ライフサイエンスコーパス: fibrillogenesis

1 availability and stepwise polymerization for fibrillogenesis.

2 e mechanical stress and increase fibronectin fibrillogenesis.

3 migration and RhoA activity, and fibronectin fibrillogenesis.

4 bilizes nonfibrillar large aggregates during fibrillogenesis.

5 llagens V and XI in the regulation of tendon fibrillogenesis.

6 nction significantly affects type I collagen fibrillogenesis.

7 ese residues was sufficient to inhibit Abeta fibrillogenesis.

8 of side chain interactions in polyglutamine fibrillogenesis.

9 We investigated the role of GAGs in LC fibrillogenesis.

10 ross-link organization, which is crucial for fibrillogenesis.

11 g, but not order, is important for efficient fibrillogenesis.

12 that was associated with the early stages in fibrillogenesis.

13 ave a functional role in modulating collagen fibrillogenesis.

14 c beads embedded within collagen gels during fibrillogenesis.

15 ion as nucleation points, thereby initiating fibrillogenesis.

16 o collagen type 1 and its impact on collagen fibrillogenesis.

17 le mechanism by which tension could initiate fibrillogenesis.

18 vin might regulate both decorin and collagen fibrillogenesis.

19 c maturation required for premelanosome-like fibrillogenesis.

20 n-independent function for hevin in collagen fibrillogenesis.

21 e increased diameter consistent with altered fibrillogenesis.

22 had an inhibitory effect on type I collagen fibrillogenesis.

23 ocytes and plays a role in the regulation of fibrillogenesis.

24 ute to collagen regulation via modulation of fibrillogenesis.

25 ld greater than is seen with Abeta(1)(-)(40) fibrillogenesis.

26 observed in the kinetics of Abeta(1)(-)(40) fibrillogenesis.

27 e mutations, Q336R caused an increase in tau fibrillogenesis.

28 n the cell) is a nucleation site of collagen fibrillogenesis.

29 c changes in beta2m at time points preceding fibrillogenesis.

30 ral evolution of early aggregates in amyloid fibrillogenesis.

31 ancient type V collagen in the regulation of fibrillogenesis.

32 leading to >tenfold increases in the rate of fibrillogenesis.

33 plore factors that either inhibit or promote fibrillogenesis.

34 e N-terminal side affect the dynamic amyloid fibrillogenesis.

35 II domain in cell spreading and fibronectin fibrillogenesis.

36 ived growth factor, did not affect fibrillin fibrillogenesis.

37 n cell spreading, migration, and fibronectin fibrillogenesis.

38 dently of its ability to mediate fibronectin fibrillogenesis.

39 ino acids in a sequence critical for Abeta40 fibrillogenesis.

40 bronectin which are critical for fibronectin fibrillogenesis.

41 ght into the integrin-mediated pathway of Fn fibrillogenesis.

42 7), to explore the role of the C terminus in fibrillogenesis.

43 back regulation of synthesis, and control of fibrillogenesis.

44 protein, is also not an inhibitor of Abeta40 fibrillogenesis.

45 nvolved in cell-matrix adhesion and collagen fibrillogenesis.

46 s, where it is involved in the regulation of fibrillogenesis.

47 rofibrils and play a central role in elastic fibrillogenesis.

48 t of putative regulator of vitreous collagen fibrillogenesis.

49 x-containing assembly is a key step in Abeta fibrillogenesis.

50 ons with other matrix components that affect fibrillogenesis.

51 rk (TGN) to the EC surface, thus allowing FN fibrillogenesis.

52 he formation of ECM contacts and fibronectin fibrillogenesis.

53 e-deficient mice demonstrated disruptions in fibrillogenesis.

54 tein specific functions in the regulation of fibrillogenesis.

55 and 210 nm under conditions consistent with fibrillogenesis.

56 ns, can also be employed to monitor collagen fibrillogenesis.

57 portance of integrin activation for early FN fibrillogenesis.

58 cell culture and inhibited in vitro collagen fibrillogenesis.

59 insight into initial steps of cell-driven FN fibrillogenesis.

60 cond mutation located at CDR3 (W91A) induced fibrillogenesis.

61 specific molecular interactions of collagen fibrillogenesis.

62 lexity domains and can decelerate pathogenic fibrillogenesis.

63 role of proteolytic cleavage in TTR amyloid fibrillogenesis.

