7/Fc, which binds to protein H and selected M proteins, displaced FH from the bacterial surface, enh

111 Mutation of S369 within the PIV5 M protein disrupted 14-3-3 binding and improved the budd

112 at low pH also resulted in an enhancement of M protein dissociation from partially permeabilized, but

113 For many paramyxoviruses, M proteins drive viral assembly and egress; however, som

114 ion curves that are sensitive to slow micros/ms protein dynamics (demonstrated with ubiquitin).

115 s human fibrinogen (hFg) binding Pattern A-C M-proteins, e.g. M1.

116 Using assays for monoclonal (M)-proteins (electrophoresis/immunofixation) and kappa-l

117 gulon that encodes virulence factors such as M protein (emm), C5a peptidase (scpA), and streptococcal

118 lence factors multiple-gene activator (mga), M protein (emm23), C5a peptidase (scpA), fibronectin-bin

119 The M protein, encoded by the emm gene, is a major virulence

120 We analyzed M-protein evaluations from 384 MM patients (excluding th

121 Among 107 patients with M-protein exclusively in serum at diagnosis who became s

122 Inhibition of RSV M protein export by leptomycin B correlated with reduced

123 HIP1 RNA decreases native and inducible IRAK-M protein expression and prevents development of endotox

124 7 (p < 0.01), and a 2-fold increase in PEPCK-M protein expression at day 7 (p < 0.01).

125 We examined IRAK-M protein expression in epithelia from asthmatic patient

126 that for both Nipah virus and Hendra virus, M protein expression in the absence of any other viral p

127 Surprisingly, ablating M protein expression reduced virion secretion but marked

128 atory syncytial virus (HRSV) lacking matrix (M) protein expression (M-null virus) from cDNA.

129 t K2hPg with recombinant a1a2 (VKK38) of the M protein from GAS isolate NS455.

130 The NH(2)-terminal sequence of the M protein from group A streptococci defines the serotype

131 with human saliva resulted in the release of M protein from the DeltaNH(2) mutant at a significantly

132 o identify regions of functional importance, M proteins from a variety of VHSV strains were tested in

133 taxonomic and functional coverage, with >7.3 M proteins from across the Tree of Life, enables FAT-CAT

134 l facilitate the design of future studies of M protein function, streptococcal virulence, epidemiolog

135 s the relationship between AP3B1 binding and M protein function.

136 PET corresponded with increased monoclonal (M) protein (g/dL) in tumor-bearing mice over time (3.29

137 E) transcription signal of the HPIV3 matrix (M) protein gene is identical to those of the nucleoprote

138 arly myeloma." It is defined as either serum M-protein >/= 3 g/L or >/= 10% monoclonal plasma cells i

139 s kappa restricted, and another case with an M-protein had a T-cell PTLD.

140 or example, one PTLD case with an IgG lambda M-protein had a tumor that was kappa restricted, and ano

141 ine (J8-DT) from the conserved region of the M protein has shown efficacy against disease that follow

142 Other paramyxovirus M proteins have been shown to dimerize, and biochemical

143 interacts with a remarkably large number of M protein HVRs (apparently approximately 90%).

144 Neutralizing antibodies typically recognize M protein hypervariable regions (HVRs) and confer narrow

145 characterize the effect of nuclear-retained M protein in a full viral context and generated a recomb

146 During primary infections, accumulation of M protein in infected nuclei results in coiling of genom

147 gene junction, in addition to wild-type (wt) M protein in its normal location, was recovered, but the

148 kt was caused by the expression of the viral M protein in the absence of other viral components, and

149 We also show that the level of M protein in the infected cell is rate limiting for vira

150 GxYR(204), was responsible for retaining the M protein in the TGN.

151 The role of the M protein in virus assembly was then examined by infecti

152 cture determination of four sequence-diverse M proteins in complexes with C4BP.

153 at trial entry the presence of two distinct M proteins in immunofixation electrophoresis.

154 y prevents overaccumulation of nonfunctional M proteins in the cytoplasm and nuclei of NiV-infected c

155 Among 161 patients with M-protein in both serum and urine at diagnosis who becam

156 potentially provide an objective tracking of M-proteins in patients with complete response.

