ライフサイエンスコーパス: procollagen

1 t one ligand in extracellular matrix (type I procollagen).

2 erfered with the intracellular maturation of procollagen.

3 involved in prolyl 3-hydroxylation in type I procollagen.

4 d with increased intracellular expression of procollagen.

5 reduced levels of phospho-Smad2/3 as well as procollagen.

6 ll expressed monocyte/macrophage markers and procollagen.

7 t markedly increased the half-life of type I procollagen.

8 ed a 3-fold increase in intracellular type I procollagen.

9 arkers, most notably expression of alpha1(I) procollagen.

10 ting some involvement in the biosynthesis of procollagens.

11 ting some involvement in the biosynthesis of procollagens.

12 eatment, causing dose-dependent increases in procollagen 1 and transforming growth factor-beta1 mRNA

13 sue inflammation, and identical increases in procollagen 1 mRNA expression, following sensitization a

14 as accompanied by markedly increased CD34(+)/procollagen 1(+) fibrocytes.

15 We show in vivo the presence of CD163(+)/procollagen-1(+)/osteocalcin(+) cells in the fibrotic an

16 as evidenced by their expression of mRNA for procollagen 1alpha1.

17 ymal markers S100A4, vimentin, alpha-SMA, or procollagen 1alpha2, although these proteins were abunda

18 Procollagen 3 and alphaSMA are regulated by distinct mec

19 n between ALI/ARDS BALF-induced alphaSMA and procollagen 3 induction (r = -.08, p = .66).

20 as shown by the inverse levels of Ki-67 and procollagen-3 N-terminal peptide versus osterix, and (ii

21 Markers of remodeling such as MMP-9, procollagen-3, and tenascin C were observed in all acute

22 creted proteins but a profound, 5-fold lower procollagen 4-hydroxyproline content and enhanced cystei

23 Type I procollagen accumulates in the Golgi of fibroblasts from

24 The extent of procollagen accumulation and PDI/P4H1 binding differs am

25 d less fibrosis and less staining for type I procollagen after imatinib mesylate treatment, but essen

26 It is generally accepted that LH2 modifies procollagen alpha chains on the endoplasmic reticulum be

27 ing NADPH oxidase activation and its link to procollagen alpha1 (I) and TGF-beta1 expression in an im

28 f apoptotic bodies by stellate cells induces procollagen alpha1 (I) and transforming growth factor be

29 d in a significant decline in TACE activity, procollagen alpha1 (I), alpha smooth muscle actin (alpha

30 idase activation resulted in upregulation of procollagen alpha1 (I); in contrast, TGF-beta1 expressio

31 Fibrosis-related transcripts including procollagen alpha1(I) (CoL1A), TIMP1, and MMP3 mRNA were

32 vivo evidence of an up to 90% suppression of procollagen alpha1(I) expression, a reduction of septa f

33 les loaded with small interfering RNA to the procollagen alpha1(I) gene specifically reduce total hep

34 les loaded with small interfering RNA to the procollagen alpha1(I) gene were retained in the liver of

35 les loaded with small interfering RNA to the procollagen alpha1(I) gene.

36 fibrolytic genes in HSCs, down-regulation of procollagen alpha1(I) messenger RNA, and blunting of pro

37 ncrease in profibrogenic transcripts Col1a1 [procollagen alpha1(I)], Tgfb1, and Timp1.

38 prominence of a homotrimeric form of type I procollagen (alpha1 trimer) during vertebrate developmen

39 rates of proliferation and the expression of procollagen-alpha1 was inhibited significantly in vitro

40 d expressing CD133, cytokeratin (CK)7, CK19, procollagen-alpha1(I), and Snail at day 5 after heat exp

41 d mRNA expression for collagen alpha1(1) and procollagen alpha2(1).

