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1 using the H score (MMPs) or pixel intensity (collagen IV).
2 for, but not limited to, the crosslinking of collagen IV.
3 of elevated glucose on deposition of FN and collagen IV.
4 o kinds of alloantibodies against allogeneic collagen IV.
5 necrosis factor-alpha or cell attachment to collagen IV.
6 on of cellular fibronectin, collagen III and collagen IV.
7 ondrial ROS production (DCF and MitoSOX) and collagen IV.
8 mmunobeads recognizing either laminin 332 or collagen IV.
9 factor (CDAF) that is processed from alpha1 collagen IV.
10 the only BMP ligand in Drosophila that binds collagen IV.
11 ith magnetic beads coated with antibodies to collagen IV.
12 hanism of BMP shuttling that is catalyzed by collagen IV.
13 culature was dual stained with isolectin and collagen IV.
14 of Perlecan, which counters constriction by Collagen IV.
15 es, polymerizing, and binding to nidogen and collagen IV.
16 mbrane, as mirrored by an increase in plasma collagen IV.
17 to the membrane of Caco-2 cells spreading on collagen IV.
18 fferentiate, but showed impaired adhesion to collagen IV.
19 l epithelial cell spreading and migration on collagen IV.
20 ulation of Caco-2 spreading and migration on collagen IV.
21 oodpasture auto-antigen, the alpha3 chain of collagen IV.
22 anoma cells did not affect their adhesion to collagen IV.
23 o both native and recombinant NC1 domains of collagen IV.
24 s by integrin signaling when cells attach to collagen IV.
25 nderlying chain selection in the assembly of collagen IV.
26 n, cell aggregation, or protease cleavage of collagen IV.
27 apico-basal polarity markers Podocalyxin and Collagen IV.
28 2-mediated crosslinking of basement membrane collagen IV.
29 tes the formation of covalent cross-links in collagen IV.
30 the formation of sulfilimine cross-links in collagen IV.
31 FIX binds tightly to collagen IV.
32 in, heparin, bovine serum albumin, mucin, or collagen IV.
34 oteinases (MMPs) have the ability to degrade collagen IV, a main component of the breast lobular base
35 o chromatin to increase the transcription of collagen IV, a major collagen upregulated in fibrosis.
36 d of an IOL placed on a membrane coated with collagen IV, a major constituent of the lens capsule.
39 etic mice, Sema3a(+) exacerbates laminin and collagen IV accumulation in Kimmelstiel-Wilson-like glom
41 lointerstitial total collagen and glomerular collagen IV accumulation) benefits were seen upon dual t
42 on in ROCK activity, albuminuria, glomerular collagen IV accumulation, and urinary collagen IV excret
45 h islets seeded onto scaffolds adsorbed with collagen IV achieved euglycemia fastest and their respon
47 D mutation in the collagen domain of COL4A2 (collagen IV alpha chain 2) in a family displaying porenc
48 neys showed significantly less expression of collagen IV, alpha-smooth muscle actin, and other marker
49 product of the alpha1alpha2alpha1 network of collagen IV (alpha1alpha2alpha1(IV) truncated protomer)
50 membrane disorder caused by mutations in the collagen IV alpha3, alpha4, or alpha5 genes that results
54 is required for sulfilimine formation within collagen IV, an event critical for BM assembly and tissu
56 llel to perlecan and in opposition to viking/collagen IV and betaPS-integrin to keep CNS lineages roo
57 tegrin interacts with two different ligands, collagen IV and CDH17, using two different binding sites
61 ockdown cells revealed increased adhesion to collagen IV and decreased invasion through the Matrigel.
