ライフサイエンスコーパス: collagen I

1 platelet-derived growth factor receptor, and collagen I).

2 face materials (no coating, Matrigel(R), and collagen I).

3 s enhanced, resembling the binding of VWF to collagen I.

4 vation of epitopes of the structural protein collagen I.

5 ion or fibrosis occurs, mostly consisting of collagen I.

6 ll adhesion to bone marrow stromal cells and collagen I.

7 ss endothelial cells and through Matrigel or collagen I.

8 tracellular matrix (ECM) proteins, including collagen I.

9 ith stimulation of tumour growth by DDRs and collagen I.

10 ber 1), connective tissue growth factor, and collagen I].

11 hibited OC (3.4-fold), Runx2 (2.8-fold), and collagen I (2.6-fold).

12 We show here that in collagen I 3D cultures in the absence of glycogen syntha

13 After T3-SCI, the MCA had more collagen I (42%), collagen III (24%), transforming growt

14 Collagen is a biological macromolecule capable of second

15 We now show that type IV collagen is a component within the morphological DEJ of

16 Fibrosis with excessive amounts of type I collagen is a hallmark of many solid tumours, and fibros

17 Overexpression of collagen is a hallmark of organ fibrosis.

18 Type I collagen is a key protein of most connective tissue and

19 gether, these findings indicate that type VI collagen is a key regulator of dermal matrix assembly, c

20 Type IV collagen is a major and crucial component of basement me

21 Type VI collagen is a nonfibrillar collagen expressed in many co

22 We recently demonstrated that type VII collagen is a novel component of the inner enamel organi

23 Collagen is a structural protein whose internal cross-li

24 BP180 (also termed type XVII collagen) is a hemidesmosomal protein and plays a critic

25 s of the extracellular matrix, in particular collagens, is a hallmark of idiopathic pulmonary fibrosi

26 how alignment occurs in biopolymers such as collagen-I (a major component of the ECM).

27 Following myocardial infarction (MI), collagen I, a major component of cardiac ECM, is cleaved

28 MMP-1 promoted MLE12 cell migration through collagen I, accelerated wound closing, and protected cel

29 Furthermore, fibronectin (not collagen-I) accumulates in the tendons of Mmp14-null mic

30 We found that lung epithelial cell-derived collagen I activates fibroblast collagen receptor discoi

31 However, collagen I affected WT-hbeta(2)m amyloid formation in co

32 ntrast agent (ProCA32.collagen1) with strong collagen I affinity.

33 site (Pro-986) in the alpha1-chain of type I collagen is almost completely 3-hydroxylated in every ti

34 ycin lung injury, and activate expression of collagen-I(alpha)1 and the myofibroblast marker alphaSMA

35 A collagen-I(alpha)1-expressing mesenchymal population of

36 n, our studies suggest a distinct lineage of collagen-I(alpha)1-expressing resident fibroblasts that

37 We studied collagen-I(alpha)1-producing cells in normal and disease

38 e and decreased expression of fibronectin-1, collagen I, alpha-smooth muscle actin, connective tissue

39 , higher expression levels of fibronectin-1, collagen I, alpha-smooth muscle actin, CTGF, and PAI-1,

40 sangial cell hypertrophy and fibronectin and collagen I (alpha2) expression.

41 sangial cell hypertrophy and fibronectin and collagen I (alpha2) production.

42 ypertrophy and expression of fibronectin and collagen I (alpha2).

43 Photochemical cross-linking of corneal collagen is an evolving treatment for keratoconus and ot

44 istep self-assembly of the fibrillar protein collagen is an important design challenge in biomimetic

45 Bone collagen is an important material for radiocarbon, paleo

46 Collagen is an insoluble protein that widely distributes

47 analysis together with a RT-PCR detection of collagen I and collagen II gene expression to show that

48 In collagen I and collagen IV (targets for MMP1 and MMP3, r

49 o map the binding interfaces on beta(2)m for collagen I and detect collagen I-induced mus-ms time-sca

50 r epithelial cell differentiation, excessive collagen I and elastin deposition, and hypercellularity

51 olithographic 3D printing, and the effect of collagen I and fibrin extracellular matrix proteins and

52 rchitecture of physiologically relevant ECMs-collagen I and fibrin-in a matter of minutes.

53 onectin-deficiency reduced the expression of collagen I and fibronectin.

