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1 l three, but show decreased proliferation on laminin 1.
2 ndary and do not enter the region containing laminin 1.
3 D82 significantly inhibited cell adhesion on laminin 1.
4 gamma1) partially compensates for the absent laminin 1.
5 olecule in adhesion of a hemopoietic cell to laminin-1.
6 ediated through up-regulation of mesenchymal laminin-1.
7 peptide could inhibit tumor cell adhesion to laminin-1.
8 he pancreatic mesenchyme diffusely expresses laminin-1.
9 ind SV2 binds with high affinity to purified laminin-1.
10 is and is required for lamellae formation on laminin-1.
11 in cells adherent to thrombospondin-1 or to laminin-1.
12 eta4 integrin inhibited clone A migration on laminin-1.
13 sion of either subunit increased adhesion to laminin-1.
14 myosin IIA or growth on high substrate-bound laminin-1.
15 neither polymerized nor co-polymerized with laminin-1.
16 nd exhibits dynamic adhesion and motility on laminin-1.
17 LSIRT) decreases the size of acini formed on laminin-1.
18 also inhibited attachment to collagen IV and laminin-1.
19 dothelial marker, von Willebrand factor, and laminin-1.
20 ned the adhesion of prostate cancer cells to laminin-1.
21 otif sufficient to increase cell adhesion to Laminin-1.
22 ic sites in the extracellular matrix protein laminin-1.
23 growth cones turn on a uniform substrate of laminin-1.
24 ombospondin-2, and the E8 fragment of murine laminin-1.
25 ng alpha6beta1 integrin-mediated adhesion to laminin-1.
27 Further study demonstrated that exogenous laminin (1-10 microg/ml) treatment induced microglial ac
28 y of the following: 1) laminin (specifically laminin-1), 2) the "cross-region" of laminin-1, and 3) t
30 h at least three different laminin isoforms (laminins 1, 2/4, and 10/11) in the blastocyst and in the
31 and a close self-assembly relationship among laminins-1, -2, and -4 were demonstrated by: (a) polymer
32 ules with either three full short arms (e.g. laminins-1-4), or molecules containing one (laminins-6-9
35 at the decrease in apoptosis is dependent on laminin 1, a ligand for surface GalT I, suggesting that
36 ation of IGF-II levels increases adhesion to Laminin-1, a basement membrane protein down-regulated in
38 ked for interaction between purified SV2 and laminin-1, a laminin isoform with a similar structure.
41 n of all the neurites, whereas inhibition of laminin-1 activity reduced the elongation of minor neuri
45 d: discontinuous epithelial BM straining for laminin-1 (alpha 1 beta 1 gamma 1), entactin/nidogen and
46 antibodies directed against beta 2 laminin, laminin-1 (alpha 1-beta 1-gamma 1), and von Willebrand f
49 ed from the COOH-terminal globular domain of laminin-1 alpha1 chain (laminin G peptides), designated
50 of the laminin alpha2-chain, as well as its laminin-1 alpha1-chain counterpart, to identify candidat
51 s involved in neuronal viability, we infused laminin-1 (alpha1,beta1,gamma1) into the mouse hippocamp
52 inin heterotrimers: they grow freely between laminin 1 (alpha1beta1gamma1) and laminin 2, fail to cro
54 previously identified 20 angiogenic sites on laminin-1 (alpha1beta1gamma1) by screening 559 overlappi
55 Fibulin-2 was also found to interact with laminin-1 (alpha1beta1gamma1) through a region (residues
60 beta 1 is the major trophoblast receptor for laminin 1 and a functional receptor for laminins 2/4 and
64 issues also expressed vimentin, collagen IV, laminin 1 and laminin beta2, whereas fibronectin was det
65 ants revealed that alpha7beta1 binds well to laminin 1 and to a mixture of laminin 2 and 4 but not to
66 become single cells or very small groups on laminin 1 and VE-cadherin localization at regions of cel
70 genesis appears to require basement membrane laminin-1 and an alpha6-containing integrin receptor; 2)
71 TAG-1 and the extracellular matrix molecules laminin-1 and chondroitin sulfate proteoglycans (CSPGs)
72 servations suggest that transcripts encoding laminin-1 and collagen (IV) are increased in the colon a
74 library to identify sequences which bind to laminin-1 and elute with heparan sulfate or peptide 11 (
75 The processes differentially contribute on laminin-1 and fibronectin due to selective actin tetheri
76 ffect was mediated in part by an increase in laminin-1 and fibronectin mRNA levels and in part by the
77 of extracellular matrix proteins, especially laminin-1 and fibronectin, suggesting altered cytoskelet
80 s suggest that fibulin-2 functions to bridge laminin-1 and laminin-5 with other extracellular matrix
81 ivity and functional relationship within the laminin-1 and LG4 as well as the functional relation bet
82 kDa skeletal muscle alpha-dystroglycan, both laminin-1 and merosin binding to 120-kDa brain alpha-dys
84 that LG4 has a unique function distinct from laminin-1 and suggest that laminin alpha1 LG4-5 may also
85 which involves the cell-binding domain(s) of laminin-1 and tumor cell surface heparan sulfate (HS).
