ライフサイエンスコーパス: type V

1 cies (type IV), and Propionibacterium acnes (type V).

2 elic disorder distal spinal muscular atrophy type V.

3 strains of Klebsiella pneumoniae to collagen type V.

4 '-UTR of BRIL causes osteogenesis imperfecta type V.

5 that is involved in osteogenesis imperfecta type V.

6 uch more hyperpolarized potentials than wild type (V(1/2) of s(infinity) curve approximately -130 mV

7 referential reliance on [1 - C] (mostly A, B types) vs (3) preferential reliance on [1 - Q] (mostly C

8 e I: 6, Type 2: 6, Type III: 6, Type IV: 11, Type V: 4.

9 ers were significantly more elevated in wild-type vs. Aag(-/-) liver after I/R.

10 mmunostaining with anticollagen type III and type V Abs).

11 main and C2 regions from type I AC (ACI) and type V AC (ACV) to identify the region on ACI that inter

12 Expression of type V AC was approximately 75% over endogenous levels a

13 To alter the above equilibrium, type V AC was overexpressed in a myocyte-specific manner

14 ism whereby Ca(2+) inhibits adenylyl cyclase type V (ACV) and adenylyl cyclase type VI (ACVI) is unkn

15 second of the two large cytosolic domains of type V adenylyl cyclase (ACV) as bait, we identified a s

16 at besides catalyzing the synthesis of cAMP, type V adenylyl cyclase (ACV) can act as a GTPase-activa

17 th Myc (PAM) interacts with the C2 domain of type V adenylyl cyclase (ACV-C2) and that purified PAM i

18 ibrary, using the N-terminal region of human type V adenylyl cyclase (hACV) as bait, we identified G

19 A truncated first cytosolic domain of type V adenylyl cyclase (VC(1)) and a truncated second c

20 tly with the C(1) but not the C(2) domain of type V adenylyl cyclase and that the inhibition by RGS2

21 Expression of mammalian type V adenylyl cyclase in a cyclase-deleted yeast strai

22 and apparent affinity for the C(1) domain of type V adenylyl cyclase in the absence of activators of

23 tuted by mixture of the C1 and C2 domains of type V adenylyl cyclase was also inhibited by Gialpha.

24 Type V adenylyl cyclase was decreased approximately 45%

25 In HEK293 cells expressing type V adenylyl cyclase, RGS2 inhibited Galpha(s)-Q227L-

26 e nature of the interaction between RGS2 and type V adenylyl cyclase.

27 our laboratory to identify mutant mammalian type V adenylyl cyclases insensitive to inhibition by G(

28 Comparisons of cells from wild-type vs. AE3(-/-) mice show that AE3 (present in hippoca

29 of the extracellular matrix protein collagen type V alpha 1 (col5a1).

30 ic cells) include aminopeptidase A, collagen type V, alpha 1, cyclin G2, DEC1/Stra13, endothelin 1, l

31 This polypeptide, which we have named alpha4 type V (alpha4(V)) collagen, contains an uninterrupted G

32 xpand on these observations to show that GBS type V, an emergent serotype, grown in a chemostat at a

33 taining (400 endotoxin units/ml) collagenase type V and "endotoxin-free" (3.1 endotoxin units/ml) Lib

34 nt manner and also appeared to bind collagen type V and laminin, but not other proteins, such as tran

35 maS and the catalytic C1 and C2 domains from type V and type II mAC (VC1.IIC2), bound to FSK and eith

36 Galpha(s) and Galpha(i) regulation of human type V and type VI adenylyl cyclase (AC V and AC VI) in

37 Type V and VI mammalian adenylyl cyclases (AC5, AC6) are

38 fication of BKV into six genotypes, of which types V and VI have not been previously recognized.

39 ithelium-derived factor (PEDF) defects cause types V and VI osteogenesis imperfecta via defective bon

40 d 29 had darker skin types (Fitzpatrick skin types V and VI).

41 (skin types I, II, III, and IV) than in skin types V and VI-which are reported to tolerate relatively

42 at efficiently cleaves gelatin, elastin, and types V and X collagen.

43 MODY5 (maturity-onset diabetes of the young, type V) and familial GCKD (glomerulocystic kidney diseas

44 Adenylyl cyclase (Type V) and its subdomains, which interact with Gsalpha,

45 meability in isolated choroid plexus of wild-type vs. AQP1 null mice, as well as intracranial pressur

46 y times of 17 +/- 0.7 vs. 55 +/- 5 s in wild-type vs. AQP4-null mice in a buried food pellet test, wh

47 ctions caused by group B streptococcal (GBS) type V are increasingly common.