54 eta1/Smad2/3 inhibitor, eliminated excessive collagen I and III accumulation induced by AAT1 knockdow

55 downregulation of alpha-smooth muscle actin, collagen I and III and decreased migration and different

56 but AAT1 knockdown mimicked the increase in collagen I and III expression, TGF- beta1 expression and

57 AAT1 overexpression blocked the increase in collagen I and III expression, transforming growth facto

58 ecretome resulted in decreased expression of collagen I and III in fibroblasts compared with control

59 downregulated SO2/AAT1 pathway and increased collagen I and III protein expression.

60 In parallel, collagen I and III showed a selective and progressive in

61 ctivated receptor-gamma 1-alpha (PGC1alpha), collagen I and III transcription, and thyroxine decrease

62 on of alpha-smooth muscle actin (alpha-SMA), collagen I and III was significantly higher in the heart

63 ith a downregulation in collagen production (collagen I and III), collagen processing, cleavage, cros

64 histochemistry markers were used to identify collagen I and III, lymphocytes (CD45), proliferation (K

65 N-terminal propeptide of collagen I and III, tissue inhibitor of matrix metallopr

66 IL-6, TGF-beta) and excessive production of collagen I and III.

67 Histologic analyses of four matrix proteins-collagen I and IV, laminin, and fibronectin-in skin biop

68 e results provide detailed insights into how collagen I and LMW-heparin impact different stages in th

69 tro, LA under TGFbeta1 stimulation increased collagen I and lysyl oxidase (LOX), the enzyme that cros

70 matrix and vascular proteins in addition to collagen I and osteocalcin.

71 s with periostin increased the expression of collagen I and stimulated the phosphorylation of FAK, p3

72 vealed decreased protein expressions of both Collagen I and TGF-beta1.

73 Here, we investigated the roles of collagen I and the commonly administered anticoagulant,

74 nt protein-1, alpha-smooth muscle actin, and collagen I and TIMP1 expression.

75 remodeling, by reducing the stiffer cardiac collagen I and titin n2b expression in the left ventricl

76 h the down regulation of mRNA expressions of Collagen I and transforming growth factor-beta1 (TGF-bet

77 qRT-PCR data showed low levels of collagen I and V, as well as keratocan for HKCs, indicat

78 on of miR-199a-3p increased TGFbeta1-induced collagen I and vimentin expression and restored SOCS7 ex

79 reatment induced fibrotic changes, including collagen I and vimentin expression, being associated wit

80 the major extracellular components, such as collagen-I and -IV, were retained in explants.

81 of E-cadherin and zona occludens-1, whereas collagen-I and alpha-smooth muscle actin were increased

82 d murine FL-fibroblasts was reduced, whereas collagen-I and alpha-smooth muscle actin were markedly e

83 n of basal PAI-1 in NL-fibroblasts increased collagen-I and alpha-smooth muscle actin.

84 Collagen-I and alphaSMA(+) fibroblasts do not correlate

85 (Ad-PAI-1) suppressed expression of uPA and collagen-I and attenuated proliferation in FL-fibroblast

86 re deficient in their packaging of fibrillar collagen-I and express less decorin, important for colla

87 tein acidic and rich in cysteine (SPARC) and collagen-I and induction of complement activation.

88 ce without lung injury also showed increased collagen-I and uPA.

89 linking sites and the MMP-1 cleavage site in collagens I and II.

90 beta1, transforming growth factor-beta2, and collagens I and III in both keloid and normal skin fibro

91 a substrate preference for collagen II over collagens I and III.

92 ssion of connective tissue growth factor and collagens I and IV.

93 ofibrotic mediators and effectors, including collagens I and V and alpha-smooth muscle actin, on the

94 ) and minor enrichment of laminin-gamma1 and collagens I and VI.

95 led to increased expression of fibronectin, collagen I, and alpha-smooth muscle actin in the TM in m

96 were identified by their expression of CD45, collagen I, and alpha-smooth muscle actin using flow cyt

97 th high affinity to immobilized fibronectin, collagen I, and collagen V.

98 lpha-actin fiber formation, up-regulation of collagen I, and down-regulation of collagen III.

99 arameters (transforming growth factor-beta1, collagen I, and fibronectin) were increased at baseline.

100 ification showed a dominance of collagen IV, collagen I, and laminin isoforms in the glomerular ECM t

101 e also decreased mRNA expression of osterix, collagen I, and osteocalcin by mesenchymal stem cells at

102 tion rate; decreased expressions of osterix, collagen I, and osteocalcin; but increased trabecular se

103 actor-beta-mediated profibrotic fibronectin, collagen I, and proinflammatory interleukin-6.