42 osteogenesis imperfecta mouse (OIM), lacking procollagen-alpha2(I) expression, represents a model of

43 s, a human HSC line, increases expression of procollagen alphaI and procollagen alphaIII mRNA and the

44 enosine A2A receptor-mediated stimulation of procollagen alphaI mRNA and collagen type I collagen exp

45 enosine A2A receptor-mediated stimulation of procollagen alphaIII mRNA and collagen type III protein

46 creases expression of procollagen alphaI and procollagen alphaIII mRNA and their translational protei

47 Mutations in ADAMTS2, a procollagen amino-propeptidase, cause severe skin fragil

48 opeptide, aminoterminal propeptide of type I procollagen, aminoterminal propeptide of type III procol

49 lloproteinases-1, and propeptide of type III procollagen and calculated ELF scores by the previously

50 odate a wide range of bulky cargo, including procollagen and chylomicrons, that is sensitive to adapt

51 YR61 expression substantially reduces type I procollagen and concurrently increases matrix metallopro

52 /porous cortical bone, reduced processing of procollagen and dentin matrix protein 1, remarkably high

53 mass spectrometry suggested types I and III procollagen and fibronectin as candidate ligands.

54 ivated receptors and decreased expression of procollagen and matrix metalloproteinases in mice fed MC

55 th factor-beta pathway, which reduced type I procollagen and raised MMP-1 expression.

56 uring posttranslational maturation of type I procollagen and that FKBP65 and HSP47 but fail to proper

57 UV irradiation-induced inhibition of type-I procollagen and upregulation of MMP-1.

58 AMTS proteases are involved in maturation of procollagen and von Willebrand factor, as well as in ext

59 structure and/or metabolism of the resultant procollagen and/or collagen protein and its function in

60 cells co-localized with PDGF receptor beta, procollagen, and periostin.

61 end products, surfactant protein-B, type III procollagen, and pro-caspase 3.

62 interaction between mutant COMP and type II procollagen are initiating events in the assembly of mat

63 HSP47 binds procollagen at a neutral pH but releases at a pH similar

64 the integrity of the triple helix of type I procollagen at the ER/cis-Golgi boundary and, when absen

65 order of action for CRTAP, P3H1 and CYPB in procollagen biosynthesis and pathogenesis of OI.

66 e partially restores the stability of mutant procollagen but not sufficiently to prevent N-anchor unf

67 nism of PCPE-1 whereby PCPE-1 interacts with procollagen, but in addition, the CUB3 domain of BMP-1 a

68 ssion, whereas overexpressing CTGF increased procollagen by a TGF-beta/Smad signaling-dependent mecha

69 matrix, enhances the cleavage of C-terminal procollagen by bone morphogenetic protein 1 (BMP1).

70 ted by a lower in vitro production of type I procollagen by dermal fibroblasts isolated from skin of

71 genes expressed in fibroblasts--collagen I, procollagen C endopeptidase enhancer 1, secreted protein

72 en C proteinases (pCPs) cleave type I to III procollagen C propeptides as a necessary step in assembl

73 The protein PCOLCE1 (procollagen C proteinase enhancer 1) is not a proteinase

74 Procollagen C proteinases (pCPs) cleave type I to III pr

75 We showed that fibulin-4 binds procollagen C-endopeptidase enhancer 1 (Pcolce), which e

76 have shown a significant correlation between procollagen C-endopeptidase enhancer protein 2 (PCPE2) s

77 ing activity requires binding of PCPE to the procollagen C-propeptide trimer, identification of the p

78 g that PCPE binds to the stalk region of the procollagen C-propeptide trimer, where the three polypep

79 We showed that the minimal procollagen C-proteinase (BMP-1 lacking the EGF and CUB3

80 r epidermal growth factor-like domains, have procollagen C-proteinase (pCP) activity and activity for

81 nc metalloproteinases, is a highly effective procollagen C-proteinase (PCP) and chordinase.

82 o as measured by a fluorogenic peptide based procollagen C-proteinase activity assay.