157 erm persistence of serum monoclonal protein (M protein) in HIV-infected patients on antiretroviral th

158 absence of intact monoclonal immunoglobulin (M protein) in the serum, and no evidence of multiple mye

159 herin to HIV-1 Vpu is a feature of all group M proteins, including those of transmitted founder virus

160 porter gene expression assay showed that the M protein inhibited viral transcription.

161 M proteins interact with the nucleocapsid (NP or N) comp

162 e analyze the mechanisms involved in RelAp43-M protein interaction.

163 nkDB 2.0 enables the holistic analysis of XL-MS protein interaction data without limitation to the cr

164 Assembly of the M protein into clusters and filaments at infected cell s

165 a protective immunity-related GTPase family M protein (IRGM) polymorphism leading to impaired cleara

166 gest that the monoubiquitination of the PIV5 M protein is important for proper virus assembly and for

167 of the N protein within IBs suggest that the M protein is involved in the transport of viral ribonucl

168 M protein is rapidly anchored at the septum, and in part

169 The M protein is required for virion assembly following infe

170 lization analyses revealed that the MERS-CoV M protein is retained intracellularly in the trans-Golgi

171 The M protein is the major surface-associated virulence fact

172 M protein is the most abundant GAS surface protein, and

173 study, it was found that the VSV matrix (VSV-M) protein is an important element in this decrease in a

174 The coronavirus membrane (M) protein is the central actor in virion morphogenesis.

175 , we found that Myomesin-2 (Myom2), encoding M-protein, is upregulated postnatally, and based on this

176 separate effects for these 3 factors and the M-protein isotype had higher discriminatory power than o

177 In the present study, a peptide from the GAS M protein (J14) representing a B cell epitope was incorp

178 We assayed monoclonal (M)-proteins, kappa/lambda free light chains (FLCs) in pr

179 on of the sequence 24-FPVI-27 within the MuV M protein led to poor VLP production, consistent with fi

180 IRAK-M protein levels were increased in asthmatic airway epit

181 ein ESI-MS method, which combines direct ESI-MS protein-ligand binding measurements and competitive p

182 Our findings indicate that MERS-CoV M protein localizes to the TGN because of the combined p

183 Dimeric M-proteins (M-Prt) in group A Streptococcus pyogenes (GA

184 l surface indirectly via fibrinogen bound to M-protein, M23.

185 ing sites upstream of the genes encoding the M protein (M49), serum opacity factor (SOF), fibronectin

186 taE background showed that expression of the M* protein markedly enhanced the growth of the DeltaE mu

187 ssue deposition of streptococcal IgA-binding M proteins may contribute to the pathogenesis of IgAN.

188 The nuclear export of the RSV M protein, mediated by the nuclear export protein export

189 Our data suggest that SYNV SIE is caused by M protein-mediated transition from replication to virion

190 brane tension perceived by mechanosensitive (MS) proteins mediates cellular responses to mechanical s

191 Glycoprotein (G protein) and M protein microdomains were not colocalized in the plasm

192 nteractions between transmembrane domains of M protein monomers.

193 streptokinase, CAMP factor, streptolysin O, M protein (more abundant in the CvfA(-) mutant), SpeB, m

194 hondrial pathways to apoptosis induced by an M protein mutant (M51R) VSV in U87 human GBM tumor cells

195 to its recombinant wt (rwt) counterpart, an M protein mutant of VSV, rM51R-M virus, stimulates matur

196 he absence of other viral components, and an M protein mutant that does not inhibit RNA polymerase II

197 However, M protein mutant viruses, such as rM51R-M virus, stimula

198 These results demonstrate the potential of M protein mutant VSVs as candidate vaccine vectors again

199 approach for attenuation that uses a matrix (M) protein mutant (rM51R) VSV as a vaccine vector agains

200 However, M protein mutants with weakened nuclear localization sig

201 Matrix (M) protein mutants of vesicular stomatitis virus (VSV),

202 Matrix (M) protein mutants of VSV have shown greater selectivity

203 at incorporates two enhancing strategies: an M protein mutation (M51R) that prevents the virus from s

204 ons included gene shifting (VSV-p1-GFP/RFP), M protein mutation (VSV-M51), G protein cytoplasmic tail

205 was mapped to a C-terminal region within the M protein, namely, 366-KTKSLP-371.