104 Cells were seeded onto collagen I, and subsequently treated with differentiatio

105 scle actin, connective tissue growth factor, collagen I, and TGF-beta; and reduced renal macrophage i

106 ctivation and the expression of miR-199a-3p, collagen I, and vimentin during TGF-beta1 treatment.

107 eased alpha smooth muscle actin (alpha-SMA), collagen-I, and transforming growth factor beta messenge

108 These collagenases cleave DDR1 and attenuate collagen I- and IV-induced receptor phosphorylation.

109 oteins fibronectin (FN) and type I collagen (collagen I) are codistributed in many tissues, and colla

110 eases following mesangial cell attachment to collagen I, associated with increased collagen I express

111 s compared with MMP-1, GVSK degraded soluble collagen I at the high but not the low Ca(2+) concentrat

112 we propose a model in which weak, multimodal collagen I-beta(2)m interactions promote exchange with a

113 he cell surface, and its ectodomain displays collagen I binding with an affinity similar to that of t

114 We quantified production of fibronectin and collagen I by HEF and HEMC in response to eosinophil pro

115 demonstrated by the increased expression of Collagen-I by HSCs incubated with either a phosphorylate

116 s the deposition of matrix proteins, such as collagen I, by hepatic stellate cells (HSCs) that culmin

117 As the size and organisation of stromal collagen is closely associated with the optical properti

118 AIR-1, a novel immunoinhibitory receptor for collagen, is closely associated with some autoimmune dis

119 n umbilical vein endothelial cells plated on collagen I-coated plates and cultured in the confluent s

120 Here, we show that stromal collagen I (Col-I) fibers in the mammary fat pad are axi

121 Using a three-dimensional collagen-I (Col-1) gel assay that simulates epithelial i

122 interacted with three different substrates: collagen-I (Col-I), bovine serum albumin, and a monolaye

123 Collagen I (COL1A1), collagen III (COL3A1), hyaluronan s

124 of pancreatic adenocarcinoma cells through a collagen I (COLI) matrix.

125 ys consisting of 32 distinct combinations of collagen I, collagen III, collagen IV, fibronectin, and

126 ific extracellular matrix proteins-including collagen I, collagen IV, and laminin V-to modulate inter

127 We found that in vivo ITF2357 decreased collagen I, collagen IV, fibronectin, integrin alphaVbet

128 b(-/-) mice revealed lower amounts of mature collagen I compared with WT mice and exhibited significa

129 ionally towards blood vessels on fibronectin-collagen I-containing extracellular matrix (ECM) fibers

130 In doxycycline-treated scar matrices, collagen I content was significantly reduced (P = 0.0317

131 etermination of amino-terminal propeptide of collagen I content.

132 Type IV collagen is critical for BM function, yet how it is dire

133 erefore, the ability to monitor the state of collagen is crucial for determining the presence and pro

134 re isolated, and fibrocytes expressing CD45, collagen I, CTGF, ETAR, or alpha-SMA were identified by

135 loxP-mediated vinculin gene disruption in 3D collagen I cultures.

136 45(+) CD4(+) IL-17(+) cells, CD45(+) CD34(+) collagen I(+) CXCR4(+) fibrocytes, and HSP47(+) activate

137 n of HE4-neutralizing antibodies accelerated collagen I degradation and inhibited fibrosis in three d

138 vs 2.45 [0.36], p<0.0001) indicating greater collagen I degradation.

139 thermore, TIMP3 modulates sDLK1 shedding and collagen I degradation.

140 down-regulation of ACTN4 by shRNA induces a collagen I-dependent amoeboidal-to-mesenchymal transitio

141 was hypoxic, and hypoxic signaling enhanced collagen I deposition by mesothelial cells.

142 uding glomerulosclerosis, where it increases collagen I deposition in vivo and promotes mesangial cel

143 e healing tendon tissues by promoting better collagen I deposition, decreased cellularity, less vascu

144 However, their implementation into synthetic collagen is difficult and requires the replacement of th

145 e of markers of fibroblast-like cells (e.g., collagen I, ecto-5'-nucleotidase, and PDGF receptor-beta

146 The medial collagen is engaged throughout the stretching process, a

147 cell-matrix adhesion by showing that type IV collagen is essential for inter-adipocyte adhesion in th

148 erance toward autologous intact alpha345(IV) collagen is established in hosts expressing this Ag, eve

149 sults demonstrate that the A1 site in type I collagen is exclusively 3-hydroxylated by P3H1, and pres

150 th a conditional knockout (CKO) of Notch1 in collagen I-expressing (mesenchymal) cells on treatment w

151 ent to collagen I, associated with increased collagen I expression and increased susceptibility to ap

152 way was identified as an important driver of collagen I expression in Fib-MCs in experiments utilizin

153 trongly inhibited 4E-BP1 phosphorylation and collagen I expression in Fib-MCs.