83 with intact COOH termini are enhanced by the procollagen C-proteinase enhancer 1 (PCOLCE1) and that m

84 teinases, is itself subject to regulation by procollagen C-proteinase enhancer proteins (PCPEs) which

85 by mTLL-2 in the presence of high levels of procollagen C-proteinase enhancer-1 (PCPE-1), for reason

86 , which enhances proteolytic cleavage of the procollagen C-terminal propeptide during procollagen pro

87 cleavage of CI and CII [C1,2C], and type II procollagen carboxy-propeptide [CPII] in serum, and C-te

88 lpha1(V) and human recombinant pro-alpha1(V) procollagen chains.

89 her in the most C-terminal domains of type I procollagen chains.

90 SERPINH1 and FKBP10, which encode the type I procollagen chaperones HSP47 and FKBP65, respectively, a

91 omains in BMP-1 and mTLL-2 did not result in procollagen cleavage and 2) the proteinase domain of mTL

92 Interestingly, however, procollagen cleavage was not affected by the presence or

93 ECM), including the expression of alpha2 (1) procollagen (Col1A2) and fibronectin 1 (FN), was seen in

94 but presumably the dissociation of the HSP47-procollagen complex is triggered by the lower pH in the

95 the molecular mechanism of transportation of procollagen containing vesicles for secretion is unknown

96 A collagen (PIIANP), C-propeptide of type II procollagen (CPII), and type II collagen neoepitope (C2C

97 Here this enzyme is identified as C-terminal procollagen endoproteinase/bone morphogenetic protein-1

98 ut instead by addition of ERGIC membranes to procollagen-enriched domains of the ER by a TANGO1-media

99 located at the ER exit site is necessary for procollagen export.

100 chemokines and cytokines, and the number of procollagen-expressing M2 macrophages in injured kidneys

101 inate decrease in CTGF, TGF-beta, and type I procollagen expression and content.

102 mad/CTGF axis likely mediates reduced type I procollagen expression in aged human skin in vivo.

103 icate that in human skin fibroblasts, type I procollagen expression is dependent on endogenous produc

104 st, overexpression of CTGF stimulated type I procollagen expression, and increased promoter activity.

105 lockade in normal dermal fibroblasts reduced procollagen expression, whereas overexpressing CTGF incr

106 y Smad7 abolished CTGF stimulation of type I procollagen expression.

107 ated UV-A1 exposures did not suppress type I procollagen expression.

108 wer surfactant protein-B and higher type III procollagen expressions compared with STEP-30/30.

109 ncrease their size to accommodate 300-400 nm procollagen fibres or chylomicrons.

110 Simvastatin significantly upregulated procollagen, fibronectin, and matrix metalloproteinase-1

111 organization was identified in which type II procollagen formed a central core surrounded by a protei

112 Regulation of type I procollagen gene (COL1A2) transcription by TGF-beta invo

113 Alternative splicing of the type II procollagen gene (COL2A1) is developmentally regulated d

114 mini-gene consisting of part of the type II procollagen gene (COL2A1), we show that TIA-1 interacts

115 t alter matrix metalloproteinase 1 or type I procollagen gene expression.

116 ages showed increases in proinflammatory and procollagen genes and decreases in genes regulating memb

117 result from dominant mutations in the type I procollagen genes, but mutations in a growing number of

118 up-regulation of cytokine, cell cycling, and procollagen genes.

119 The folding mechanism of type I procollagen has been well characterized, and protein dis

120 s essential for efficient assembly of type I procollagen heterotrimers.

121 P4H enzyme activity, which is essential for procollagen hydroxylation and secretion.

122 the transport of large cargo, such as 300-nm procollagen I (PC1) molecules, from the endoplasmic reti

123 ation, partly via biosynthetic processing of procollagen I and DMP1, provides novel insights into key

124 a concentrations of key collagen precursors (procollagen I and III N-terminal propeptides [PINP, PIII

125 tin-positive myofibroblasts, reduced hepatic procollagen I and tissue inhibitor of metalloproteinase

126 nces of the bound SPARC to the C-terminus of procollagen I and to the closest end of collagen I.

127 of inhibiting the biosynthetic processing of procollagen I by cells.

