ライフサイエンスコーパス: COMP

1 profile Number 1 (24% for HM II vs. 39% for COMP).

2 in, and cartilage oligomeric matrix protein (COMP).

3 ions in cartilage oligomeric matrix protein (COMP).

4 of the cartilage oligomeric matrix protein (COMP).

5 protein cartilage oligomeric matrix protein (COMP).

6 biomarkers of local skin disease, THBS1 and COMP.

7 ay mortality for HM II was 4% versus 11% for COMP.

8 ing of TGF-beta1 to the C-terminal domain of COMP.

9 nding site is present in the TSP3 repeats of COMP.

10 d bacterial pathogens, bind large amounts of COMP.

11 t at 1 year was 85% for HM II versus 70% for COMP.

12 its ADAMTS-7/ADAMTS-12-mediated digestion of COMP.

13 network between GEP, ADAMTS-7/ADAMTS-12, and COMP.

14 fied to be up-regulated transcriptionally by COMP.

15 required and sufficient for association with COMP.

16 t with the other three functional domains of COMP.

17 rocytes, and this stimulation is enhanced by COMP.

18 n in the C-terminal globular domain (CTD) of COMP.

19 er genetic factors influence serum levels of COMP.

20 einase found to bind directly to and degrade COMP.

21 rum levels of the cartilage matrix biomarker COMP.

22 sary and sufficient for its interaction with COMP.

23 required and sufficient for association with COMP.

24 nt COMP forms mixed pentamers with wild type COMP.

25 the glycosylation of the pilin-like protein ComP.

26 fragments clearly distinguishable from total COMP.

27 nt demonstrating a joint tissue source for D-COMP.

28 nificant heritability (PIIANP 0.57, HA 0.49, COMP 0.43, C2C 0.30; P < or = 0.01 for all).

29 A comproportionation rate constant, k(comp) = 1 x 10(6) M(-1) s(-1), was determined by tip pul

30 We show that comp-1 functions in sperm to modulate their migration th

31 Contrary to previously described models, comp-1 mutant sperm show no defects in size or velocity,

32 n Caenorhabditis elegans to identify a gene, comp-1, whose function is specifically required in compe

33 th an adjusted OR of 1.31 per SD increase in COMP (95% CI 1.02-1.68) and adjusted OR of 1.38 per SD i

34 ions in cartilage oligomeric matrix protein (COMP), a pentameric glycoprotein found in cartilage, ten

35 ents of cartilage oligomeric matrix protein (COMP), a prominent noncollagenous matrix component in ar

36 Cartilage oligomeric matrix protein (COMP), a secreted glycoprotein synthesized by chondrocyt

37 effort to define the biological functions of COMP, a functional genetic screen based on the yeast two

38 ollagen IX knock-out but not associated with COMP ablation, indicating specific involvement in the ab

39 e underlying mechanisms, we examined D469del-COMP activation of the unfolded protein response and cel

40 te that cartilage oligomeric matrix protein (COMP) acts as a major endogenous plasma- and platelet-de

41 The repeated modular structure of COMP allows it to "bridge" and assemble multiple cartila

42 ization and further revealed the presence of COMP along with collagens XII and XIV in anchoring plaqu

43 With its modular structure, COMP also has the potential to act as a scaffold for gro

44 hat the cartilage oligomeric matrix protein (COMP), an abundant component of cartilage ECM, is expres

45 mediators in vitro would induce fragments of COMP analogous to natural disease.

46 This suggests that stalling of mutant COMP and an interaction between mutant COMP and type II

47 ECM proteins was observed in 1-month-old WT-COMP and C57BL\6 control mice.

48 We found that ComX, ComP and ComA affect the same set of genes, indicating t

49 he first evidence linking the association of COMP and GEP and identifying a previously unrecognized g

50 Data on COMP and HA levels and extensive joint radiographic and

51 iteria) and obtained sera for measurement of COMP and hyaluronan (HA).

52 ndin E2, and their effects on the release of COMP and its cleavage patterns were characterized.

53 in Cab45 impairs oligomerization, as well as COMP and LyzC sorting.

54 pecifically bind secretory proteins, such as COMP and LyzC, in a Ca(2+)-dependent manner in vitro.

55 ion was associated with dramatically reduced COMP and matrilin-3, consistent with known interactions.

56 were associated with higher serum levels of COMP and NTX (P < 0.05 for each) compared with the no RH

57 indicating the likelihood of baseline serum COMP and NTX levels to be predictive of the development

58 Higher baseline serum COMP and NTX levels were associated with an increased ri

59 isk of RHOA progression with higher baseline COMP and NTX levels.