154 TGFbeta3-microS yielded significantly higher collagen I expression in the AP bands compared with the

155 myofibroblasts and significantly diminished collagen I expression relative to those from control mic

156 and mTORC2 signaling and leads to increased collagen I expression via the mTORC1-dependent 4E-BP1/eI

157 on systemic sclerosis and is known to induce collagen I expression, but the mechanism(s) behind this

158 HSCs and their alpha-smooth muscle actin and collagen I expression, thus increasing tumor fibrosis.

159 reased mTORC1 signaling was shown to augment collagen I expression.

160 H cellular signaling pathway and mouse/human collagen I expression.

161 ratio was shifted toward higher abundance of collagen I fibers.

162 chanical strain sensors and demonstrate that collagen I fibres preferentially co-localize with more-r

163 nct tissue-specific effect of collagen VI on collagen I fibrillogenesis.

164 Interestingly, collagen I fibrils did not suppress surface-mediated ass

165 We previously found that collagen I fibrils induced the formation of peculiar lin

166 lass transition temperature, we propose that collagen I fibrils may be in a glassy state while hydrat

167 ed and characterized the function of CD45(+)/collagen I(+) fibrocytes in acutely injured skeletal mus

168 enafil substantially blocked the increase in collagen I, fibronectin 1, TGFbeta, and CTGF mRNA in Ctr

169 l remodeling, including vimentin, TGF-beta1, collagen I, fibronectin, and matrix metalloproteases, an

170 In vitro, eCRT strongly induces collagen I, fibronectin, elastin, alpha-smooth muscle ac

171 to RELM-beta increased TGF-beta1, TGF-beta2, collagen I, fibronectin, smooth muscle alpha-actin, lami

172 unostaining of tumor-xenograft sections with collagen-I, fibronectin (major extracellular-matrix prot

173 A 5-fold increase in collagen I fibrosis is detected in the remote surviving

174 Gelatin, which is derived from collagen, is frequently used as a brain simulant materia

175 emonstrate a step-by-step process to isolate collagen I from commercially available animal byproducts

176 the ones expressing the scrambled shRNA on a collagen I gel (two-dimensional) although these two cell

177 estores the amoeboidal morphology and limits collagen I gel compaction.

178 n of WM1158 cells into the three-dimensional collagen I gel, a representative of the dermis.

179 n and growth/survival in a three-dimensional collagen I gel.

180 cue the amoeboidal morphology and to compact collagen I gel.

181 we validate the utility of DS-OCT using pure collagen I gels and 3D mammary fibroblast cultures seede

182 l, 1.0 mg/ml, and 2.0 mg/ml acid-solubilized collagen I gels forming at 27 degrees C, 32 degrees C, a

183 al ovarian cancer cells on three-dimensional collagen I gels led to a dramatic down-regulation of the

184 Interestingly, in three-dimensional collagen I gels, ACTN4 KD cells are more polarized compa

185 an alignment of these fossil sequences with collagen (I) gene transcripts from available mammalian g

186 st often caused by dominant mutations in the collagen I genes COL1A1/COL1A2, whereas rarer recessive

187 rating polymer networks (mIPNs) comprised of Collagen I, HA and poly(ethylene glycol) diacrylate.

188 This is the first time that crosslinking of collagen I has been shown to enhance metastatic growth.

189 Although type IV collagen is heavily glycosylated, the influence of this

190 Collagen is highly valued both as a food additive and a

191 The mechanical strength of fibrillar collagens is highly dependent on the formation of covale

192 Here, we combine the usefulness of a collagen I hydrogel membrane with entrapped ribonuclease

193 physiological barrier function are formed in collagen I hydrogels with stiffness matching that of hum

194 Expression of collagen I, III, and IV (COL1A1, COL3A1, COL4A1) transcr

195 was more severe with increased deposition of collagen I, III, and IV.

196 The expression of collagens I, III, and IV (COL I, COL III, and COL IV) an

197 rity of RV dysfunction, whereas the ratio of collagen I/III expression was only elevated in severe RV

198 Therefore, aggravation of the collagen I/III ratio and cardiac stiffening by excess n-

199 Excess dietary LA increased the collagen I/III ratio in the mouse myocardium, leading to

200 a, metalloproteinase-2, metalloproteinase-9, collagen I/III, and reduced connexin 43 phosphorylation

201 and Fast Green and analyzed to determine the collagen I:III ratio.