128 a1), connective tissue growth factor (CTGF), procollagen I carboxy-terminal propeptide (PICP), amino-

129 Alternatively, disruption of procollagen I ER export could activate the unfolded prot

130 increased alpha-smooth muscle cell actin and procollagen I expression as well as induced transforming

131 required for the export of the equally bulky Procollagen I from the ER.

132 we found that cleavage of full-length human procollagen I heterotrimers by either meprin alpha or me

133 cell layers and decreased the processing of procollagen I in SPARC-null cells.

134 ydroxylation of specific proline residues in procollagen I in vitro.

135 Autophagic vesicles and more procollagen I molecules were present in the cytoplasm of

136 osparactic fibroblasts, suggesting a role in procollagen I processing during musculoskeletal developm

137 ADAMTS3 induced procollagen I processing in dermatosparactic fibroblasts

138 In vitro, procollagen I produced by SPARC-null dermal fibroblasts

139 of the SPARC-binding sites on collagen I and procollagen I provides useful information for further un

140 Loss of TANGO1 leads to procollagen I retention in the ER, which promotes UPR-me

141 Disruption of secretion led to procollagen I retention within the ER, induction of the

142 We investigated the role of TANGO1 in procollagen I secretion in HSCs and liver fibrogenesis.

143 NA Hic-5 knockdown mesangial cells increased procollagen I transcription to a lesser degree after 48

144 Hic-5 expression within 2-4 h and increased procollagen I transcription within 12 h, whereas adding

145 ase-1 (MMP-1), was decreased, while elastin, procollagen I type I, fibronectin, COL1alpha1, and tissu

146 ndicate that Col-I and aggregated, insoluble procollagen I undergo intracellular degradation via auto

147 tudy, the binding of SPARC to collagen I and procollagen I was verified by surface plasmon resonance.

148 The SPARC-binding sites on collagen I and procollagen I were identified by directly visualizing th

149 clude that SPARC mediates the association of procollagen I with cells, as well as its processing and

150 broad distribution of SPARC binding sites on procollagen I with the most preferred binding region loc

151 the uncleaved precursor of type I collagen (procollagen I) and a reduction in dentin matrix protein

152 +/-0.7%; P<0.05), expression of fibronectin, procollagen I, and connective tissue growth factor mRNA,

153 ighly enriched for mRNAs encoding periostin, procollagen I, fibronectin I, vimentin, discoidin domain

154 and three markers of osteoblastic activity, procollagen I, osteocalcin, and alkaline phosphatase.

155 on several of its known substrates including procollagen I, procollagen III, pN-collagen V, and proly

156 These EPDCs also stained positive for procollagen I, suggesting that the EPDCs themselves synt

157 pression profile in penile tissue (including procollagen I, TGF-beta(1), and plasminogen activator in

158 Fibrogenic signals drive transcription of procollagen I, which enters the endoplasmic reticulum (E

159 In contrast, procollagen I, with its large globular C-propeptide, per

160 ARC interacts with the collagen I precursor, procollagen I.

161 gen), and tissue levels of messenger RNA for procollagens I and III and for TGFbeta1 and TGFbeta2.

162 like proteinases cleave the C-propeptides of procollagens I-III.

163 t the binding of monomeric (inactive) LH2 to procollagen Ialpha1.

164 is study shows that MAGP-2 stabilizes type I procollagen, identifying an important function of MAGP-2

165 lls expressing R75C, R519C, R789C, and G853E procollagen II mutants, we found that the R789C mutation

166 hexapeptide derived from the C-propeptide of procollagen IIalpha1 (i.e. chondrocalcin).

167 result of reduced collagen turnover, because procollagen III (alpha1) mRNA levels and fractional coll

168 22, P<0.001) and aminoterminal propeptide of procollagen III (beta=0.12, P=0.035) at follow-up when a

169 thout advanced fibrosis, terminal peptide of procollagen III (PIIINP) was the only marker found to be

170 A missense point mutation in the procollagen III amino terminal propeptide segment (PIIIN

171 tissue inhibitor of metalloproteinase 1, and procollagen III aminopeptide were measured and entered i

172 Plasma procollagen III N-terminal peptide was not associated wi

173 We related plasma TIMP-1, procollagen III N-terminal peptide, and MMP-9 to the inc

174 1 (TIMP-1), metalloproteinase-9 (MMP-9), and procollagen III N-terminal peptide.