206 ple myeloma (MM) require monoclonal protein (M-protein)-negative status on both serum immunofixation

207 by using chimeras between MERS-CoV M and the M protein of infectious bronchitis virus (IBV).

208 entified 14-3-3 as a binding partner for the M protein of parainfluenza virus 5 (PIV5).

209 a conserved helical peptide epitope from the M protein of Streptococcus pyogenes, were designed by ex

210 host innate immunity response in contrast to M protein of vaccine strains, which have lost this prope

211 e during rabies virus infection and that the M protein of wild isolates of rabies virus is a viral im

212 hogenicity, and colocalization of the HN and M proteins of NDV, indicating that these residues of the

213 The VLP is composed of the NP and M proteins of Newcastle disease virus (NDV) and a chimer

214 complex, AP3B1, as a binding partner for the M proteins of the zoonotic paramyxoviruses Nipah virus a

215 racterized the ubiquitination of the matrix (M) protein of a paramyxovirus, parainfluenza virus 5 (PI

216 In this work, we replaced the membrane (M) protein of the model coronavirus mouse hepatitis viru

217 Nup98) are host cell targets for the matrix (M) protein of vesicular stomatitis virus (VSV).

218 The matrix (M) protein of wild isolates of rabies virus such as Tha

219 ed region synthetic peptide derived from the M-protein of GAS and containing only 12 aa from GAS, whe

220 neighbouring helical turns, but not between M-proteins of different turns, as is observed for the re

221 y SK2a and SK2b coupled with the coinherited M-proteins of these strains.

222 ing T cells that respond to short homologous M protein or keratin peptides.

223 that did not involve association with either M protein or RNA.

224 Sortase is not required for translocation of M protein or SfbI at their respective locations.

225 e not associated with significant changes in MS protein or methionine levels.

226 logical niches or population immunity to the M protein, or they may require several infections over a

227 Paramyxovirus matrix (M) proteins organize virus assembly, linking viral glyco

228 Plasminogen (Plg)-binding M protein (PAM) is a group A streptococcal cell surface

229 n receptor, Pg-binding group A streptococcal M protein (PAM), and the human Pg activator streptokinas

230 uman Pg (hPg)) binding Group A streptococcal M-protein (PAM) as its major cell surface M-protein.

231 r, plasminogen-binding group A streptococcal M-protein (PAM).

232 for DENV replication, the functional role of M protein, particularly the alpha-helical domain (MH), w

233 We determined that matrix protein (M protein) partitions into plasma membrane microdomains

234 gression were amount of urinary excretion of M protein per 24 h, proportion of bone marrow plasma cel

235 Coronavirus membrane (M) proteins play key roles in virus assembly, through M-

236 The RSV matrix (M) protein plays key roles in virus assembly and budding

237 Measurement of monoclonal antibodies (M-proteins) plays an important role in the diagnosis and

238 w-affinity binding (K(d) greater, >or= 0(-7) M) proteins prefer ordered structures, whereas only high

239 ) of a specific subtype of bacterial surface M protein, present in all GAS pattern D strains.

240 ain) and without (5448 Deltasda1(M-) strain) M protein production.

241 analyzing large-scale affinity precipitation-MS protein-protein interactomes.

242 er((R)) ampoule, Ironorm((R)) capsule, and V.M. Protein((R)) powder).

243 lAsH (green) revealed that newly synthesized M protein reaches the plasma membrane in less than 30 mi

244 ne is the same domain 3 that is critical for M protein recognition during assembly.

245 t achieved minimal response (serum and urine M-protein reduction of >/= 25% and >/= 50%) could receiv

246 ermaphrodite X chromosomes transition from a MES protein-regulated state to DCC-mediated repression.

247 Our model suggests that the rhabdovirus M protein regulates the transition from replication to v

248 Coronavirus M proteins represent the major protein component of the

249 Second-site mutations affecting M protein restored interaction with altered NP proteins

250 nhibition of host gene expression by the VSV M protein resulted in the degradation of Mcl-1 but not B

251 in lacking the gene that encodes the matrix (M) protein (RSV M-null) was developed.