64 RBP, but not thyroxine, inhibited subsequent fibrillogenesis.

65 supplement information about early events in fibrillogenesis.

66 her intramelanosomal vesicles can facilitate fibrillogenesis.

67 ross-links are introduced at early stages of fibrillogenesis.

68 assays demonstrate that mPPCs suppress Abeta fibrillogenesis.

69 e ECM protein fibronectin (FN) and FN matrix fibrillogenesis.

70 accepted as the critical step in TTR amyloid fibrillogenesis.

71 ow structural heterogeneity of collagen upon fibrillogenesis.

72 specific effect of collagen VI on collagen I fibrillogenesis.

73 ion along with complementary measurements of fibrillogenesis.

74 a potential rate-limiting step during Abeta fibrillogenesis.

75 of TSP2-null mice, such as abnormal collagen fibrillogenesis, accelerated wound healing, and increase

76 l oligomers that normally occur during Abeta fibrillogenesis, acting as a potent inhibitor of Abeta1-

77 c phospholipids in membrane-catalyzed amylin fibrillogenesis and aggregation.

78 lular domain (ECD) of DDR2 inhibits collagen fibrillogenesis and alters the morphology of collagen ty

79 proteoglycan gene family, regulates collagen fibrillogenesis and cell growth.

80 It also supported fibrillogenesis and cell spreading and controlled cell m

81 In comparison of the fibrillogenesis and cellular toxicity of EV40 to the wil

82 neously enhance amyloid beta-protein (Abeta) fibrillogenesis and decrease cellular toxicity, as measu

83 s of other factors, such as collagenases, on fibrillogenesis and degradation.

84 role(s) of type I/V collagen interactions in fibrillogenesis and elucidate the mechanism whereby half

85 he collagen triple helix and may also affect fibrillogenesis and folding of the peptide chains.

86 d the mechanism of TGFbeta-induced fibrillin fibrillogenesis and its relationship to myofibroblasts.

87 ype V collagen in the regulation of collagen fibrillogenesis and matrix assembly.

88 here may be important for the activation of fibrillogenesis and matrix assembly.

89 wild-type mice because of impaired collagen fibrillogenesis and maturation in the infarcts as reveal

90 ant synucleins, showed a correlation between fibrillogenesis and mean beta-strand propensity, hydroph

91 ructure sets viscoelasticity during collagen fibrillogenesis and more broadly highlights the utility

92 uding the inhibition of amyloid beta (Abeta) fibrillogenesis and oligomer formation and the reverse p

93 ecorin (Dcn), leading to defects in collagen fibrillogenesis and possibly less stable collagen fibril

94 signals from TGF-beta and Wnt for fibrillin fibrillogenesis and profibrotic gene expression.

95 ructure, should allow further elucidation of fibrillogenesis and protein misfolding.

96 dentifying the regions that promote Josephin fibrillogenesis and rationalizing the mechanisms that pr

97 re simultaneously employed to track collagen fibrillogenesis and reconcile the information reported b

98 nce of the IIICS domain, blocked fibronectin fibrillogenesis and required sulfated proteoglycans to m

99 urs on timescales that are short compared to fibrillogenesis and results in assembly into preamyloid

100 bryos inhibit gastrulation, fibronectin (FN) fibrillogenesis and the ability of ectodermal cells to s

101 e E22Q Dutch and D23N Iowa mutations enhance fibrillogenesis and the pathogenicity of Abeta toward HC

102 e glycolipids, gangliosides, can mediate the fibrillogenesis and toxicity of Alzheimer's disease amyl

103 ic wild-type and mutant Abeta40 peptides for fibrillogenesis and toxicity toward cultured human cereb

104 cently that decorin, a regulator of collagen fibrillogenesis and transforming growth factor-beta acti

105 initial phase of membrane disruption before fibrillogenesis, and does not prevent the formation of s

106 nal (3D) cell and tissue culture, studies of fibrillogenesis, and investigation of multiscale force t

107 roles in controlling collagen cross-linking, fibrillogenesis, and mineralization.