60 Baseline serum levels of COMP and NTX were measured by enzyme-linked immunosorben

61 An association between COMP and OA has been shown, yet the precise factors gove

62 characterized by intracellular retention of COMP and other extracellular matrix (ECM) proteins, whic

63 We studied the binding interaction between COMP and TGF-beta1 in vitro and determined the effect of

64 We conclude that TGF-beta1 binds to COMP and that TGF-beta1 bound to COMP has enhanced bioac

65 was able to block the prosurvival effect of COMP and the induction of XIAP and survivin, indicating

66 to date cluster in the TSP3 repeat region of COMP and the mutant protein is retained in the rough end

67 le 44 (IFI44) and sialoadhesin (Siglec-1) to COMP and TSP-1 in multiple regression analyses significa

68 utant COMP and an interaction between mutant COMP and type II procollagen are initiating events in th

69 tion in cartilage oligomeric matrix protein (COMP) and confirmed, by mass spectroscopy, the presence

70 Higher baseline ln(COMP) and ln(HA) levels were associated with incident kn

71 -1 (THBS1) and cartilage oligomeric protein (COMP) and stained for myofibroblasts.

72 d genes cartilage oligomeric matrix protein (COMP) and thrombospondin 1 (TSP-1) correlated moderately

73 nity Hospital Comprehensive Cancer Programs (COMPs), and 50 Community Hospital Cancer Programs (CHCPs

74 ein interactions with ADAMTS-7/ADAMTS-12 and COMP, and 2) inhibition of TNFalpha-induced ADAMTS-7/ADA

75 actions between GEP, ADAMTS-7/ADAMTS-12, and COMP, and 2) map the binding sites required for the inte

76 ate that serum concentrations of PIIANP, HA, COMP, and C2C have substantial heritable components, and

77 requencies for 5 genes (ASPN, CALM1, COL2A1, COMP, and FRZB) previously tested for association with h

78 ity, as mutations in Col9a1, Col9a2, Col9a3, Comp, and Matn3 genes cause multiple epiphyseal dysplasi

79 rt by 6 months was 91% for HM II and 80% for COMP, and the Kaplan-Meier survival for patients remaini

80 included COL7A1, COL18A1 (endostatin), DAF, COMP, and VEGFB.

81 Seventy-one percent of NCI-CCCs, 36% of COMPs, and 15% of CHCPs were conducting reflex IHC/MSI f

82 102 also abolished the antileakage effect of COMP-Ang1 at 7 days.

83 ilization by the angiopoietin-1 (Ang1) mimic COMP-Ang1 for 7 days.

84 by GEP is dramatically inhibited by an anti-COMP antibody.

85 In addition, COMP appears to be required for GEP-mediated chondrocyte

86 the epidermal growth factor (EGF) domain of COMP as bait led to the discovery of ADAMTS-7.

87 rsor (GEP), an autocrine growth factor, as a COMP-associated partner.

88 upted along with the distribution of several COMP-binding proteins.

89 COMP binds directly to ADAMTS-7 in vitro and in native a

90 However, it is not known whether COMP binds growth factors.

91 In addition to binding collagen I, COMP binds to collagens XII and XIV via their C-terminal

92 ospondin motifs) was shown to associate with COMP both in vitro and in vivo.

93 Finally, we show that COMP-bound TGF-beta1 causes increased TGF-beta1-dependen

94 the epidermal growth factor repeat domain of COMP but not with the other three functional domains of

95 haADAR1 binding with the GAC hairpin stem in COMP can lead to a non-genetic, RNA editing-mediated sub

96 Mutations in COMP cause two skeletal dysplasias, pseudoachondroplasia

97 he cartilage oligomeric matrix protein gene (COMP) cause pseudoachondroplasia (PSACH).

98 ions in cartilage oligomeric matrix protein (COMP) cause two skeletal dysplasias, pseudoachondroplasi

99 GPP is available online at http://comp.chem.nottingham.ac.uk/glyco/.

100 4.3 for PIIANP (chromosome 8p23.2), 3.2 for COMP (chromosome 8q11.1), 2.0 for HA (chromosome 6q16.3)

101 COMP co-localizes with GEP predominantly in the pericell

102 Binding of COMP correlates with survival of M. catarrhalis in human

103 sn(64)) COMP epitopes (mean 0.95% deamidated COMP (D-COMP) relative to native COMP) in cartilage.

