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

5 ll expressed monocyte/macrophage markers and procollagen.

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

7 d with increased intracellular expression of procollagen.

8 ting some involvement in the biosynthesis of procollagens.

9 ting some involvement in the biosynthesis of procollagens.

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

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

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

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

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

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

16 Procollagen 3 and alphaSMA are regulated by distinct mec

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

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

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

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

21 Type I procollagen accumulates in the Golgi of fibroblasts from

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 Here, analyzing endogenous procollagen and a new engineered GFP-tagged form, we sho

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

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

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

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

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

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

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

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

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

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

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

58 transport of large matrix proteins, such as procollagen, and are implicating less well-defined carri

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

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

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

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

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

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

65 CM in a dose-dependent manner and that, like procollagen, BMP-1 colocalizes with FN fibrils in the ma

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

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

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

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

70 emoval of N- and C-terminal propeptides from procollagens by metalloproteinases of the ADAMTS (a disi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 ed, addition of heparin enhanced the rate of procollagen cleavage by matrix-bound BMP-1.

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

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

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

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

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

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

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

93 he formation of a transport intermediate for procollagen export.

94 fies key biophysical events in TANGO1-driven procollagen export.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 ed collagen proportional area (p < 0.04) and procollagen I and III expression.

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

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

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

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

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

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

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

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

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

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

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

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

130 ADAMTS3 induced procollagen I processing in dermatosparactic fibroblasts

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

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

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

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

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

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

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

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

139 BMP-1-FN interactions and BMP-1 cleavage of procollagen I were both enhanced by the presence of hepa

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

141 of a fibroblast ECM showed colocalization of procollagen I with FN fibrils, and proteolytic cleavage

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

143 +/-0.7%; P<0.05), expression of fibronectin, procollagen I, and connective tissue growth factor mRNA,

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

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

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

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

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

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

150 iring enzyme 1alpha (IRE1alpha) in a SMAD2/3-procollagen I-dependent manner.

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

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

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

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

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

156 22, P<0.001) and aminoterminal propeptide of procollagen III (beta=0.12, P=0.035) at follow-up when a

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

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

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

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

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

162 1 (TIMP-1), metalloproteinase-9 (MMP-9), and procollagen III N-terminal peptide.

163 EF severity and fibrosis biomarkers (PIIINP [procollagen III N-terminal peptide], CITP [C-telopeptide

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

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

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

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

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

169 istochemical staining for myofibroblasts and procollagen III was observed in the nonprotective group,

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

171 I collagen, and aminoterminal propeptide of procollagen III.

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

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

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

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

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

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

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

179 ring around ER exit sites (ERES), and links procollagens in the ER lumen to COPII machinery, tethers

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

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

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

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

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

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

186 ansport intermediate commensurate with bulky procollagens is then facilitated by two complementary me

187 ypoxia-induced expression of the crosslinker procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2 (PLOD

188 Procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2 (PLOD

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

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

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

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

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

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

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

196 Owing to the size of fibril-forming procollagen molecules it is assumed that they are transp

197 ffected infant make some overmodified type I procollagen molecules.

198 culum before the formation of triple helical procollagen molecules.

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

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

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

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

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

204 recursor is proteolytically processed by the procollagen N-proteinases ADAMTS2 and ADAMTS14 between A

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

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

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

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

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

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

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

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

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

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

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

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

217 C-terminal proteolytic processing of soluble procollagen precursors.

218 N-terminal propeptide of type 3 procollagen (PRO-C3) is a biomarker of liver fibrosis in

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

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

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

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

223 We examined the role of FN matrix in procollagen processing by the C-propeptide proteinase bo

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

225 caffold to organize enzyme and substrate for procollagen processing.

226 the procollagen C-terminal propeptide during procollagen processing.

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

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

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

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

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

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

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

234 th HIV, PCOLCE (enzymatic cleavage of type I procollagen) significantly increased after pitavastatin

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

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

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

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

239 The result is nocturnal procollagen synthesis and daytime collagen fibril assemb

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

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

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

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

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

245 with FN fibrils, and proteolytic cleavage of procollagen to initiate fibril formation was significant

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

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

248 ide an important insight into the process of procollagen trafficking and reveal a short-loop pathway

249 of endoplasmic reticulum-to-plasma membrane procollagen transport by the sequential rhythmic express

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

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

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

253 Decreased levels of serum procollagen type 1 amino-terminal propeptide and tartrat

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

255 We measured plasma levels of procollagen type 1 N-terminal propeptide (P1NP) and C-te

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

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

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

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

260 rease of HSP47 and FKBP65 along with reduced procollagen type I in culture media.

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

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

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

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

265 ad significantly elevated gene expression of procollagen type I, procollagen type III, and alpha-smoo

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

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

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

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

270 Blood samples for 25(OH)VD and the procollagen type III N-terminal peptide (P3NP) were coll

271 -10, specific markers of cardiac remodeling (procollagen type III N-terminal peptide, matrix metallop

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

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

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

275 vated gene expression of procollagen type I, procollagen type III, and alpha-smooth muscle actin, are

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

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

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

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

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

281 e., increased carboxy-terminal propeptide of procollagen type-I) has been described in heart failure

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

290 n is required for TANGO1-dependent export of 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.