202 e, an effect that could not be observed with collagen I in the absence of DDR induction.

203 agen IV in the basal lamina and of fibrillar collagen I in the adjacent interstitium in the dual infe

204 y; indeed, apigenin dose-dependently reduced collagen I in the human HSC line, TWNT-4.

205 owed double the amino-terminal propeptide of collagen I in their blood, indicating increased collagen

206 The emergence of collagen I in vertebrates resulted in a dramatic increas

207 xhibit enhanced secretion of fibronectin and collagen I, increased migratory/invasive abilities, and

208 Asn(260), Asn(371), and Asn(394)), result in collagen I-independent constitutive phosphorylation.

209 rfaces on beta(2)m for collagen I and detect collagen I-induced mus-ms time-scale dynamics in the bet

210 task-induced increases in serum CCN2 and pro-collagen I intact N-terminal protein.

211 often caused by mutations in genes encoding collagen I-interacting proteins.

212 strate that upon miR-200 loss integrin beta1-collagen I interactions drive 3D in vitro migration/inva

213 Collagen I is a major tendon protein whose polypeptide c

214 MMP-9, and MMP-13, whereas non-cross-linked collagen I, IV, and natively glycosylated SLRPs are susc

215 uman liver ECM to its individual components; Collagen I, Laminin-521 and Fibronectin.

216 is of ECM components such as fibronectin and collagen I, leading to an impairment in cell motility an

217 Mesangial cell attachment to collagen I led to increased Hic-5 expression within 2-4

218 expression in mesangial cells by adhesion to collagen I led to TGF-beta expression, which was abolish

219 ated albumin-induced increases in TIMP-1 and collagen-I levels.

220 eedback regulation of DBL-1/BMP signaling by collagens is likely to be contact independent due to phy

221 In vitro, collagen I limited the lipolytic flux between acinar cel

222 nal breast cancer cells in three-dimensional collagen I matrices in vitro.

223 e membranes by dedifferentiated RPE cells on collagen I matrices.

224 ed these partially reprogrammed spheroids in collagen-I matrices of varying densities, mimicking diff

225 Collagen I matrix assembly in vivo requires active fibro

226 ult, rounded-amoeboid melanoma cells degrade collagen I more efficiently than elongated-mesenchymal c

227 nts.Measurements and Main Results: Fibrillar collagen is not only increased but also highly disorgani

228 including fibrotic disease states with high collagen, is now utilizing 'omics data sets and is revea

229 peptide analog of the cell-binding domain of collagen I, on the in vitro progression of osteogenic ce

230 magnification electron microscopy shows that collagen is organized into perimysial cables which incre

231 Galectin-3 (Gal-3), N-terminal propeptide of collagen I (PINP), and N-terminal propeptide of collagen

232 Collagen I-positive cells (89.43% +/- 6.53%) in day 28 a

233 Collagen is post-translationally modified by prolyl and

234 stress of the collagen fibrils, whereas the collagen is predominantly responsible for the material's

235 al-to-mesenchymal transition and intensified collagen I production and MUC5AC expression.

236 Increased TGF-beta1 and TGF-beta1-dependent Collagen I production in intestinal mesenchymal cells re

237 ous vacuoles in the cytoplasm, a decrease in collagen I production, and augmented LC3 II expression.

238 assay (LDH), electronic microscopy analysis, collagen I production, flow cytometry lysosome compartme

239 Interstitial fibrosis with cross-linked collagen is prominent in HF hearts, with presence of act

240 tor is stimulated with collagenase-resistant collagen I (r/r) or with a triple-helical peptide harbor

241 y, we show that mutant DDR1 that cannot bind collagen is recruited into DDR1 signalling clusters.

242 ies, where a polymer matrix of nanofibrillar collagen is reinforced by apatite mineral crystals.

243 on and secondary accumulation of MSC-derived collagen is responsible for hematopoietic failure in aut

244 efit of surgery and exercise training (e.g., collagen I: RYGB -41% vs. RYGB + ET -76%; P <= 0.0001).

245 Fibre stretch-assay studies reveal that collagen I's Fn-binding domain is responsible for the me

246 method to manufacture unidirectional laminar collagen I scaffolds.

247 role for TANGO1 and the UPR in facilitating collagen I secretion and fibrogenesis.