62 IV modifying enzymes rescued ER retention of collagen IV and EC apoptosis and resulted in normal deve
63 rosis, mesangial expansion, and ECM protein (collagen IV and fibronectin) accumulation as well as inc
64 uction in EC resulted in impaired folding of collagen IV and its retention in the endoplasmic reticul
65 extracellular matrix (ECM), with a focus on collagen IV and its variant, spongin short-chain collage
73 trated a 2-fold increase in the levels of BM collagen IV and LOX, key determinants of capillary BM st
76 ver, in Col4a3(-/-) Alport mice, both intact collagen IV and NC1 hexamers from murine GBM elicited Ig
77 ion, respectively) Caco-2 sheet migration on collagen IV and noticeably inhibited lamellipodial exten
80 ation, altered peritracheal distributions of collagen IV and Perlecan, misregulated ASP growth, and a
83 hos-Foxo3a, phos-NF-kappaB, fibronectin, and collagen IV and reduced expressions of Sirt1 and total-F
84 ow that p53 induces the expression of alpha1 collagen IV and release of Arresten-containing fragments
85 issues, is primarily composed of laminin and collagen IV and serves as a structural barrier to cancer
86 1 knockdown decreased melanocyte adhesion to collagen IV and shifted melanocyte localization in a man
88 hesion of both fetal and adult beta-cells to collagen IV and vitronectin also results in the marked s
89 pendent adhesion of fetal beta-cells to both collagen IV and vitronectin induces significant glucose-
90 remodeling in old mice, including increased collagen IV and XVI and decreased Fraser syndrome comple
92 connective tissue growth factor (CTGF), and collagens IV and VI found in diabetic wild-type mice was
93 own to bind decay-accelerating factor (DAF), collagen IV, and carcinoembryonic antigen-related cell a
94 ses Col4a2 and intracellular accumulation of collagen IV, and decreases the proteolytic release of co
96 (4) significant accumulation of perivascular collagen IV, and fibrin deposits (5) significantly incre
99 rticipates in regulation of cell adhesion on collagen IV, and is required for maximal PAK1 kinase act
100 llular matrix proteins-including collagen I, collagen IV, and laminin V-to modulate intercellular Eca
101 ment membrane (BM) constituents, laminin 10, collagen IV, and nidogen-2 (but not perlecan) are consid
104 th invasive outgrowths, their degradation of collagen IV, and their secretion of urokinase-type plasm
105 capillary knot, dysregulation of nephrin and collagen IV, and ultrastructural changes in the trilamin
106 that the structural and genomic features of collagen IV are homologous to those of non-bilaterian an
108 opy after immunohistochemically staining for collagen IV basement membrane markers, in addition to ex
111 n this article, we show that adhesion by the collagen IV-binding integrin alpha1beta1 unexpectedly in
113 integrin consistent with the modification of collagen IV by hypochlorous (HOCl) and hypobromous acids
114 bilized the expression of full-length alpha1 collagen IV by upregulation of alpha(II) prolyl-hydroxyl
115 n as PLOD3) into newly identified post-Golgi collagen IV carriers and that VIPAR-dependent sorting is
116 he 7/10/22 subfamily and broadly distributed collagen IV chains (alpha1/2) promote clustering of syna
119 our previous studies, establish that the six collagen IV chains are organized into three canonical pr
120 tress arising from defective localization of collagen IV chains in human podocytes contributes to the
122 ted by pathogenic anti-GBM alloantibodies to collagen IV chains present in the renal allograft but ab
127 protein quantification showed a dominance of collagen IV, collagen I, and laminin isoforms in the glo
128 tivity of structural ECM genes (fibronectin, collagen IV, collagen VI, myocilin), matricellular genes
131 (trans), microvessel volume, and circulating collagen IV correlated with duration of overall survival
135 ent in vivo was associated with increases in collagen IV, decreases in laminin, and varied changes in
137 An inhibitor of FN matrix assembly prevented collagen IV deposition, demonstrating dependence of coll
140 foot processes, lowered proteinuria, lowered collagen IV deposits in the mesangial matrix, diminished
143 orms of the major ECM components laminin and collagen IV did not reproduce the effect; or (3) inhibit
145 stress are potential therapeutic options for collagen IV diseases including haemorrhagic stroke.