48 l of endogenous nucleotide bound to the wild-type V-ATPase and to a mutant (the A subunit mutant R483

49 This protease is a founding member of the type V (autotransporter) secretion system and is conside

50 stems, one putative Type IV system and three Type V autotransporters.

51 2c1 is a newly identified guide RNA-mediated type V-B CRISPR-Cas endonuclease that site-specifically

52 hat are secreted via the autotransporter (or type V) bacterial secretion pathway.

53 Type I and type V behaviors of the International Union of Pure and

54 ted that dimerizing with the beta 2m(a) (NOD type) vs beta 2m(b) isoform (NOR type) alters the struct

55 for heterogeneity = .037, between BRAF-wild-type vs BRAF-mutated cancer risks).

56 ngs to the widely conserved, uncharacterized type V branch of P-type ATPases, a large family of ion p

57 ious observations about the emergence of GBS type V, but our data caution that conclusions about sero

58 of amylose-lipid complexes (Resistant Starch Type V) by the addition of different lipids/fatty acids

59 ted by conjugates prepared with purified GBS type V capsular polysaccharide (CPS) than among those ev

60 ted with a greater percentage of Type IV and Type V cases.

61 robability of release (0.27 vs 0.46 for wild-type vs CaSR(-/-) pairs) with little change in quantal s

62 The fact that several GBS type V cell wall-associated and membrane proteins were e

63 asodepressor responses to bradykinin and the type V cGMP-selective phosphodiesterase inhibitor zaprin

64 udes a myosin motor-like sequence fused to a type V chitin synthase gene.

65 ifferential RNA sequencing (RNA-seq) of wild-type V. cholerae and a locked low-cell-density QS-mutant

66 n exbB1 or exbD1 were introduced into a wild-type V. cholerae background, no defect in iron transport

67 only those amino acids was secreted by wild-type V. cholerae but not by an epsD mutant, establishing

68 ited for vaccination and challenge with wild-type V. cholerae El Tor Inaba.

69 However, acid-adapted wild-type V. cholerae exhibited a major competitive advantage

70 In this work, we have isolated the wild-type V. cholerae monolayer and demonstrated that the env

71 ingested approximately 1 x 10(5) CFU of wild-type V. cholerae O1 El Tor Inaba strain N16961 10 days o

72 ed with 10(6) CFU (one 50% lethal dose) wild-type V. cholerae O1 El Tor strain N16961.

73 Wild-type V. cholerae strains 3038 and C7258 and a vaccine ca

74 , significantly increased attachment of wild-type V. cholerae to Caco-2 cells.

75 By comparing TcpP diffusion in wild-type V. cholerae to that in mutant strains lacking eithe

76 n for the V. cholerae T2S system, since wild-type V. cholerae was found to secrete the biofilm matrix

77 t expression of a lacZ reporter gene in wild-type V. cholerae, although the -128 promoter fragment di

78 Like E. coli, but unlike wild-type V. cholerae, motility of some V. cholerae strains c

79 Unlike wild-type V. cholerae, mutants lacking wigR fail to recover f

80 indistinguishable from those formed by wild-type V. cholerae.

81 requirements for monolayer formation by wild-type V. cholerae.

82 ty was not detected in cell extracts of wild-type V. cholerae.

83 allograft rejection is mediated by collagen type V (col(V)) specific T-helper-cell 17 (Th17) cells.

84 We recently identified the collagen type V [col(V)] alpha1(V) chain as a key autoantigen dri

85 e role of cell-mediated immunity to collagen type V [col(V)] in this process.

86 Autoimmunity to type V collagen (col(V)) is a major risk factor for lung

87 We reported that anti-type V collagen (col(V)) T cell immunity was strongly as

88 ne response to a native protein in the lung, type V collagen (col(V)), and that col(V)-induced oral t

89 Immunity to type V collagen [col(V)] contributes to lung transplant

90 Aberrant expression of the type V collagen alpha1(V) chain can underlie the connect

91 Type V collagen also exists as an alpha1(V)alpha2(V)alph

92 ion involves IL-17-regulated autoimmunity to type V collagen and alloimmunity, which could be enhance

93 ) specifically enhance its ability to cleave type V collagen and gelatin, respectively.

94 Transforming growth factor-beta and type V collagen are targets for regulating the initial f

95 trimers, thus completing characterization of type V collagen biosynthetic processing.