108 n cartilaginous tissues, influences collagen fibrillogenesis, and modulates chondrocyte differentiati

109 ositive stress fibers, increased fibronectin fibrillogenesis, and production of a stiff ECM with orie

110 s a more complicated role in inhibiting IAPP fibrillogenesis, and that other factors, such as the low

111 and mature OGN can regulate type I collagen fibrillogenesis, and that processing of the prodomain by

112 atterns continued to change slowly after the fibrillogenesis appeared to be complete, due to dissocia

113 Fibronectin (FN) assembly and fibrillogenesis are critically important in both develop

114 lass of organofluorine inhibitors of amyloid fibrillogenesis are described.

115 Implications for fibronectin fibrillogenesis are discussed.

116 However, the mechanisms controlling corneal fibrillogenesis are incompletely understood and the cond

117 how that procollagen processing and collagen fibrillogenesis are initiated in Golgi to plasma membran

118 n gene delivery does not jeopardize collagen fibrillogenesis as no significant differences in collage

119 exclusion chromatography, KLVFF-K6 inhibited fibrillogenesis, as measured by thioflavin T fluorescenc

120 an amyloid tissue deposits and could inhibit fibrillogenesis, as shown in fibril formation and extens

121 In an in vitro fibrillogenesis assay, Sh collagen showed accelerated fi

122 Fibrillogenesis assays further demonstrated that DMP1 ac

123 In vitro fibrillogenesis assays indicated that hevin enhanced fib

124 , surface property measurements, and amyloid fibrillogenesis assays on islet amyloid polypeptide and

125 Fibrillogenesis assays using recombinant decorin and big

126 ctivity in both phosphorylation and collagen fibrillogenesis assays.

127 sessed by immunocytochemical and fibronectin fibrillogenesis assays.

128 nd, inhibition of COX-2 reduces the collagen fibrillogenesis associated with involution, as well as t

129 Understanding fibrillogenesis at a molecular level requires detailed s

130 ranule, significantly inhibits hIAPP amyloid fibrillogenesis at concentrations similar to those found

131 s, we propose a generic mechanism for beta2m fibrillogenesis at neutral pH that is consistent with th

132 could bypass an unfavorable folding step in fibrillogenesis, because the lactam linkage "preforms" a

133 with collagen was found to modulate collagen fibrillogenesis both in vitro and in cell-based assays.

134 ithout interfering with cell spreading or FN fibrillogenesis but perturbs both epiboly and convergenc

135 the lack of seeding of full-length alpha-syn fibrillogenesis by 1-120.

136 ored, cell-surface protein, affects collagen fibrillogenesis by cells.

137 bly in vivo requires active fibronectin (Fn) fibrillogenesis by cells.

138 demonstrated that brazilin inhibited Abeta42 fibrillogenesis by directly binding to Abeta42 species v

139 al mechanistic principles of in vivo amyloid fibrillogenesis by globular proteins, a previously obscu

140 uggest that the catalysis of type I collagen fibrillogenesis by nonhelical telopeptides is due to spe

141 The modulation of collagen fibrillogenesis by the DDR1 ECD elucidates a novel mecha

142 Here we show that TTR fibrillogenesis by the mechano-enzymatic pathway is inde

143 beta(1) integrins induce initial fibronectin fibrillogenesis by transmitting cytoskeleton-generated t

144 Fibrillogenesis can be resolved in immature tissue by di

145 he capacity of decorin to influence collagen fibrillogenesis, catabolism of decorin may have importan

146 s with amylin fibrils, rather than enhancing fibrillogenesis catalytically.

147 binding may potentially impact upon collagen fibrillogenesis, cell-collagen attachment, and collagen

148 ose a model in which the attractive force of fibrillogenesis comes from a structural reorganization o

149 enesis assay, Sh collagen showed accelerated fibrillogenesis compared with the controls.

150 tudy focuses on the characterization of this fibrillogenesis competency of collagen.

151 involved in extracellular matrix formation, fibrillogenesis, complement activation, and angiogenesis

152 s, but it has no apparent effect on critical fibrillogenesis concentration at physiological NaCl and

153 previously reported increase in the critical fibrillogenesis concentration of collagen is caused by p

154 a modulator of extracellular matrix protein fibrillogenesis, decorin can inhibit the cellular respon

155 monstrated to be a key regulator of collagen fibrillogenesis; decorin deficiencies lead to irregularl

156 Loss of Sparc results in tendon collagen fibrillogenesis defects and Sparc-/- tendons are less ab

157 We further show that while the inhibition of fibrillogenesis depends on the phosphatase activity of x

158 inhibitors of wild type beta2-microglobulin fibrillogenesis, doxycycline and single domain antibodie

159 d type V collagen were required for collagen fibrillogenesis during remodeling of adult liver tissue.

