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 concentrations at baseline and the area under the c

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

5 COMP expression is detected in the dermal compartment of

6 COMP haplotypes that were associated with susceptibility

7 COMP interacts directly with the ubiquitous surface prot

8 COMP levels were determined by an inhibition enzyme-link

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

70 einase found to bind directly to and degrade COMP.

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

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

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

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

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

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

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

78 tified and characterized within the enriched COMP fragments.

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

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

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

82 4.3 for PIIANP (chromosome 8p23.2), 3.2 for COMP (chromosome 8q11.1), 2.0 for HA (chromosome 6q16.3)

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

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

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

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

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

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

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

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

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

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

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

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

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

96 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

97 Mutations in COMP cause two skeletal dysplasias, pseudoachondroplasia

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

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

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

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

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

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

104 In adjusted models, ln COMP was higher in African American women than in Caucas

105 Levels of ln COMP were associated with age, BMI, and all definitions

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

107 .15-2.89]) increased with higher baseline ln(COMP) levels.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 d bacterial pathogens, bind large amounts of COMP.

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

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

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

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

142 3 repeats and the C-terminal domain (CTD) of COMP to 3.15-A resolution limit by X-ray crystallography

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

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

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

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

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

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

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

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

151 t with the other three functional domains of COMP.

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

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

154 102 also abolished the antileakage effect of COMP-Ang1 at 7 days.

155 = 0.0156 at 3 weeks), and skin expression of COMP exhibited a strong downward trend in both groups.

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

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

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

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

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

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

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

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

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

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

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

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

168 er genetic factors influence serum levels of COMP.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

187 vels of cartilage oligomeric matrix protein (COMP) and ethnicity (African American or Caucasian) and

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

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

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

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

192 e human cartilage oligomeric matrix protein (COMP) gene have been linked to the development of pseudo

193 in the cartilage oligomeric matrix protein (COMP) gene to the 4, 6 or 7mers in the etiology of pseud

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

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

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

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

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

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

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

201 -3, and cartilage oligomeric matrix protein (COMP) is essential for cartilage matrix stability, as mu

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

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

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

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

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

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

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

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

210 , serum cartilage oligomeric matrix protein (COMP), are related to disease outcome over a 5-year peri

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

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

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

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

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

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

217 ions in cartilage oligomeric matrix protein (COMP).

218 of the cartilage oligomeric matrix protein (COMP).

219 protein cartilage oligomeric matrix protein (COMP).

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

221 -1 (THBS1) and cartilage oligomeric protein (COMP) and stained for myofibroblasts.

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

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

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

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

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

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

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

229 Serum COMP concentrations were higher during periods of radiog

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

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

232 Serum COMP levels rose significantly after TKR; however, after

233 Serum COMP levels were measured by enzyme-linked immunosorbent

234 Serum COMP levels were quantified by sandwich enzyme-linked im

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

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

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

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

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

240 hypermobility is associated with lower serum COMP levels.

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

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

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

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

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

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

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

248 Disease-specific COMP fragments were isolated by affinity chromatography

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

269 Mutations in the COMP gene cause pseudoachondroplasia and multiple epiphy

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

271 ponsible for triplet repeat mutations in the COMP gene.

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.