175 ntrations were quantified by Luminex, plasma procollagen III N-terminal propeptide (PIIINP) by enzyme

176 Procollagen III N-terminal propeptide (PIIINP) was 3.8-f

177 Serial procollagen III peptide (PIIINP) results were recorded.

178 Procollagen III peptide, TE, and FibroTest results, as w

179 amts2(-/-) mice showed widespread defects in procollagen III processing.

180 ts known substrates including procollagen I, procollagen III, pN-collagen V, and prolysyl oxidase.

181 I collagen, and aminoterminal propeptide of procollagen III.

182 of liver fibrosis such as hyaluronic acid or procollagen-III-peptide.

183 explains the presence of some processed skin procollagen in dermatosparaxis.

184 a with a time course coincident with that of procollagen in the airways.

185 ouse embryonic fibroblasts show retention of procollagen in the cell layer and associated dilated end

186 t we have tested but induces accumulation of procollagen in the endoplasmic reticulum when expressed

187 elease both C- and N-propeptides from type I procollagen in vitro and in vivo and contribute to the i

188 ity against Chordin, probiglycan, and type I procollagen in vitro.

189 xtracellular processing of newly synthesized procollagen into mature collagen fibrils.

190 Type I procollagen is a heterotrimer composed of two proalpha1(

191 Reduced production of type I procollagen is a prominent feature of chronologically ag

192 L-2) does not cleave chordin or procollagen; procollagen is cleaved by mTLL-2 in the presence of high

193 us BMP1 substrates Chordin, probiglycan, and procollagen is demonstrated to be strikingly reduced in

194 The supramolecular cargo procollagen is loaded into coat protein complex II (COPI

195 dual and a population of the secreted type I procollagen is protease sensitive.

196 ntiated chondrocytes synthesize the type IIB procollagen isoform by exon 2 skipping (exclusion).

197 Chondroprogenitor cells produce the type IIA procollagen isoform by splicing (including) exon 2 durin

198 PLOD2 (procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2) hydr

199 , and ascorbic acid supplementation improved procollagen maturation and lowered sulfenic acid content

200 hat exogenously added Sfrp2 inhibited type I procollagen maturation in primary cardiac fibroblasts.

201 FKBP10, PLOD2 and SERPINH1, that act during procollagen maturation to contribute to molecular stabil

202 AGP-2 overexpression had no effect on type I procollagen messenger RNA, but markedly increased the ha

203 me proliferator-activated receptor alpha and procollagen messenger RNA.

204 Assembly of the type I procollagen molecule begins with interactions among the

205 slow to assemble into trimers, and abnormal procollagen molecules concentrate in the RER, and bind t

206 ffected infant make some overmodified type I procollagen molecules.

207 culum before the formation of triple helical procollagen molecules.

208 bstantially reduced the expression of type I procollagen mRNA, protein, and promoter activity.

209 nduced expression of alpha1(I) and alpha2(I) procollagen mRNAs.

210 pha1(I), alpha2(I), alpha1(V), and alpha2(V) procollagen mRNAs.

211 anases (ADAMTS1, 4, 5, 8, 9, 15 and 20), the procollagen N-propeptidases (ADAMTS2, 3 and 14), the car

212 se mutations prevent or delay removal of the procollagen N-propeptide by purified N-proteinase (ADAMT

213 n of the NH(2)-terminal propeptide of type I procollagen (N-propeptide) is poorly understood.

214 ADAMTS, as exemplified by the actions of the procollagen-N-propeptidases in collagen fibril assembly

215 ked beta C-telopeptide (betaCTX), and type 1 procollagen-N-propeptide (P1NP).

216 oduction or post-translational processing of procollagen or alter bone homeostasis.