87 ation in C2C12 myotubes, which suggests that laminin-1 and V. villosa agglutinin do not compete for t
92 upportive if III(7-10), supportive if pFN or laminin-1) and suggest that efficient interaction of fre
95 fically laminin-1), 2) the "cross-region" of laminin-1, and 3) the alpha6 moiety of the integrin rece
96 RNA-7 decreased Caco2-BBE cell attachment on laminin-1, and CD98 overexpression recovered this inhibi
97 s were considerably more spread on Matrigel, laminin-1, and collagen I than the mock transfectants an
99 f fibronectin, heparan sulfate proteoglycan, laminin-1, and entactin was observed in the GBM of the a
100 local loss of beta1C integrin, of its ligand Laminin-1, and of IGF-II in the tumor microenvironment m
101 hesion to the matrix components fibronectin, laminin-1, and thrombospondin-1 differentially regulates
102 DWS repeats, is involved in cell adhesion to laminin-1, and we specifically implicate the repeat sequ
107 idly phosphorylated on S518 by Pak following laminin-1 binding to beta1 integrin, and by protein kina
109 solid phase microtiter assay, 125I-laminin (laminin-1) bound to purified alpha-dystroglycan in a spe
112 These peptides inhibited cell attachment to laminin-1 but not to collagen I, suggesting these active
114 the same low concentrations, only Drosophila laminin-1, but neither recalphaL nor recalphaS supported
116 )-neutralizing Ab 6A11 inhibited adhesion to laminin-1 by 98% (p < 0.05), demonstrating a novel role
118 e regeneration occurred within 6 h after the laminin-1 chase by forming a morphologically complete ba
119 agated in 3-dimensional cultures composed of laminin-1, collagen I, or mixtures of the two, and analy
120 es and to E3, an elastase digest fragment of laminin-1 containing AG73, is specific, since other lami
122 hypothesis that the increased expression of laminin-1 contributes to the failure of crest-derived ce
123 tained in muscle; however, in pathway cells, laminin 1 declined modestly, and laminin beta2 decreased
125 trength of alpha6beta1-dependent adhesion to laminin-1, defined forces (0-1.5 nN) were applied to mag
126 in neurite outgrowth and also suggests that laminin-1 degradation by plasmin contributes to the proc
127 ull lens capsules exhibited higher levels of laminin-1 deposition relative to their wild-type counter
132 ainst alpha6 integrin, beta1 integrin or the laminin-1/E8 domain recognized by alpha6beta1 integrin,
135 nents (type IV, collagen, perlecan, bamacan, laminin-1, entactin-nidogen, fibronectin) in SEF areas a
140 cells cultured with and without TGF-beta1 to laminin-1, fibronectin, and vitronectin along with expre
141 e ability of an LCMV isolate to compete with laminin-1 for receptor binding is determined by its bind
144 east partially due to the interaction of the laminin-1 gamma1 chain with endogenous laminin-10, becau
145 protein because infusion of plasmin-digested laminin-1 gave similar results; 2) was posttranscription
146 ere we demonstrate that elastase cleavage of laminin-1 generates fragments, which stimulate proteinas
147 1-chain (SRARKQAASIKVAVSADR), whereas intact laminin-1 has no effect on proteinase expression by macr
149 and hence other isoforms, act redundantly to laminin 1 in posterior notochord and ISV development.
151 lular beta1 integrin ligands fibronectin and laminin-1 in a cohort of 249 breast cancer patients who
154 nces between the functions of collagen I and laminin-1 in regulating endothelial cell morphogenesis.
158 larger acinar-like structures on exposure to laminin-1 in vitro and smaller, more differentiated tumo
160 ion of PMA-stimulated cultured mast cells to laminin-1 increased from 5.3 +/- 3.6% (mean +/- SEM) in
162 src and fyn and found that neural agrin and laminin-1 induced normal clustering of AChRs and that ag
165 nhibited agrin-, V. villosa agglutinin-, and laminin-1-induced acetylcholine receptor clustering in C
173 -dimensional model, we present evidence that laminin-1 is capable of inducing epigenetic change by in
177 ryonic pancreas supports the conclusion that laminin-1 is important in the induction of exocrine (duc
181 on proteoglycans and was more effective than laminin-1, L1-Fc, or intact tenascin-C, thus demonstrati
182 eptide for blocking adhesion to fibronectin, laminin 1, laminin 5, and collagen IV was 2.4 microg, 1.