160 epeat protein subfamily in the regulation of fibrillogenesis during tendon development were defined.

161 haemodynamic forces regulate FN assembly and fibrillogenesis during vascular remodelling.

162 ionality unrelated to regulation of collagen fibrillogenesis, e.g. modulation of epithelial cell adhe

163 ditional kinetic and thermodynamic assays of fibrillogenesis efficacy with direct measurements of int

164 Here, we perform in vitro IAPP fibrillogenesis experiments in the presence and in the a

165 trations, our X-ray diffraction and in vitro fibrillogenesis experiments suggest that this binding pl

166 tin-independent mechanism of type I collagen fibrillogenesis following adult liver injury.

167 provide new insights into the regulation of fibrillogenesis for cellular homeostasis.

168 By contrast, amylin fibrillogenesis has a sigmoidal dependence on heparin fr

169 Detailed structural information about fibrillogenesis has remained elusive due to the highly i

170 fic structural features that might favor TTR fibrillogenesis have not yet been identified.

171 The kinetics of fibrillogenesis, however, occur without the typical lag

172 ce and has been implicated as a regulator of fibrillogenesis; however, a specific role has not been e

173 tion of CD spectra before, during, and after fibrillogenesis identified a unique fibril spectrum dist

174 1-overexpression robustly increased collagen fibrillogenesis in atherosclerotic plaque.

175 y, and that a similar mechanism may underlie fibrillogenesis in certain natural systems.

176 ow seeding mechanism likely precedes a rapid fibrillogenesis in determining the extent of amyloid dep

177 king regulates cell adhesion and fibronectin fibrillogenesis in epithelial cells, as well as alpha5 l

178 otein fibrinogen in addition to enhancing FN fibrillogenesis in fibroblasts.

179 gnificant control over this process and over fibrillogenesis in general.

180 copy (AFM) to visualize initial stages of FN fibrillogenesis in living fibroblasts at high resolution

181 copy (AFM) to visualize initial stages of FN fibrillogenesis in living fibroblasts at high resolution

182 known about their molecular interactions and fibrillogenesis in mixtures with normal heterotrimers.

183 the lag and fiber state were used to monitor fibrillogenesis in real time.

184 similar to scleroderma to evaluate collagen fibrillogenesis in the absence of MCP-1.

185 ncrease in FN matrix assembly that parallels fibrillogenesis in the embryo.

186 Furthermore, Abeta12-28P reduces Abeta fibrillogenesis in the presence of apoE, and Abeta/apoE

187 The decreased Abeta fibrillogenesis in the presence of EGb761 was observed b

188 all these results, we propose a model for AS fibrillogenesis in the presence of phospholipid vesicles

189 Prior to evaluating tendon fibrillogenesis in type XIV collagen-deficient mice, the

190 orm, DeltaN6 is able to efficiently nucleate fibrillogenesis in vitro at physiological pH.

191 ata are consistent with a model for beta(2)m fibrillogenesis in vitro involving the association of pa

192 ified a new mechano-enzymatic pathway of TTR fibrillogenesis in vitro, catalysed by selective proteol

193 E interacts with Abeta and facilitates Abeta fibrillogenesis in vitro.

194 n accelerates both Abeta oligomerization and fibrillogenesis in vitro.

195 l membrane may provide a mechanism for Abeta fibrillogenesis in vivo, and Abeta-induced disruption of

196 n-controlled aggregation mechanism for Abeta fibrillogenesis in vivo.

197 purified, soluble protein, inhibits collagen fibrillogenesis in-vitro.

198 on about transcriptional control of collagen fibrillogenesis, in addition to implicating for the firs

199 Our data show that fibrillogenesis increases the side chain and backbone st

200 nk inhibition, suggesting that LOX regulates fibrillogenesis independently of these molecules.

201 The inhibitors showed strong activity in fibrillogenesis inhibition and disassembly, and even gre

202 s a dual functional compound in both Abeta42 fibrillogenesis inhibition and mature fibril remodeling,

203 ding scenarios suggest several mechanisms of fibrillogenesis inhibition: 1), fibril inhibition of lon

204 H(2)-KLVFFAE-CONH(2) (Abeta16-22), is a weak fibrillogenesis inhibitor.

205 l amino acids in consecutive order, is not a fibrillogenesis inhibitor.