96 Digestion of type V collagen by the gelatinases is an important step

97 Type V collagen can exist as a heterotrimer, [alpha1(V)]

98 date the mechanism whereby half-reduction of type V collagen causes abnormal connective tissue biogen

99 The reduced type V collagen content is associated with a 50% reducti

100 The type V collagen domain but not the alpha4(V) N-terminal

101 the new 75-kDa chicken gelatinase lacks the type V collagen domain that is found in all mammalian ge

102 and spreading on dishes coated with various type V collagen domains revealed that Schwann cells adhe

103 Previously, we identified a type V collagen family member, alpha4(V) collagen, which

104 Type V collagen has been implicated in the regulation of

105 e findings further confirm the importance of type V collagen in the causation of EDS type II, and the

106 gene that encodes the proalpha1(V) chain of type V collagen in the classical form of the Ehlers-Danl

107 ose of this study was to define the roles of type V collagen in the regulation of collagen fibrilloge

108 a central role for the evolutionary, ancient type V collagen in the regulation of fibrillogenesis.

109 Type V collagen incorporates into type I collagen fibril

110 Type V collagen is a quantitatively minor fibrillar coll

111 data, we identified and then confirmed that type V collagen is an MMP-20 substrate.

112 orne mrkD gene product to mediate binding to type V collagen is associated frequently with strains of

113 e complete dependence of fibril formation on type V collagen is indicative of the critical role of th

114 Since type V collagen is not present in dental enamel but is a

115 reported recently preliminary evidence that type V collagen is required for collagen fibril nucleati

116 d the data are consistent with a mutation in Type V collagen leading to haploinsufficiency with the f

117 e found to be critical for interactions with type V collagen model substrates and inhibitors and to p

118 a1(V) mRNA relative to the levels of another type V collagen mRNA, proalpha2(V), were also observed i

119 a highly basic region (not present in other type V collagen NTD) as the site responsible for high af

120 erential modification of alpha1(V) chain and type V collagen properties.

121 evidence that the alpha chain composition of type V collagen remains alpha1(V)(2)alpha2(V) even in th

122 broblasts secreted only 65% of the amount of type V collagen secreted by normal controls.

123 Previously we reported that type V collagen synthesized by Schwann cells inhibits th

124 Type V collagen transcripts of affected individuals were

125 Binding to type V collagen was not associated solely with one parti

126 , denatured or monomeric type I collagen, or type V collagen was substituted for type I collagen, no

127 aling by transforming growth factor-beta and type V collagen were required for collagen fibrillogenes

128 production from alloantigen- or autoantigen (type V collagen)-reactive lymphocytes.

129 pe IV collagen alpha1 and alpha2 chains, (2) type V collagen, (3) type VI collagen, and most recently

130 reviously, we reported the cloning of alpha4 type V collagen, a novel member of the collagen type V g

131 haploinsufficiency of proalpha1(V) chains of type V collagen, a quantitatively minor collagen that co

132 ppressed DTH responses to donor antigens and type V collagen, abrogated local production of tumor nec

133 e (THP) models of the MMP-9 cleavage site in type V collagen, alpha1(V)436-450 THP and alpha1(V)436-4

134 tivity (DTH) responses to donor antigens and type V collagen, an autoantigen involved in the rejectio

135 in the COL5A1 and COL5A2 genes, which encode type V collagen, have been identified in several individ

136 ucted and found to selectively inhibit MMP-9 type V collagen-based activities compared with interstit

137 The type V collagen-deficient mice demonstrate a virtual lac

138 seen in cases with structural alterations in type V collagen.

139 endow the enzyme with the ability to cleave type V collagen.

140 ivity but does not bind to either type IV or type V collagen.

141 t with type I collagen, type II collagen, or type V collagen.

142 s against lung-restricted self-Ags, collagen type V (ColV), and k-alpha1 tubulin (KAT).

143 GBS type V conjugate vaccines are safe and immunogenic and w

144 sensitivity to gap junction blockers in wild-type vs. connexin36 knockout mice.

145 PR-Cas systems, including type II-C Cas9 and type V Cpf1 systems, and can facilitate precise gene edi

146 th type V CPS is for chemically desialylated type V CPS (dV CPS).

147 cited in humans by a conjugate prepared with type V CPS is for chemically desialylated type V CPS (dV

148 as a mechanism for enhancing the ability of type V CPS to induce IgM-to-IgG switching.