147 ch involves degradation or reorganization of collagen IV (EMB-9), whereas FBL-1 opposes GON-1 by stab
148 microenvironment, and as a component of BM, collagen IV enabled the assembly of a fundamental archit
149 nity of the extracellular alpha1 I domain to collagen IV enhances outside-in signaling by potentiatin
150 dermal-epidermal junction, we propose that a collagen-IV-enriched DEJ may, in part, explain its well-
151 immunization with native forms of allogeneic collagen IV exclusively elicited antibodies to quaternar
152 erular collagen IV accumulation, and urinary collagen IV excretion compared with untreated db/db mice
153 for diabetic vs. treated) and a reduction in collagen IV expression following sTbetaRII.Fc treatment
155 Follicle epithelia mutant for integrin or collagen IV fail to rotate and elongate, which results i
156 helial colony-forming cells (ECFCs), deposit collagen IV, fibronectin, and laminin that assemble to a
158 d that in vivo ITF2357 decreased collagen I, collagen IV, fibronectin, integrin alphaVbeta3 expressio
159 of lactide and glycolide were adsorbed with collagen IV, fibronectin, laminin-332 or serum proteins
160 llagen III as well as mixtures of collagen I/collagen IV/fibronectin as having a positive effect on L
162 nesis because it was necessary for export of collagen IV from EC and deposition in vascular basement
165 als at longer range in vivo, indicating that collagen IV functions to immobilize free Dpp in the embr
167 agen IV + heparan sulfate + laminin (CHL) or collagen IV + gelatin + heparan sulfate (CGH) demonstrat
168 ereditary nephropathy caused by mutations in collagen IV genes and characterized by ultrastructural l
169 ereditary nephropathy caused by mutations in collagen IV genes and characterized by ultrastructural l
170 ar matrix proteins fibronectin, laminin, and collagen IV have been shown to function as receptors for
172 able to compete for the alpha1 I domain from collagen IV (IC(50) approximately 3 mum), GFOGER is much
173 sue from P1 and P2 was found to have reduced collagen IV immunoreactivity at the muscle basement memb
178 We identified basement membrane (BM) and collagen IV in Ctenophora, and show that the structural
179 valuated expression of MMPs 2, 9, and 14 and collagen IV in LCIS and adjacent normal breast tissue am
180 the N- and C-termini of agrin, laminin, and collagen IV in mouse and human GBM revealed a highly ori
183 llagen III in the liver and collagen III and collagen IV in the heart; this is induced by HF feeding.
184 resulted in markedly decreased deposition of collagen IV in the mesangium and less beta-galactosidase
185 itions under which Arresten is released from collagen IV in vivo or whether the protein functions in
186 ood vessels, localized to the same region as collagen IV, in 2 representative human tissues: liver an
187 cumulation of the basement membrane protein, collagen IV, in LVV-forming endothelial cells (EC), and
188 BA treatment reduced ER stress and increased collagen IV incorporation into BMs, the persistence of d
192 tion proteins, did not affect degradation of collagen IV induced by the tMCAO, but altered cell types
196 endent release of bioactive NC1 domains from collagen IV is critical for integrating collagen IV synt
198 overed that the extracellular matrix protein collagen IV is important for BMP gradient formation.
199 es and the vascular basement membrane marker collagen IV is mislocalized, suggesting that ECs fail to
201 here is a novel strain-specific alternative collagen IV isoform switch that is associated with the d
202 y GBM components (fibronectin, laminins, and collagen IV isoforms), or podocyte integrins could be ob
205 extract (Adipogel) comprising ECM proteins (collagen IV, laminin, hyaluronan, and fibronectin) and i
208 vessel volume, and the change of circulating collagen IV levels, all after a single dose of cediranib
209 g glucose-mediated oxidative modification of collagen IV lysine residues rescued the alterations in c
210 ce the function of transplanted islets, with collagen IV maximizing graft function relative to the ot
211 ibitors of MAPK and 2-oxoglutarate dependent collagen IV modifying enzymes rescued ER retention of co
213 re detected within the assembly interface of collagen IV NC1 domains isolated from renal ECM of diabe
216 MN) and Alport syndrome (AS) are progressive collagen IV nephropathies caused by mutations in COL4A3/
218 pha5(IV) heterotrimer, which forms the major collagen IV network of the glomerular basement membrane
219 inforcing sulfilimine cross-links within the collagen IV network, an event essential to basement memb
220 rt GBM is effective at restoring the missing collagen IV network, slowing kidney disease progression,
223 important structural cross-linking domain of collagen IV networks that provide mechanical stability t
224 r, the mechanism whereby podocytes adhere to collagen IV networks, a major component of the glomerula
225 us (NC1) hexamers, key connection modules of collagen IV networks, are modified via oxidation and chl
226 modifications of renal ECM, and specifically collagen IV networks, contribute to functional protein d
227 molecular machinery that forms cross-linked collagen IV networks, which are essential for glomerular
233 ysis and muscle damage could be rescued with collagen IV overexpression, matrix metalloproteinase (MM
235 ting and treating established adult ICH, but collagen IV patients will require stratification based o
237 ell death, and basement membrane constituent collagen IV production were examined in an organotypic d
238 eterozygous mice in association with reduced collagen IV production, decreased N1ICD, and attenuated
239 ericytes with TNF-alpha and IL-17A augmented collagen IV production, similar to in vivo remodeling.