252 A database of 175 representative M-protein sequences was used to analyze the protein dive

253 Knockdown of 9 out of 28 human MED proteins significantly impaired viral replication wi

254 M protein stability was dependent on the coexpression of

255 PR) and 10 patients obtaining some degree of M protein stabilization or decrease.

256 GAS) are serious human pathogens of multiple M protein strains that upregulate expression of virulenc

257 SK2b is secreted by skin-tropic Pattern D M-protein strains that also express plasminogen (human P

258 In the presence of the E.T proteins, the M protein subunits accumulated into detergent-insoluble

259 Viruses with wt M protein, such as recombinant wild-type (rwt) virus, st

260 possible to define a short linear region of M protein sufficient for assembly with N.

261 expression, leading to downregulation of the M protein surface fibril and secreted cysteine protease

262 How Rae1 functions in mRNA export and how M protein targets both Rae1 and Nup98 are not understood

263 ed the sequence requirements of the SARS-CoV M protein that are necessary for interaction with SARS-C

264 The streptococcal M protein that is used as the substrate for epidemiologi

265 n 48 emm-clusters containing closely related M proteins that share binding and structural properties

266 The sequences of M proteins, the major surface-associated virulence facto

267 membrane translocation of surface proteins: M protein to the septum, and SfbI to the poles.

268 ing residues are evolutionarily conserved in M proteins to enable functional interactions necessary f

269 ituent of the virion envelope, the membrane (M) protein, to facilitate assembly and budding.

270 After synthesis in the cytoplasm, the MS protein translocates to the endoplasmic reticulum, wh

271 den within the antigenic variability of many M protein types, are sequence patterns conserved for rec

272 30 to arginines led to an altered pattern of M protein ubiquitination and impaired viruslike particle

273 s 79, 80, 130, and 247 to arginines restored M protein ubiquitination and VLP production, suggesting

274 In a 30-valent M-protein vaccine, emm types accounted for 91% of isolat

275 duction of mumps VLPs occurred only when the M protein was coexpressed together with other viral prot

276 Using (33)P labeling, phosphorylated M protein was detected in PIV5-infected cells, and this

277 The M protein was highly cross-reactive to TGEV and PRCV ant

278 expected, the interaction of N protein with M protein was not affected in either of the chimeric vir

279 itis virus (MHV) in which all or part of the M protein was replaced by its phylogenetically divergent

280 The EXOC5CTS-m protein was stable and could bind other members of the

281 However, the interaction between HN and M proteins was dramatically reduced in the Cav-1 null MC

282 ent cells tested, translation of RSV matrix (M) protein was specifically stimulated, as judged by a g

283 the growth of the DeltaE mutant and that the M* protein was incorporated into assembled virions.

284 tify additional roles for this region of the M protein, we constructed a mutant of M5 group A strepto

285 The F and M proteins were both found to traffic through Rab11-posi

286 E121Q and E121L M proteins were capable of forming virus-like particles

287 M proteins were detected in only two patients with NHL (

288 These findings suggest that M* proteins were repeatedly selected as surrogates for t

289 M-proteins were present in 91% of PTLD cases versus 50%

290 itin is attached to alternative sites on the M protein when the primary ones have been removed.

291 Only the MuV matrix (M) protein when expressed by itself was capable of induc

292 g the translation of the rate-limiting viral M protein, which is a new paradigm in antiviral defense.

293 eGFP-DeltaM-Mtc and VSV-DeltaM-Mtc) encoding M protein with a carboxy-terminal tetracysteine tag (Mtc

294 ant of M5 group A streptococci expressing an M protein with a deletion of amino acid residues 3-22 (D

295 se findings suggest that the interactions of M protein with both E and S protein are more complex tha

296 An M protein with seven lysine residues changed to arginine

297 A recombinant virus encoding an M protein with seven lysines mutated was generated, and

298 Transport and subsequent association of M protein with the plasma membrane were shown to be inde

299 e hypervariability of its major antigen, the M protein, with >200 different M types known.

300 ndings support a model in which a portion of M protein within PIV5-infected cells is phosphorylated a