104 fic inhibitor of ADAMTS-7/ADAMTS-12-mediated COMP degradation and may play a significant role in prev

105 The molecular mechanism of COMP degradation and the enzyme(s) responsible for it, h

106 More importantly, GEP inhibited COMP degradation by ADAMTS-7/ADAMTS-12 in a dose-depende

107 ha-induced ADAMTS-7/ADAMTS-12 expression and COMP degradation in cartilage explants was also analyzed

108 e and thus may play an important role in the COMP degradation in the initiation and progression of ar

109 The COMP-degrading activity of ADAMTS-12 requires the presen

110 COMP directly binds to GEP both in vitro and in vivo, as

111 be exposed on the filaments surface and that ComP displays an exquisite binding preference for DNA up

112 Disease-causing mutations in COMP disrupt calcium binding, disulfide bond formation,

113 of deamidated (Asp(64)) and native (Asn(64)) COMP epitopes (mean 0.95% deamidated COMP (D-COMP) relat

114 ding to intracellular accumulation of mutant COMP, especially in chondrocytes.

115 these data suggests a mutation in the CTD of COMP exerts a dominant-negative effect on both intra- an

116 = 0.0156 at 3 weeks), and skin expression of COMP exhibited a strong downward trend in both groups.

117 Because COMP exists as a homopentamer, only one mutant COMP subu

118 and cIAP2 are significantly elevated in the COMP-expressing cells and down-regulation of survivin an

119 ese results suggest a model in which D469del-COMP expression induces persistent endoplasmic reticulum

120 COMP expression is detected in the dermal compartment of

121 rates were similar or lower for HM II versus COMP for all events.

122 nfluenced by the signal peptide that targets COMP for secretion.

123 Additionally, we demonstrate that mutant COMP forms mixed pentamers with wild type COMP.

124 This ELISA quantifies COMP fragments clearly distinguishable from total COMP.

125 Disease-specific COMP fragments were isolated by affinity chromatography

126 Enriched COMP fragments were separated by SDSPAGE followed by in-

127 tified and characterized within the enriched COMP fragments.

128 istinct cartilage oligomeric matrix protein (COMP) fragments derived from cartilage and released into

129 nced the proteolytic cleavage and release of COMP from tendon explants, whereas PGE2 had no catabolic

130 ian) and sexes and indicate a role for ASPN, COMP, FRZB, and COL2A1 in Caucasians.

131 sis of these observations, we postulate that COMP functions as an adapter protein in human skin, simi

132 Cartilage oligomeric matrix protein (COMP) functions as a structural component in cartilage,

133 nse variant, c.1141G>C (p.Asp369His), in the COMP gene (allelic frequency = 0.026%, P = 4.0 x 10(-12)

134 Mutations in the COMP gene cause pseudoachondroplasia (PSACH), a severe d

135 Mutations in the COMP gene cause pseudoachondroplasia and multiple epiphy

136 lar mechanism by which GAC expansions in the COMP gene lead to skeletal dysplasias is poorly understo

137 Genetic variations of the COMP gene may account for some subgroups of benign joint

138 first and second halves of follow-up in the Comp group, were calculated.

139 A separate comparison (Comp) group with unoperated glaucoma (71 eyes of 65 pati

140 The differences between the Trab and Comp groups were significant (P < 0.0001, chi-square tes

141 urea nitrogen were lower in the HM II versus COMP groups, and there were fewer patients in the highes

142 In contrast, the structure of the MT-COMP growth plate recapitulated the findings of human PS

143 COMP haplotypes that were associated with susceptibility

144 a1 binds to COMP and that TGF-beta1 bound to COMP has enhanced bioactivity.

145 n human cartilage oligomeric matrix protein (COMP) have been linked to the development of pseudoachon

146 ents of cartilage oligomeric matrix protein (COMP) have been observed in arthritic patients.

147 population) and were more likely to occur in comp/hom and het individuals with decreased serum phosph

148 Compound heterozygous and homozygous (comp/hom) mutations in solute carrier family 34, member

149 The physiological enzyme(s) that degrade COMP, however, remain unknown.

150 f serum cartilage oligomeric matrix protein (COMP), hyaluronan (HA), high-sensitivity C-reactive prot

151 This study demonstrates the presence of D-COMP in articular cartilage and the systemic circulation

152 Total COMP in cartilage did not vary by joint site or proximit

153 Accumulated COMP in growth plate chondrocytes activates endoplasmic

154 ssion of human mutant (MT) or wild-type (WT) COMP in mice by using a tetracycline-inducible promoter.