149 Levels of serum antibodies to type V CPS were measured by ELISA, and functional activi

150 CPS-tetanus toxoid (TT) vaccine (n=15), GBS type V CPS-cross-reactive material (CRM(197)) conjugate

151 V-TT-induced type V CPS-specific antibodies promoted the opsonophagoc

152 Type V CPS-specific gene was present in 66% of the isola

153 Four-fold or greater increases in type V CPS-specific IgG concentrations were noted in pos

154 V-TT CV elicited significant increases in type V CPS-specific immunoglobulin (Ig) G, IgM, and IgA

155 Significant increases in type V CPS-specific immunoglobulin G (IgG) were elicited

156 Type V CPS-specific immunoglobulin M was a dominant isot

157 ized to receive an intramuscular dose of GBS type V CPS-tetanus toxoid (TT) vaccine (n=15), GBS type

158 id not affect the structural conformation of type V CPS.

159 Cpf1 is an RNA-guided endonuclease of a type V CRISPR-Cas system that has been recently harnesse

160 Collagen type V, decorin, fibromodulin, and tenascin-X proteins w

161 reasing severity of periodontal disease, and Type V defined referrals for needs other than periodonta

162 (HSP) and distal hereditary motor neuropathy type V (dHMN-V).

163 g proteins (VCBPs) consist of immunoglobulin-type V domains and a chitin-binding domain (CBD).

164 D (CMT2D) and distal spinal muscular atrophy type V (dSMA-V) are axonal neuropathies characterized by

165 D (CMT2D) and distal spinal muscular atrophy type V (dSMA-V) are axonal peripheral neuropathies inher

166 ly defined as distal spinal muscular atrophy type V (dSMA-V) in three families, Charcot-Marie-Tooth d

167 haride types, leading us to hypothesize that type V emerged from a recombination event in a type IX b

168 The C1b domain of the type V enzyme contributed to affinity for Gialpha, but t

169 th in a glycerol/tryptone-based medium, wild-type V. fischeri cells initially excrete acetate but, in

170 As predicted, in the presence of NO, wild-type V. fischeri grew more slowly on hemin than a hnoX d

171 ion levels relative to that achieved by wild-type V. fischeri.

172 and by injection in vivo of TWEAK into wild-type vs Fn14-deficient mice.

173 The type V (for variable) promyelocytic leukemia retinoic ac

174 sphorylated or unphosphorylated form of wild-type v-Fps, with binding of the second Mg(2+) ion unaffe

175 sphorylated or unphosphorylated form of wild-type v-Fps, with substrate binding unaffected.

176 system, it is not expressed in the ventral D-type (VD) GABAergic motorneurons, which are defective in

177 The safety and immunogenicity of type V GBS capsular polysaccharide (CPS)-tetanus toxoid

178 ies promoted the opsonophagocytic killing of type V GBS in vitro.

179 est the potential for prevention of invasive type V GBS infections in healthy elderly adults through

180 e V collagen, a novel member of the collagen type V gene family that is expressed by Schwann cells in

181 ifies p200 as a novel member of the collagen type V gene family.

182 machandran et al. argued that ICC neurons of types V, I, and O, respectively, receive their predomina

183 to heart allografts from MHC-mismatched wild-type vs ICAM-1(-/-) donors were tested.

184 les promoted opsonophagocytic killing of GBS type V in vitro, whereas those from placebo recipients d

185 n receptor antagonists and phosphodiesterase type V inhibitor have been shown to be useful to treat t

186 organ development and function depend on the type V intermediate filament proteins, the lamins, which

187 The low abundance fibrillar collagen type V is incorporated into and regulates the diameters

188 The low abundance fibrillar collagen type V is widely distributed in tissues as an alpha1(V)(

189 to the extracellular space (Type I, Type IV, Type V) is required for establishing the symbiosis with

190 A shift of type V isolates into profile 4 subgroups may be indicati

191 Two-thirds of the type V isolates within profile group 4 were classified i

192 es in profile group 4 were highly related to type V isolates, as demonstrated by PFGE profiles, we in

193 strated by PFGE profiles, we investigated 45 type V isolates.

194 ostructural with SIFSIX-14-Cu-i, exhibited a type V isotherm and no phase change.

195 The wild-type V/K(malate) pH-rate profile exhibits the requiremen

196 GANP promoter activity was higher in wild-type vs Lyn-deficient cells.

197 ts in an enzyme that retains 24% of the wild-type V(max) value with a modest 5-fold increase in the K

198 pE and demonstrate that it is secreted via a type V mechanism.

199 nterval, 12.6-883) compared with other clone type/V-MIC combinations.