206 would facilitate the targeting and design of fibrillogenesis inhibitors.

207 n strategies in designing and optimizing TTR fibrillogenesis inhibitors.

208 Prior studies have shown that Abeta fibrillogenesis involves conformational changes leading

209 The study showed that collagen fibrillogenesis is a hierarchical process that depends o

210 regulated by its synthesis and turnover, and fibrillogenesis is a multistep, integrin-dependent proce

211 Collagen fibrillogenesis is a tightly controlled process in which

212 Protein fibrillogenesis is a universal tool of nano-to-micro sca

213 Collagen fibrillogenesis is an entropy-driven process promoted by

214 Understanding the nucleation of fibrillogenesis is critical so that this process can be

215 Fibrillogenesis is critically dependent on the pH and th

216 ediate species formed early in the course of fibrillogenesis is dependent upon solvent conditions.

217 Collagen fibrillogenesis is finely regulated during development o

218 FN fibrillogenesis is initiated by cytoskeleton-derived ten

219 The ability to inhibit TTR fibrillogenesis is known for several classes of compound

220 liquid phase, suggesting that inhibition of fibrillogenesis is mediated by TTR tetramer binding to A

221 ed collagen-binding proteins affect collagen fibrillogenesis is not well understood.

222 ssing are normal in these mice, and collagen fibrillogenesis is only slightly altered.

223 the process of amyloid-beta protein (Abeta) fibrillogenesis is responsible for triggering a cascade

224 uch as circular dichroism (CD) spectroscopy, fibrillogenesis is typically measured by alternative met

225 The formation of FN fibrils, fibrillogenesis, is a tightly regulated process involvin

226 nt regulator of immune function and collagen fibrillogenesis, is expressed at reduced levels in endot

227 Zinc has a dual effect on hIAPP fibrillogenesis: it increases the lag-time for fiber for

228 a-sheets has strikingly different effects on fibrillogenesis kinetics and fibril morphology.

229 ion and oligomerization state in controlling fibrillogenesis kinetics.

230 sn or His-->Gln substitutions showed altered fibrillogenesis kinetics.

231 mportant role in regulating its aggregation, fibrillogenesis, Lewy body formation, and neurotoxicity

232 Our findings indicate that ongoing amyloid fibrillogenesis may be an essential mechanistic process

233 f oligomers or protofibrils, suggesting that fibrillogenesis may occur directly from assembly of dena

234 -old rats, to examine the effect of aging on fibrillogenesis, mechanical and contractile properties o

235 In addition to defects in tendon collagen fibrillogenesis, Mkx(-/-) mutant mice exhibited abnormal

236 se data in the context of the phase-mediated fibrillogenesis model (PMF) and conclude through experim

237 These findings demonstrate that, once Abeta fibrillogenesis occurs, apoE4 favors the formation of CA

238 to be governed by the conditions under which fibrillogenesis occurs, exhibiting variation as a functi

239 Here we compare in vitro fibrillogenesis of all three purified synucleins.

240 and C-terminal strands in the initiation of fibrillogenesis of beta(2)m by creating point mutations

241 ould target molecular mechanisms that induce fibrillogenesis of cells with intracardiac origin.

242 discoidin domain receptor 2 (DDR2) inhibits fibrillogenesis of collagen endogenously secreted by the

243 overexpression of full length DDR2 inhibits fibrillogenesis of collagen type 1.

244 In addition to fibrillogenesis of collagen under the conventional condi

245 obic "core domain" of Abeta that inhibit the fibrillogenesis of full-length Abeta.

246 Fibrillogenesis of IAPP is catalyzed by synthetic and hu

247 Nanomolar misTTR inhibits fibrillogenesis of misfolded TTR under micromolar concen

248 telopeptides, two factors implicated in the fibrillogenesis of native collagen, the Col108 mini-fibr

249 As the fibrillogenesis of the 20-29 peptide often requires cond

250 quire the structural organization imposed by fibrillogenesis of the extracellular matrix.

251 brils formed from these two peptides enhance fibrillogenesis of the intact protein.

252 iological conditions and primes in vitro the fibrillogenesis of the wild-type beta2-microglobulin.