155 These data point to a new role for COMP in protecting cells against death.

156 re found to be significantly associated with COMP in regression analysis, taking the effects of these

157 , the functions of both wild-type and mutant COMP in the skeletogenesis remain unknown.

158 ly, we have shown that expression of D469del-COMP in transgenic mice causes intracellular retention o

159 and intact ADAMTS-7 are capable of digesting COMP in vitro.

160 ecombinant ADAMTS-12 is capable of digesting COMP in vitro.

161 deamidated COMP (D-COMP) relative to native COMP) in cartilage.

162 A comparison group (COMP) included all patients (n = 169 at 27 centers) enro

163 emained unextracted, e.g. asporin, CILP, and COMP, indicating cross-linking.

164 the IAP family members were not increased by COMP, indicating that a translational/post-translational

165 owever, in both HeLa cells and chondrocytes, COMP induced survivin mRNA by 5-fold.

166 , we report developmental studies of D469del-COMP-induced chondrocyte pathology from the prenatal per

167 when most chondrocytes are retaining D469del-COMP), inflammation, oxidative stress, and DNA damage co

168 Moreover, COMP inhibits phagocytic killing of M. catarrhalis by hu

169 Altogether, these data suggest that mutant COMP initiates and perhaps catalyzes premature intracell

170 with the Coronal Multi-Channel Polarimeter (CoMP) instrument at the National Solar Observatory, New

171 se findings indicate that ADAMTS-12 is a new COMP-interacting and -degrading enzyme and thus may play

172 COMP interacts directly with the ubiquitous surface prot

173 H chondrocytes, but it is unknown how mutant COMP interacts with these proteins.

174 sveratrol from birth to P28 decreased mutant COMP intracellular retention and chondrocyte cell death,

175 was disrupted, thus alleviating both D469del-COMP intracellular retention and premature chondrocyte c

176 Importantly, COMP is detected in resident macrophages and monocytes,

177 Although mutant COMP is not retained within the rER there is an unfolded

178 Mutant COMP is secreted into the extracellular matrix, but its

179 ame set of genes, indicating that the kinase ComP is the only receptor for the signalling molecule Co

180 Cartilage oligomeric matrix protein (COMP) is a cartilage matrix macromolecule.

181 Cartilage oligomeric matrix protein (COMP) is a component of cartilage, synovium, ligament, a

182 Cartilage oligomeric matrix protein (COMP) is a pentameric extracellular protein expressed in

183 Cartilage oligomeric matrix protein (COMP) is a secreted glycoprotein found in the extracellu

184 Cartilage oligomeric matrix protein (COMP) is an important non-collagenous cartilage protein

185 -3, and cartilage oligomeric matrix protein (COMP) is essential for cartilage matrix stability, as mu

186 n (HA), cartilage oligomeric matrix protein (COMP), keratan sulfate (KS-5D4), aggrecan neoepitope (CS

187 Levels of serum HA, COMP, KS-5D4, and TGFbeta1 increased significantly from

188 Six biomarkers (serum C2C, C1,2C, COMP, KS-5D4, TGFbeta1, and urinary CTX-II) were associa

189 uggest that serum and urine sampling for HA, COMP, KS-5D4, TGFbeta1, CPII, urinary CTX-II, and urinar

190 ene for cartilage oligomeric matrix protein (COMP) leads to pseudoachondroplasia, a skeletal abnormal

191 ated with a significantly reduced mean serum COMP level (P < 0.0001 adjusted for age).

192 association and to test the hypothesis that COMP levels are associated with hypermobility in patient

193 Synovial fluid COMP levels correlated most strongly with the early-phas

194 Synovial fluid COMP levels correlated strongly with 2 indicators of kne

195 Serum COMP levels correlated with the total-body bone scan sco

196 Serum COMP levels correlated with total-body joint disease sev

197 A classic twin study was conducted using COMP levels in serum obtained from healthy female twin v

198 correlation between synovial fluid and serum COMP levels was significant (r = 0.206, P = 0.006).

199 COMP levels were determined by an inhibition enzyme-link

200 geal joint) and knee OA and lower mean serum COMP levels, both in the total cohort and in non-hand-OA

201 correlation of the bone scan scores with the COMP levels.

202 of each joint site to the variance in serum COMP levels.

203 hypermobility is associated with lower serum COMP levels.

204 r serum cartilage oligomeric matrix protein (COMP) levels, and early-onset osteoarthritis (OA) are ph

205 .15-2.89]) increased with higher baseline ln(COMP) levels.

