ライフサイエンスコーパス: M protein

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

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

3 virus harboring an S369A mutation within the M protein.

4 red mutations that mainly affected the viral M protein.

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

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

7 oviruses encoding and incorporating a tagged M protein.

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

9 it to the viral membrane by associating with M protein.

10 ng the M-line-specific proteins myomesin and M protein.

11 ther PrtF1/SfbI shares other properties with M protein.

12 ith exogenous or endogenous wild-type beta(2)m protein.

13 ecessary and sufficient for interaction with M protein.

14 NP protein is incompatible with mumps virus M protein.

15 onserved but hidden sequence patterns in the M protein.

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

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

18 ntial disease through deposition of secreted M proteins.

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

20 S1 is a structural paralogue of hRSV 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 e output when coexpressed with the membrane (M) protein.

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

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

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

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

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

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

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

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

32 Expression of M protein alone, but not NP, F-K115Q, or HN protein indi

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

34 The VSV-M protein altered the intracellular distribution of muri

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

36 n septum and colocalize with areas of active M protein anchoring.

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 M protein and protein F1 (PrtF1/SfbI) are differentially

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

46 pression of the major virulence factors, the M protein and the capsule, indicates that these proteins

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

48 in helping mediate interactions between the M protein and the nucleocapsid.

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

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

51 h reduced S complexing with virion membrane (M) proteins and consequent exclusion of S from virions.

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

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

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

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

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

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

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

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

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

61 enotypic typing (based on cell surface T and M protein antigens and opacity factor [OF] production) a

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

63 The M protein appears to facilitate core particle envelopmen

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

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

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

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

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

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

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

71 s, myomesin1 (Myom1) and myomesin2 (Myom2 or M-protein) at the structural, mRNA, and protein levels b

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

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

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

75 arrow plasma cells (BMPCs) and size of serum M proteins (BMPC>or=10% and serum M protein>or=3 g/dL; B

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

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

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

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

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

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

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

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

84 in] by at least 50%, and a decrease in urine M-protein by at least 90%).

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

86 a (ie, decrease in serum monoclonal protein [M-protein] by at least 50%, and a decrease in urine M-pr

87 E viruses had second-site changes within the M protein carboxy tail that were partially compensatory.

88 mediating interaction between the membrane (M) protein carboxy tail and nucleocapsids.

89 The coronavirus membrane (M) protein carboxy tail interacts with the nucleocapsid

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 The sizes of the M-protein-containing microdomains outside the virus budd

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

107 t combinations of proteins in the absence of M protein did not result in particle release.

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

120 7 (p < 0.01), and a 2-fold increase in PEPCK-M protein expression at day 7 (p < 0.01).

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

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

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

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

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

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

127 nd to heparin, C-reactive protein (CRP), and M protein from Streptococcus pyogenes, it has been hypot

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

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

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

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

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

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

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

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

136 or=10% but serum M protein<3 g/dL; and serum M protein>or=3 g/dL but BMPC<10%).

137 e of serum M proteins (BMPC>or=10% and serum M protein>or=3 g/dL; BMPC>or=10% but serum M protein<3 g

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

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

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

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

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

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

144 Thus, at its core, MS/MS protein identification relies on the relative predict

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

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

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

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

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

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

151 The encoded beta m-proteins in fish, amphibian, and avian species are bet

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

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

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

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

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

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

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

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

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

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

162 Taken together, the results show that M protein is necessary and sufficient for NDV budding.

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

164 We demonstrated that expression of the NiV M protein is sufficient to produce budding virus-like pa

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

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

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

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

169 n serial measurements of serum FLC and urine M-protein is inadequate to abolish the serial 24-hour ur

170 sion of Fruitless transcription factors (Fru(M) proteins) is necessary and sufficient to confer the p

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

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

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

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

175 ears following diagnosis, a persistent serum M protein level of 5 g/L (0.5 g/dL) or higher was an add

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

177 patients achieved at least a 90% decrease in M-protein levels.

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

179 In placental mammals beta m-proteins lost their ancestral functions, accumulate in

180 m M protein>or=3 g/dL; BMPC>or=10% but serum M protein<3 g/dL; and serum M protein>or=3 g/dL but BMPC

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

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

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

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

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

186 ear to have added value in patients who have M-proteins measurable by electrophoresis.

187 er 2 months of therapy was superior to early M-protein measurement to predict overall response.

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

189 nteractions between transmembrane domains of M protein monomers.

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

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

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

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

194 ht to determine the ability of a recombinant M protein mutant virus (rM51R-M virus) to mature DC in v

195 ral mRNAs occurred in cells infected with an M protein mutant virus that is defective in host shutoff

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

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

198 In contrast, an M protein mutant with a degree of attenuation similar to

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

200 These results support the use of M protein mutants of VSV as vaccine vectors.

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

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

203 Matrix (M) protein mutants of vesicular stomatitis virus have re

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

232 Thus, the VSV-M protein plays an important role in permitting the viru

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

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

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

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

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

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

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

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

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

242 Higher response quality (100% M-protein reduction) was associated with longer response

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

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

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

246 Analysis of 32 strains of 17 distinct M protein serotypes revealed that MalR is highly conserv

247 Analysis of 28 strains of 22 distinct M protein serotypes showed that MalE is highly conserved

248 ry well conserved in GAS strains of distinct M protein serotypes.

249 anning the length of the protein whereas the M protein showed a consistent mutation, threonine to iso

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

251 M protein stability was dependent on the coexpression of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

269 30 to arginines led to an altered pattern of M protein ubiquitination and impaired viruslike particle

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

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

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

273 We also determined whether G protein or M protein was colocalized with VSV nucleocapsid protein

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

275 The M protein was distributed throughout the infected cell,

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

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

278 In contrast to the case for G protein, M protein was not colocalized with these areas of nucleo

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

280 in the mouse hepatitis coronavirus (MHV) A59 M protein was suggested to participate in intermolecular

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