ライフサイエンスコーパス: COMP

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

2 COMP co-localizes with GEP predominantly in the pericell

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

4 COMP expression is detected in the dermal compartment of

5 COMP haplotypes that were associated with susceptibility

6 COMP interacts directly with the ubiquitous surface prot

7 COMP levels were determined by an inhibition enzyme-link

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

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

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

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

12 l-length pentameric TSP-4, but neither TSP-5/COMP of the pentamer-forming subgroup B nor TSP-2 of the

13 Mutations in the T3 repeats of TSP-5/COMP, which cause two human skeletal disorders, are pred

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

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

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

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

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

19 Accumulated COMP in growth plate chondrocytes activates endoplasmic

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

21 Although COMP/TSP5 abnormalities are associated with several path

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

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

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

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

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

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

28 biomarkers of local skin disease, THBS1 and COMP.

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

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

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

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

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

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

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

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

37 rum levels of the cartilage matrix biomarker COMP.

38 oter, to recruit HDAC1, and to regulate both COMP gene expression and chondrogenic differentiation.

39 rocytes, and this stimulation is enhanced by COMP.

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

41 fied to be up-regulated transcriptionally by COMP.

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

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

44 biomarkers only 4 (serum Coll2-1 NO2, CS846, COMP and urinary CTXII) were consistently associated wit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

71 einase found to bind directly to and degrade COMP.

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

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

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

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

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

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

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

79 tified and characterized within the enriched COMP fragments.

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

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

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

83 4.3 for PIIANP (chromosome 8p23.2), 3.2 for COMP (chromosome 8q11.1), 2.0 for HA (chromosome 6q16.3)

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

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

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

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

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

89 f CS-A and CS-E [4- and 4,6-sulfated CS-GAG (COMP)] matrices compared with monosulfated (4-sulfated)

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

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

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

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

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

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

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

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

98 focal adhesions in F98 cells encapsulated in COMP matrices and blocked CD133 and antichondroitin sulf

99 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

100 Mutations in COMP cause two skeletal dysplasias, pseudoachondroplasia

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

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

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

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

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

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

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

108 .15-2.89]) increased with higher baseline ln(COMP) levels.

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

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

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

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

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

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

115 mechanisms underlying the murine mutant (MT)-COMP model of pseudoachondroplasia, increased midline-1

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

117 egulator of mTORC1, PP2A was evaluated in MT-COMP growth plate chondrocytes.

118 Rapamycin treatment in MT-COMP mice reduced mTORC1 signaling and intracellular ret

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

141 d bacterial pathogens, bind large amounts of COMP.

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

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

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

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

146 3 repeats and the C-terminal domain (CTD) of COMP to 3.15-A resolution limit by X-ray crystallography

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

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

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

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

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

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

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

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

155 t with the other three functional domains of COMP.

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

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

158 102 also abolished the antileakage effect of COMP-Ang1 at 7 days.

159 = 0.0156 at 3 weeks), and skin expression of COMP exhibited a strong downward trend in both groups.

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

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

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

163 LRF showed dose-dependent inhibition of COMP-specific reporter gene activity, and exogenous over

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

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

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

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

168 These data suggest that serum levels of COMP and NTX are modest risk markers for the development

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

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

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

172 er genetic factors influence serum levels of COMP.

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

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

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

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

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

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

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

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

181 RC1 signaling and intracellular retention of COMP, and increased proliferation, but did not change in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

200 Cartilage oligomeric matrix protein (COMP) is a large, multifunctional extracellular protein

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

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

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

204 -3, and cartilage oligomeric matrix protein (COMP) is essential for cartilage matrix stability, as mu

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

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

207 ene for cartilage oligomeric matrix protein (COMP) was the most significantly upregulated.

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

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

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

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

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

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

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

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

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

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

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

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

220 ions in cartilage oligomeric matrix protein (COMP).

221 of the cartilage oligomeric matrix protein (COMP).

222 protein cartilage oligomeric matrix protein (COMP).

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

224 -1 (THBS1) and cartilage oligomeric protein (COMP) and stained for myofibroblasts.

225 ited increased cartilage oligomeric protein, COMP mRNA expression.

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

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

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

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

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

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

232 nd exogenous overexpression of LRF repressed COMP gene expression in both rat chondrosarcoma cells an

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

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

235 Serum COMP levels were measured by enzyme-linked immunosorbent

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

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

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

239 that on average, a 1-unit increase in serum COMP levels increased the probability of radiographic pr

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

241 hypermobility is associated with lower serum COMP levels.

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

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

244 However, sequential measurements of serum COMP levels may identify patients whose OA is likely to

245 The mean +/- SD serum COMP concentration at baseline was significantly higher

246 The data suggest that serum COMP is related to progressive joint damage in knee OA.

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

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

249 Disease-specific COMP fragments were isolated by affinity chromatography

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

270 Mutations in the COMP gene cause pseudoachondroplasia and multiple epiphy

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

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

273 previously cloned the promoter region of the COMP gene and delineated a minimal negative regulatory e

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

275 ription factor found to bind directly to the COMP gene promoter, to recruit HDAC1, and to regulate bo

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

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

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

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

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

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

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

283 fragments clearly distinguishable from total COMP.

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

285 nt COMP forms mixed pentamers with wild type COMP.

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

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

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

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

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

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

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

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

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

295 required and sufficient for association with COMP.

296 required and sufficient for association with COMP.

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

298 sary and sufficient for its interaction with COMP.

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

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