206 HRs per unit increase in ln(COMP), ln(HA), and ln(KS) were higher among knees with c

207 ssion levels of MMP-3, type II collagen, and COMP messenger RNA, which are tightly associated with th

208 Treatment of MT-COMP mice with aspirin or resveratrol from birth to P28

209 esent in the joints of untreated juvenile MT-COMP mice, but were undetectable in treated mice.

210 This inducible transgenic D469del-COMP mouse is the only in vivo model to replicate the cr

211 Using a MT-COMP mouse model of PSACH that recapitulates the molecul

212 Importantly, by crossing the D469del-COMP mouse onto a Chop null background (Ddit3 null), the

213 rom a mouse model of mild PSACH harbouring a COMP mutation.

214 Most COMP mutations identified to date cluster in the TSP3 re

215 sm of PSACH resulting from C-terminal domain COMP mutations remain largely unknown.

216 ndrocytes and in chondrocytes with different COMP mutations, indicating a common pattern of interacti

217 n (HA), cartilage oligomeric matrix protein (COMP), N-propeptide of type IIA collagen (PIIANP), C-pro

218 etinohypothalamic tract (Leak and Moore [] J Comp Neurol 433:312-334).

219 urce code of eCEO is available at http://www.comp.nus.edu.sg/~wangzk/eCEO.html.

220 his equated to an estimated heritability for COMP of 40% (95% CI 20-60%).

221 pidermal growth factor-like repeat domain of COMP of the four functional domains tested.

222 -beta1 in vitro and determined the effect of COMP on TGF-beta1-induced signal transduction in reporte

223 pe and mutant COMP secretion directed by the COMP or BM40 signal peptide in HEK-293 cells and rat cho

224 Cartilage oligomeric matrix protein (COMP), or thrombospondin-5 (TSP-5), is a secreted glycop

225 In a joint replacement study, serum D-COMP (p = 0.017), but not total COMP (p = 0.5), declined

226 udy, serum D-COMP (p = 0.017), but not total COMP (p = 0.5), declined significantly after replacement

227 me the precise mechanisms underlying D469del-COMP pathology in pseudoachondroplasia and suggest that

228 lphavbeta3-binding FN3 monobody with a short COMP pentamerization domain through a linker that facili

229 We find that COMP protects these cells against death, either in the p

230 s from the intracellular retention of mutant COMP protein and premature death of growth-plate chondro

231 Our results demonstrate that mature COMP protein binds to multiple TGF-beta1 molecules and t

232 We further observed that COMP reduces bacterial adhesion and uptake by human lung

233 COMP epitopes (mean 0.95% deamidated COMP (D-COMP) relative to native COMP) in cartilage.

234 he precise factors governing serum levels of COMP remain unclear.

235 n system, we examined the effects of D469del-COMP retention after 4 days of mRNA expression and then

236 before the induction of significant D469del-COMP retention during which endoplasmic reticulum stress

237 D469del-COMP retention was limited prenatally and did not negati

238 icant role in processes that mediate D469del-COMP retention.

239 The comparison of wild type and mutant COMP secretion directed by the COMP or BM40 signal pepti

240 a and multiple epiphyseal dysplasia, disturb COMP secretion leading to intracellular accumulation of

241 Serum levels of COMP showed a correlation of 0.72 (95% confidence interv

242 An Asp(64), D-COMP-specific ELISA was developed using a newly created

243 Retention of D469del-COMP stimulated Chop (Ddit3) and Gadd34 (Ppp1r15a) and t

244 MP exists as a homopentamer, only one mutant COMP subunit may result in an abnormal complex that is a

245 ma file for SBRML is available at http://www.comp-sys-bio.org/SBRML under the Academic Free License (

246 the proposed method are available at http://comp-sysbio.org/miR_Path/ SUPPLEMENTARY INFORMATION: sup

247 e substantially enhances secretion of mutant COMP that accumulates in endoplasmic reticulum-like stru

248 enetic, RNA editing-mediated substitution in COMP that may then play a crucial role in the developmen

249 that activates a receptor histidine kinase (ComP) that activates a response regulator transcription

250 Patients were randomized to mWB (1 U mWB) or COMP therapy (1 U RBC+ 1 U plasma) immediately on arriva

251 of 107 patients were randomized (55 mWB, 52 COMP therapy) over 14 months.