183 eptide for blocking adhesion to fibronectin, laminin 1, laminin 5, and collagen IV was 6.9 microg, 5.
184 ound to laminin-5 and laminin-10, but not to laminin-1, laminin-2, fibronectin, various collagens, ni
185 ttach to and extend neurites on substrata of laminin-1 (LN-1) during late embryogenesis, in a time fr
186 minins' functions, we examined the motion of laminin-1 (Ln-1) in physiological buffers using atomic f
187 urons lose the ability to extend neurites on laminin-1 (LN-1) with increasing developmental age yet s
188 eurites on the extracellular matrix molecule laminin-1 (LN-1), despite the fact that they retain expr
190 ases the adhesive strength of these cells on laminin-1 matrices, although it does not increase their
193 he most potent gamma1 chain peptide, blocked laminin-1-mediated adhesion and was the only gamma1 chai
195 aring the distribution of agrin with that of laminin-1, merosin (laminin-2), neurofilament, and neura
196 (KQNCLSSRASFRGCVRNLRLSR) in the G domain of laminin-1, modeled as a right-handed alpha-helix, carrie
198 hR clustering in C2 myotubes is specific for laminin-1; neither laminin-2 (merosin) nor laminin-11 (a
201 lamina proteins from chick embryos, such as laminin-1, nidogen-1, collagens IV and XVIII, perlecan,
204 isruption of the endogenous laminin layer by laminin-1 or anti-laminin gamma1 antibody renders the tP
205 forces exerted through alpha6beta4 on either laminin-1 or on an anti-alpha6 antibody, demonstrating t
207 ivation of integrin receptors by adhesion to laminin-1 or Semaphorin 7A also promotes neurite branchi
208 ue for carcinoma cells migrating randomly on laminin-1 or stimulated to migrate on collagen I with ly
209 ophin is increased by the addition of either laminin-1 or the isolated laminin alpha1 globular domain
210 amount of cAMP decreases in the presence of laminin-1 or YIGSR, suggesting a possible mechanism for
211 nhibited adhesion of MDA-MB-435 cells to the laminin-1 peptide GD6, which contains a potential integr
214 is revealed increased sinusoidal PECAM-1 and laminin-1 protein expression, suggesting gain of adheren
216 An uneven and aggregated distribution of laminin-1 protein was apparent in the anterior region of
217 nt membrane and, in particular, contact with laminin-1 provides a potent signal to down-regulate MMP-
218 , the chemotactic migration of A431 cells on laminin-1 requires not only the formation of F-actin-ric
219 trimers exert distinct effects on subsets of laminin-1-responsive cells, suggesting that isoform dive
220 me-lapse videomicroscopy of clone A cells on laminin-1 revealed that their migration is characterized
223 ses, epithelial cells in direct contact with laminin-1 seem to differentiate into ducts and acini, wh
224 all three proteins was inhibited by EDTA and laminin-1 short arm fragments, (b) polymerization of lam
225 either chain results in the dramatic loss of laminin 1 staining throughout the embryo and prevents fo
231 components (e.g., growth factors) other than laminin-1 that can sustain both carbonic anhydrase II ex
232 trate that plasminogen specifically bound to laminin-1, the interaction resulted in increased plasmin
233 integrin functions in carcinoma migration on laminin-1 through its ability to promote the formation a
235 th alpha1:SRARKQAASIKVAVSADR, but not intact laminin-1, triggers protein kinase C-dependent activatio
236 , a peptide derived from the alpha1-chain of laminin-1, triggers protein kinase C-dependent activatio
237 espite such differences in binding, LCMV and laminin-1 use, in part, an overlapping binding site on a
238 anism that locally supports cell adhesion to Laminin-1 via IGF-II is selectively regulated by the bet
239 ion and survival of HPPL in culture, whereas laminin-1 was a crucial component of Matrigel for induci
240 Increased adhesion of MMC homologues to laminin-1 was also stimulated by FcepsilonRI cross-linki
241 Moreover, during NGF-induced neuritogenesis, laminin-1 was degraded, and this cleavage was catalyzed
244 1 short arm fragments, (b) polymerization of laminin-1 was inhibited by fragments of laminins-2 and -
245 ng at the marginal edges of clone A cells on laminin-1 was resistant to solubilization with Triton X-
247 e alpha-, beta-, and gamma-chain subunits of laminin-1 were expressed in all combinations, transientl
248 concentrations of V. villosa agglutinin and laminin-1 were strictly additive with respect to acetylc
249 ast carcinoma cells, normally nonadherent to laminin 1, were stably transfected with cDNA for mouse a
250 ng the alpha 7-X2 variant adhered rapidly to laminin 1, whereas those expressing alpha 7-X1 failed to
251 a7X1 coupled with beta1A failed to adhere to laminin-1, whereas cotransfectants expressing alpha7X1 a