200 mice expressing restricting MHC on all cell types vs mice that specifically lack restricting MHC on

201 properties of alpha4(V)-containing collagen type V molecules suggest a unique and important role for

202 velopment, Schwann cells synthesize collagen type V molecules that contain alpha4(V) chains.

203 95% CI 0.40-0.65 for KRAS mutant [KRAS wild type vs mutant, pinteraction=0.74]; HR 0.50, 95% CI 0.40

204 CI 0.32-0.89 for PIK3CA mutant [PIK3CA wild-type vs mutant, pinteraction=0.85]) or circulating DNA c

205 etween fitting different datasets (e.g. wild type vs. mutant).

206 edian overall survival of patients with wild-type vs. mutated ATM in MCL.

207 mmetry (e. g. SHE genes) in yeast identified type V myosin among other proteins.

208 MYO2 encodes a type V myosin heavy chain needed for the targeting of va

209 Delivery of Aip3p also requires the type V myosin motor Myo2p and its regulatory light-chain

210 ify She3p as an adaptor protein that links a type V myosin motor to specific ribonucleoproteins.

211 cterize the interaction between Sro7 and the type V myosin Myo2 and show that this interaction is imp

212 late Golgi elements to the bud requires the type V myosin Myo2p, further suggesting that actin plays

213 is most important for ring constriction, and type V myosin Myo51 aids the other two myosins." Zambon

214 the type II myosins Myo2p and Myp2p and the type V myosin Myo51p [2].

215 nization during cytokinesis, distribution of type V myosin Myo52 to the division site, and timely rec

216 Here, we show that the type V myosin myoJ localizes to CV membranes and is requ

217 In addition, this process requires the type V myosin protein Myo2, the microtubule end-binding

218 Myo4p is a nonessential type V myosin required for the bud tip localization of A

219 COPI coatomer subunit in the targeting of a type V myosin to the late Golgi in yeast.

220 We show that Mlc1p, a light chain for Myo2p (type V myosin) and Iqg1p (IQGAP), is the essential light

221 and have delocalized actin patch and myo52p (type V myosin) distributions.

222 vement is specifically dependent on Myo2p, a type V myosin, and not on Myo4p, another type V myosin,

223 sites, bundling by cross-linkers, pulling by type V myosin, and severing by cofilin are simulated as

224 originally identified as a light chain for a type V myosin, Myo2p; however, a cytokinesis defect asso

225 , a type V myosin, and not on Myo4p, another type V myosin, or Myo3p and Myo5p, type I myosins.

226 ecruiting the She2p-mRNA complex to Myo4p, a type V myosin.

227 Finally, the vacuole-specific type-V myosin adapter Vac17p interacts with Atg18p, perh

228 Focalization requires Fus1 and type V myosins and happens asynchronously always in the

229 Type V myosins are essential for fusion and concentrate

230 py and live-cell imaging of Fus1, actin, and type V myosins revealed an aster of actin filaments whos

231 otation and this requires both actin and two type V myosins, Myo51 and Myo52.

232 Type V neurons provide information mainly about ITDs and

233 Type V:NH:E was isolated from 22 (79%) of the 28 patient

234 In type V, no renin was found in the arteriole.

235 Lamins, the type V nuclear intermediate filament proteins, are repor

236 Type V occurred more frequently in the northeast region

237 y widespread answer to these problems is the type V (or autotransporter) secretion pathway.

238 the first biochemical characterization of a type V P-type ATPase, implicates Cod1p in ER function an

239 tition assay between the DeltatoxRS and wild-type V. parahaemolyticus strains marked with the beta-ga

240 The wild-type V pH-rate profile decreases below a pK of 5.2 and i

241 Type V phosphodiesterase (PDE V) metabolizes cyclic guan

242 LTD by a 30 min treatment of slices with the type V phosphodiesterase inhibitor zaprinast (20 microm)

243 sfer of eNOS, alone or in combination with a type V phosphodiesterase inhibitor, may constitute a new

244 he first characterization of an F. nucleatum Type Vd phospholipase class A1 autotransporter (strain A

245 essing of the most prevalent in vivo form of type V procollagen.

246 ette C, containing an IFN-antagonistic, wild-type V protein (rBC), (ii) an isogenic recombinant virus

247 bits minigenome replication as does the wild-type V protein.

248 Type V represents another different three-component syst

249 for common ancestral origins of type III and type V RTKs.