252 Compared with COMP therapy, WB did not reduce transfusion volumes in s

253 ce causes intracellular retention of D469del-COMP, thereby recapitulating pseudoachondroplasia chondr

254 of biochemical markers, i.e., MMP-3, CTX-II, COMP, TIMP-1, Pyr, and Glc-Gal-Pyr, correlated significa

255 3 repeats and the C-terminal domain (CTD) of COMP to 3.15-A resolution limit by X-ray crystallography

256 small interfering RNAs blocks the ability of COMP to enhance survival.

257 ) to search for proteins that associate with COMP to identify an interaction partner that might degra

258 R suggest a molecular model in which D469del-COMP triggers apoptosis during the first postnatal week.

259 caspases indicated that retention of D469del-COMP triggers cell death in chondrocytes by necroptosis,

260 Although COMP/TSP5 abnormalities are associated with several path

261 t this domain can mediate the interaction of COMP/TSP5 and aggrecan.

262 cyte attachment and that the RGD sequence in COMP/TSP5 and the integrin receptors alpha5beta1 and alp

263 olid-phase binding assay, we have shown that COMP/TSP5 can bind aggrecan.

264 se results are the first to demonstrate that COMP/TSP5 can mediate chondrocyte attachment through int

265 We show that COMP/TSP5 can support chondrocyte attachment and that th

266 OMP/TSP5 with the integrins are dependent on COMP/TSP5 conformation.

267 Using recombinant COMP/TSP5 fragments, we found that the "signature domain

268 s undertaken to delineate the function(s) of COMP/TSP5 in cartilage, especially regarding its interac

269 These data indicate that COMP/TSP5 in different conformations can utilize differe

270 Chondrocyte attachment to COMP/TSP5 in the calcium-replete conformation was inhibi

271 In summary, our data indicate that COMP/TSP5 is an aggrecan-binding protein, and this inter

272 Through these interactions, COMP/TSP5 may be able to regulate cellular activities an

273 Our results suggest that COMP/TSP5 may function to support matrix interactions in

274 unction-blocking antibodies, suggesting that COMP/TSP5 mediates attachment through chondrocyte alphaV

275 We also tested a COMP/TSP5 mutant, designated MUT3 that accounts for 30%

276 ther hand, chondrocyte attachment to reduced COMP/TSP5 was instead sensitive to alphaVbeta3 function-

277 Cell attachment to reduced COMP/TSP5 was not inhibited by beta1 antibodies.

278 his binding was decreased with MUT3, or when COMP/TSP5 was treated with EDTA, indicating the presence

279 The interactions of COMP/TSP5 with the integrins are dependent on COMP/TSP5

280 oligomeric matrix protein/thrombospondin 5 (COMP/TSP5) is a major component of the extracellular mat

281 oligomeric matrix protein/thrombospondin 5 (COMP/TSP5) is a major component of the extracellular mat

282 ilar to cartilage oligomeric matrix protein (COMP/TSP5), but its function is unknown.

283 affinity co-electrophoresis, we showed that COMP/TSP5, in its calcium-replete conformation, bound to

284 ns on aggrecan and the "signature domain" of COMP/TSP5.

285 s binding was reduced with EDTA treatment of COMP/TSP5.

286 showed weaker binding than calcium-repleted COMP/TSP5.

287 ted by the calcium-sensitive conformation of COMP/TSP5; interaction of COMP with aggrecan can be medi

288 such as cartilage oligomeric matrix protein (COMP), type II collagen, and Sox9, whereas anti-miR-199a

289 re surrounded by a protein network of mutant COMP, type IX collagen, and MATN3.

290 y transcription factor activated directly by ComP, under the conditions tested.

291 Comp-utational function prediction methods are therefore

292 ype IV pili bind DNA through the minor pilin ComP via an electropositive stripe that is predicted to

293 ject controlled for age, gender, and race, D-COMP was associated with radiographic hip (p < 0.0001) b

294 In contrast, total COMP was associated with radiographic knee (p < 0.0001)

295 The heritability of COMP was determined by comparing correlation among 160 m

296 D-COMP was higher in soluble proteins extracted from hip c

297 1), and cartilage oligomeric matrix protein (COMP) were assessed in serially obtained serum samples.

298 en, and cartilage oligomeric matrix protein (COMP) were examined by quantitative real-time reverse tr

299 t with the other three functional domains of COMP, whereas the four C-terminal TSP motifs of ADAMTS-7

300 ve conformation of COMP/TSP5; interaction of COMP with aggrecan can be mediated through the GAG side

301 s, nor does it require interaction of mutant COMP with other matrix proteins prior to transport from