217 [CTX], and N-terminal propeptides of type I procollagen [P1NP]) markers were measured.

218 ain receptor 2 expression was unchanged, but procollagen peptide I and III expression and collagen ty

219 molecular mechanisms that govern binding to procollagen peptides and triple helices in the endoplasm

220 els of serum C-terminal propeptide of type I procollagen (PICP) were significantly higher in mutation

221 (TIMP-1), amino-terminal peptide of type III procollagen (PIIINP), hyaluronic acid (HA), and YKL-40 l

222 N-terminal propeptide of type I procollagen (PINP) and C-telopeptide of type I collagen

223 Procollagens, pre-chylomicrons, and pre-very low-density

224 ties that include biosynthetic processing of procollagen precursors into mature collagen monomers.

225 C-terminal proteolytic processing of soluble procollagen precursors.

226 CRT(-/-) MEFs also have reduced type I procollagen processing and deposition into the extracell

227 ing identified multiple proteins involved in procollagen processing and maturation as potential fibul

228 hat SPARC plays a key role in post-synthetic procollagen processing and the development of mature cro

229 concentration inhibited human and rat type I procollagen processing by Bmp1 in vitro.

230 e (SPARC) plays a key role in post-synthetic procollagen processing in normal and pressure-overloaded

231 the procollagen C-terminal propeptide during procollagen processing.

232 ospho-eIF2alpha, thus suggesting a defect in procollagen processing.

233 d like-2 (mTLL-2) does not cleave chordin or procollagen; procollagen is cleaved by mTLL-2 in the pre

234 cell response to immune activation increased procollagen production and subsequent deposition as fibr

235 n dermal fibroblasts and no effect on type I procollagen production by these cells.

236 stitial collagenase) were reduced and type I procollagen production was increased.

237 ting in depletion of ascorbic acid, impaired procollagen proline 4-hydroxylation, and a noncanonical

238 gene constructs of proximal 2.2-kb alpha1(I) procollagen promoter to demonstrate that a region proxim

239 agen (CII) messenger RNA, C-terminal type II procollagen propeptide (CPII), the collagenase cleavage

240 B collagen messenger RNA, C-terminal type II procollagen propeptide (CPII), the collagenase cleavage

241 r of metalloproteinases 2, C-terminal type I procollagen propeptide (PICP), and the immature collagen

242 C1 fed a high-fat diet increased the hepatic procollagen protein level, suggesting a role in the deve

243 nd COL1A2, which encode the chains of type I procollagen, result in dominant forms of OI, and mutatio

244 tivity of FKBP65 has several effects: type I procollagen secretion is slightly delayed, the stabiliza

245 reflect a diminished amount of normal type I procollagen, small populations of overmodified heterotri

246 Hsp47/SERPINH1 is a procollagen-specific molecular chaperone that, unlike ot

247 oxylation of (2 S)-proline (Pro) residues in procollagen strands.

248 cent protein, alpha-smooth muscle actin, and procollagen, suggesting that a population of cells formi

249 associated with a marked reduction in type I procollagen synthesis and impairment in adhesion.

250 roteins on the membrane is required to cargo procollagen than other molecules and suggest that the SE

251 Langerin bound to type I procollagen that was immunoprecipitated from fibroblast

252 ) with that of supramolecular cargoes (e.g., procollagen) that are proposed to traverse the Golgi by

253 fects on mRNA transcript levels of fibrillar procollagens, their modifying enzymes, small leucin-rich

254 e proteinases act to proteolytically convert procollagens to the major fibrous components of the extr

255 necessary for collagen precursor molecules (procollagens) to acquire final shape and function.

256 riction, yet inhibited Sar1 organization and procollagen transport from the endoplasmic reticulum (ER

257 wo modules are presented in more detail, the procollagen type 1 alpha2 gene and the ADAM17/tumor necr

258 d lead, plasma biomarkers of bone formation (procollagen type 1 amino-terminal peptide (PINP)) and re

259 of bone formation, including osteocalcin and procollagen type 1 N propeptide.