244 5R, which binds better than wild-type FIX to collagen IV, provides better hemostasis than wild-type F
245 rabbit anti-VWF, rat ani-CD105, rabbit anti-collagen IV, rat anti-ICAM-2, rabbit anti-desmin, and ra
246 ecause the molecular mechanisms whereby this collagen IV receptor mediates endothelial cell functions
247 ient recombinant laminins, with retention of collagen IV, reiterating the basement membrane (BM) chan
248 othelial denudation, exposing the underlying collagen IV-rich basal lamina, which promotes both intra
249 tended to localize in close proximity to the collagen IV-rich basement membranes of either the airway
250 mbrane from the lens capsule of the eye is a collagen IV-rich matrix that can easily be extracted and
253 ely, our findings establish that the triad-a collagen IV scaffold with sulfilimine cross-links, perox
254 ysine residues to structurally reinforce the collagen IV scaffold, a function critical for basement m
256 stigate the alpha121, alpha345, and alpha565 collagen IV scaffolds and to develop therapies for manag
258 ole for the chloride ring in the assembly of collagen IV scaffolds of BMs, a critical event enabling
262 Mouse mesangial cells plated on MGO-modified collagen IV showed decreased adhesion and migration.
265 tein receptor type 2 (BMPR2) and its target, collagen IV, signaling of the phosphorylated form of the
270 r an order of magnitude of stiffness values, collagen IV surfaces lead to enhanced motility compared
271 from collagen IV is critical for integrating collagen IV synthesis and proteolysis with epithelial pr
272 bstitutions have enhanced down-regulation of collagen IV synthesis, which is mediated by the ERK/MAPK
275 Previously, we reported the engineering of collagen IV-targeting nanoparticles (NPs) and demonstrat
276 lymeric NPs were surface functionalized with collagen IV-targeting peptides and loaded with paclitaxe
278 study in vivo the biogenesis and assembly of Collagen IV, the main constituent of BMs, we used a GFP-
279 hough the cells adhered to the BrM component collagen IV, these cells preferentially adhered to lamin
280 ing in EC that is necessary for EC export of collagen IV, thus permitting the development of LVV and
281 2) is required by both cell types to produce collagen IV to activate ILK (integrin-linked kinase).
282 tein functionality, including the ability of collagen IV to interact with glomerular mesangial cells.
283 e microelectrodes in the MEA was coated with collagen IV to promote cell adhesion and further single-
284 h blood vessels (labeled with an antibody to collagen IV) to measure the coverage of vessel walls by
285 LNNd was found to mediate laminin binding to collagen IV, to bind to galactosyl sulfatide, and to sel
288 intracerebral haemorrhage (ICH), and common collagen IV variants are a risk factor for sporadic ICH.
289 nset disease were studied with antibodies to collagens IV, VIIIA1, VIIIA2, fibronectin, and laminin.
290 ing VNC, the extracellular matrix components Collagen IV, Viking and Peroxidasin are not deposited ar
294 , alpha-Actinin), and the basement membrane (Collagen IV), were down-regulated upon SRF depletion.
295 a its N-terminal CUB domains, interacts with Collagen IV, which enhances Tolloid activity towards its
296 oteins that contain this amino acid, such as collagen IV, which is an important structural component
299 ucts, and in a zymography assay, reaction of collagen IV with products of A2E photodegradation result