248 Depletion of TANGO1 in HSCs blocked collagen I secretion without affecting other matrix prot

249 th intact endogenous TANGO1 impairs cellular collagen I secretion.

250 ion 1 (TANGO1) as a potential participant in collagen I secretion.

251 DDR1b- or DDR2-expressing HT1080 cells with collagen I significantly accelerated tumour growth rate,

252 Although both groups showed high collagen I staining, content of collagen I was significa

253 the collagen receptor, CD167a, responded to collagen I stimulation at the primary tumor to promote l

254 were more likely to invade into Matrigel and collagen I substrates than cell lines derived from high-

255 express DDR1 and that short-term exposure to collagen is sufficient to activate DDR1 in Hodgkin lymph

256 breast cancer cells readily transfer to new collagen I surfaces, and away from basement membrane pro

257 icate that calpain mediates cytokine-induced collagen-I synthesis and proliferation of ASMCs via the

258 ted cytokine-induced phosphorylation of Akt, collagen-I synthesis, and cell proliferation of ASMCs an

259 nd serum from patients with asthma increased collagen-I synthesis, cell proliferation, and phosphoryl

260 Collagen-I synthesis, cell proliferation, and phosphoryl

261 s occurs in Col-r/r mice that have a mutated collagen-I that is uncleavable by MMPs.

262 (ECM) is comprised of biopolymers, primarily collagen I, that are created and maintained by stromal f

263 Collagen is the fundamental structural component of a wi

264 Collagen is the main structural and load-bearing element

265 Fibrillar type I collagen is the major organic component in bone, providi

266 iculum (rER), and the triple-helical protein collagen is the most abundant extracellular matrix compo

267 Collagen is the most abundant protein family in mammals.

268 Collagen is the most abundant protein in the extracellul

269 Type I collagen is the most abundant protein in the human body

270 Type I fibrillar collagen is the most abundant protein in the human body,

271 Collagen is the most abundant secreted protein in verteb

272 Collagen is the most prevalent component of the extracel

273 Type I collagen is the predominant collagen in mature tendons a

274 Collagen is the primary component of the extracellular m

275 alpha2beta1 integrin, the receptor of type I collagen, is the major collagen-binding integrin express

276 In vivo, collagen I, the major structural protein in human body,

277 MCs to increase secretion of fibronectin and collagen I; this was inhibited by blocking transforming

278 d ECM genes/proteins with new ones emerging (collagen-I, thrombospondin-I, plasminogen activator inhi

279 reduced collagen III levels and the ratio of Collagen I to Collagen III.

280 Our study suggests collagen I to have evolved as a radical sponge against m

281 the ubiquitous interstitial matrix component collagen I to undergo metastatic reactivation in multipl

282 into microfluidic devices and modified with collagen (I) to promote hepatocyte adhesion.

283 ncreased adhesion and aggregate formation on collagen I under flow, and accelerated clot retraction a

284 The amino acid composition of collagen is unique due to its high (33%) glycine content

285 conclude that in atherosclerosis, type VIII collagen is up-regulated in the absence of ApoE and func

286 Type VIII collagen, a short-chain collagen, is up-regulated in atherosclerosis; however, l

287 disassembly of fibrils formed from purified collagen I using turbimetry, probe the fibril morphology

288 A recombinant bacterial collagen is utilized to characterize the sequence requir

289 play cell surface alpha smooth muscle actin, collagen I/V, and mediate angiogenesis.

290 enesis, was increased, whereas expression of collagen I was reduced in the corresponding region of th

291 showed high collagen I staining, content of collagen I was significantly higher in PRP-treated tendo

292 The ratio of collagen III to collagen I was significantly lower in PRP samples (p=0.0

293 Type VI collagen is well known for its role in muscular disorder

294 of alpha-smooth muscle actin (alpha-SMA) and Collagen I were reduced as was the activity of matrix me

295 In vivo, MMP-1 and GVSK degraded collagen I when perfused in Zucker rat ventral skin and

296 iorycteropus, obtained from the bone protein collagen (I), which places the 'Malagasy aardvark' as mo

297 inhibitor of metalloproteinase (TIMP)-1 and collagen-I, which were blocked by HIF-1alpha shRNA.

298 Here, we show that copolymerization of collagen I with polyacrylamide produces minimal matrix m

299 hat in self-seeded reactions, interaction of collagen I with WT-hbeta(2)m amyloid fibrils attenuates

300 In non-lesional tissue the axial period of collagen is within the range 63.6-63.7 nm (formalin fixe