260 Serum procollagen type 1 N-terminal propeptide (P1NP) and urin

261 f type I collagen (CTX)) and bone formation (procollagen type I amino-terminal peptide (PINP)) were e

262 th muscle actin expression, and synthesis of procollagen type I and eotaxin-1.

263 n, increased fibrosis intensity (assessed by procollagen type I carboxy-terminal propeptide [PICP]),

264 rved increased alpha-smooth muscle actin and procollagen type I mRNAs, large fibrotic areas in alpha-

265 markers (osteoprotegerin [OPG], osteocalcin, procollagen type I N-terminal propeptide, and C-terminal

266 AFs synthesized more procollagen type I than did DLFs at baseline (twofold hi

267 n of structural changes, serum propeptide of procollagen type I, a marker of the deposition of type I

268 p and included carboxyterminal propeptide of procollagen type I, carboxyterminal telopeptide of type

269 growth factor, hepatocyte growth factor, and procollagen type I.

270 caused by dominant-negative mutations in the procollagen type III (COL3A1) gene.

271 The level of N-terminal propeptide of procollagen type III (PIIINP) was significantly higher i

272 ing growth factor-beta-mediated induction of procollagen type III and tenascin-C in isolated cardiac

273 -10, specific markers of cardiac remodeling (procollagen type III N-terminal peptide, matrix metallop

274 Higher urine levels of procollagen type III N-terminal propeptide (PIIINP) mark

275 sforming growth factor- beta (TGF-beta), and procollagen type III N-terminal propeptide (PIIINP), wit

276 ansforming growth factor-beta (TGF-beta) and procollagen type III N-terminal propeptide (PIIINP), wit

277 are caused by a semidominant mutation in the procollagen type IV alpha 1 gene (Col4a1) in mice, which

278 mutation in the mouse Col4a1 gene, encoding procollagen type IV alpha1, predisposes both newborn and

279 owest tertile, higher levels of osteocalcin, procollagen type-1 N-terminal propeptide, and tartrate-r

280 e in the upper two tertiles for osteocalcin, procollagen type-1 N-terminal propeptide, or tartrate-re

281 ient increases in the bone formation markers procollagen type-I N-terminal propeptide (PINP), osteoca

282 alysis, aminoterminal propeptide of type III procollagen/type 1 collagen telopeptide ratio </=1 (odds

283 ide and aminoterminal propeptide of type III procollagen/type 1 collagen telopeptide ratio </=1, meas

284 Low aminoterminal propeptide of type III procollagen/type 1 collagen telopeptide ratio (</=1) at

285 Western blotting with antibodies specific to procollagen types Iota and IotaIotaIota.

286 F and higher C-terminal propeptide of type I procollagen values also had higher mean pulmonary artery

287 einase-2 and C-terminal propeptide of type I procollagen values than hypertensive controls.

288 8, however only Syntaxin 18 was required for Procollagen VII export.

289 n is required for TANGO1-dependent export of procollagen VII from the endoplasmic reticulum (ER).

290 TANGO1 binds and exports Procollagen VII from the endoplasmic reticulum (ER).

291 Knockdown of SLY1 by siRNA arrested Procollagen VII in the ER without affecting the recruitm

292 TANGO1 is thus pivotal in concentrating procollagen VII in the lumen and recruiting ERGIC membra

293 ntermediate Compartment (ERGIC) membranes to procollagen VII-enriched patches on the ER.

294 f this individual revealed that ER export of procollagen was inefficient and that ER tubules were dil

295 Procollagen was retained intracellularly with concomitan

296 bitor 1, and C-terminal propeptide of type I procollagen were determined in 28 patients with HFpEF an

297 llagen, aminoterminal propeptide of type III procollagen) were measured 1 month after MI in 218 patie

298 proteins traverse the Golgi much faster than procollagen while moving through the same stack.

299 nd post-translational modification of type I procollagen, without which bone mass and quality are abn

300 ction of both TANGO1 and TALI, the export of procollagen XII by the same cells requires only TANGO1.