250 For the p-type and one of the n-type v-SAND-based OFETs, the performance (under vacuum a

251 Collagen type V(SC) blocked axonal outgrowth in the presence of o

252 hat in embryonic peripheral nerves, collagen type V(SC) plays a dual role in regulating cell migratio

253 ganglion neurons and Schwann cells, collagen type V(SC) promoted axon fasciculation and association o

254 om Schwann cell conditioned medium (collagen type V(SC)) promoted migration of Schwann cells but inhi

255 mbrane protein IcsA belongs to the family of type V secreted (autotransported) virulence factors.

256 The type V secreted autotransporter serine protease EspP and

257 leatum strains contain genomic expansions of Type V secreted effectors (autotransporters) that are cr

258 detect, track, and characterize the role of Type Vd secreted phospholipases in Gram-negative bacteri

259 Many proteins secreted by the type V secretion system (autotransporters) have been lin

260 are outer membrane proteins belonging to the type V secretion system family, and many have been shown

261 rters (ATs) are exoproteins belonging to the type V secretion system family, with many playing roles

262 and flagella-specific type III, type IV, and type V secretion systems as well as adhesins, invasins,

263 e bacteria exchange polymorphic toxins using type V secretion systems.

264 Whereas the role of Type Vd secretion in bacteria remains unidentified, we s

265 en two different strains of C. elegans (wild-type vs slcf-1 mutant).

266 ting for vesicle-associated membrane protein type v-SNARE proteins (or synaptobrevins) reveals charac

267 ormation by the engineered but not the 'wild type' v-Src, establishing that changes in cellular signa

268 lture conditions, compared with that of wild-type V strains.

269 brains at ages of E13 and P5 (in particular type V), suggesting roles in early neural development an

270 Here we show that an antitoxin from a type V system (GhoS, an endoribonuclease specific for th

271 ependent growth inhibition system (CDI) is a Type V system, using a long beta-helical cell surface pr

272 The type V TGF-beta receptor (TbetaR-V) mediates IGF-indepen

273 The type V TGF-beta receptor (TbetaR-V)/IGFBP-3 receptor med

274 majority of the collagen mass, and collagen type V, the functions of which are poorly understood, is

275 For type V, the relative risk was 0.3 (95% CI, .01-3.1), cor

276 compound 2a is of comparable potency in wild type vs thymidine kinase deficient LM cells.

277 these five proteins inhibited binding of GBS type V to ME-180 cells by > or =85%.

278 ions were equally severe in Fitzpatrick skin types V to VI and I to IV, with minimal erythemal doses

279 The type V transforming growth factor beta (TGF-beta) recept

280 esponse, has recently been identified as the type V transforming growth factor-beta receptor (TbetaR-

281 Tartrate-resistant acid phosphatase (type V) (TRAP) was used as the bait in a biopanning proc

282 vered via diverse secretory systems, such as Type V, Type VI, PVC and a novel PrsW-like intramembrane

283 potent and specific blocker of the vacuolar-type (V-type) ATPase, which eliminates the driving force

284 The membrane rotor ring from the vacuolar-type (V-type) sodium ion-pumping adenosine triphosphatas

285 cines are immunogenic in healthy adults, but type V vaccines have not previously been tested.

286 0.88 for type I/II, type III/IV and advanced type V/VI lesions, respectively (p < 0.03).

287 ups: the first group comprised of vulnerable type V/VI lesions; the second group, stable type I/II le

288 holinergic receptors, Galpha(s), and cardiac types V/VI adenylyl cyclase distribute between caveolae

289 suggest that Schwann cells bind to collagen type V via syndecan-3-dependent binding to a novel high

290 ) increases alternative mRNA splicing of the type V, voltage-gated cardiac Na+ channel alpha-subunit

291 e most common rtxA1 gene variant in clinical-type V. vulnificus encodes a toxin with reduced potency

292 collagen domain of pepsin-digested collagen type V was poorly adhesive for Schwann cells.

293 phas-insensitive mutants of adenylyl cyclase type V were used to test the hypothesis that heterologou

294 pes III and II, followed by either type I or type V, while types IV and VI are the least abundant.

295 The N-propeptide of collagen type V/XI and the NC2 domain of type IX collagen both co

296 All three B-clade type V/XI collagen chains revealed the same three sites

297 nomer is type II as in articular cartilage), type V/XI collagen consisted of a mix of five geneticall

298 Collagen type V/XI is a minor but essential component of collagen

299 ations were obtained when contributions from types V/XI and IX collagen were included in the simulati

300 hancement of NK cell activation through wild-type vs. Y238F mutant NKp44.