253 outside this core in the context of in vitro fibrillogenesis of the wild-type peptide at physiologica

254 Without exception, fibrillogenesis of these peptides involved an oligomeric

255 l, indicating that periostin alters collagen fibrillogenesis or cross-linking and leads to stiffening

256 vel treatment strategies aimed at inhibiting fibrillogenesis or destabilizing existing amyloid deposi

257 N binding site facilitates either negligible fibrillogenesis or produces FN fibrils that are neither

258 ine rich proteoglycan that mediates collagen fibrillogenesis, organization, and tensile strength.

259 ation of compressive strain, and fibronectin fibrillogenesis over time.

260 An important, recognized fibrillogenesis parameter is amino acid content, whereas

261 ld modulator of the lag phase of the variant fibrillogenesis, potently inhibits fibril elongation of

262 epend on the conditions under which collagen fibrillogenesis proceeds, and developing a fuller unders

263 conversion and aggregation during the entire fibrillogenesis process from random coil to mature fibri

264 er structure, which considerably affects the fibrillogenesis process, the architecture of the resulti

265 anisms rather than being key elements in the fibrillogenesis process.

266 corneal transparency by regulating collagen fibrillogenesis, promoting corneal epithelial wound heal

267 operties of collagen gels over the course of fibrillogenesis provides fundamental insight into biopol

268 manner, is a direct and rapid inducer of the fibrillogenesis required for TGF-beta-induced cell migra

269 FN fibrillogenesis requires cell-generated forces, which ex

270 lved in cell adhesion, motility, fibronectin fibrillogenesis, signaling, and growth factor receptor t

271 TGF-beta signaling is dispensable for rapid fibrillogenesis, stable interactions between the cytopla

272 Soluble intermediates in A beta fibrillogenesis, termed protofibrils, have been identifi

273 nal beta-sheet has a more profound effect on fibrillogenesis than disruption of the C-terminal beta-s

274 e potently inhibits D76N beta2-microglobulin fibrillogenesis than doxycycline with complete abrogatio

275 have different stability and less efficient fibrillogenesis than heterotrimers.

276 in mutations in this protein promote amyloid fibrillogenesis, there are no reports of this type of am

277 mechanical stretching of FN-III1 may induce fibrillogenesis through this partially unfolded intermed

278 se a recently developed biophysical model of fibrillogenesis to test competing hypotheses for the loc

279 al interior of the tissue biases Fibronectin fibrillogenesis to the tissue surface lacking cell-cell

280 Here, we investigate type I collagen fibrillogenesis using confocal rheology-simultaneous con

281 fles (CDRs), cell migration, and fibronectin fibrillogenesis via Src- and integrin-linked kinase (ILK

282 FN fibrillogenesis visualized by time-lapse AFM thus provid

283 known activator of integrin adhesion to FN, fibrillogenesis was accelerated almost threefold to 0.68

284 sing real-time quantitative kinetic methods, fibrillogenesis was characterized as a function of prote

285 agen under the conventional conditions, some fibrillogenesis was conducted alongside a 12-T magnetic

286 lack the amino terminus of the IIICS domain, fibrillogenesis was not inhibited and cell spreading was

287 The impact of these changes on fibrillogenesis was tested by treating cells with blebbi

288 teoglycan decorin, also involved in collagen fibrillogenesis, was increased compared with CTRL (all P

289 the role of integrin dynamics in fibronectin fibrillogenesis, we developed an antibody-chasing techni

290 We propose a model for cell-mediated fibrillogenesis whereby cell traction force initiates a

291 introduce a kinetic model of de novo protein fibrillogenesis which we imaged at the nanoscale and in

292 mediates are the most toxic compounds of Tau fibrillogenesis, which effectively decrease cell viabili

293 e assembly of ECM and controls elastic fiber fibrillogenesis, which is of fundamental importance in E

294 multiple FN-FN binding sites predicts robust fibrillogenesis, which minimally depends on individual d

295 Rather, neprilysin may act by reducing hIAPP fibrillogenesis, which we showed to be the case by fluor

296 ti-amyloid drugs and in the study of amyloid fibrillogenesis with a cell-based model.

297 ike homotrimeric helices that are capable of fibrillogenesis with the production of D-periodic microf

298 ype XIV collagen in early stages of collagen fibrillogenesis with tissue differences.

299 direct use of trafficked and recycled FN for fibrillogenesis, with a striking role for TGF-beta in th

300 ion, integrin translocation, and fibronectin fibrillogenesis without affecting focal contacts.