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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 myosin IIA or growth on high substrate-bound laminin-1.
13 eta4 integrin inhibited clone A migration on laminin-1.
14 sion of either subunit increased adhesion to 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
79 s suggest that fibulin-2 functions to bridge laminin-1 and laminin-5 with other extracellular matrix
80 ivity and functional relationship within the laminin-1 and LG4 as well as the functional relation bet
81 kDa skeletal muscle alpha-dystroglycan, both laminin-1 and merosin binding to 120-kDa brain alpha-dys
83 that LG4 has a unique function distinct from laminin-1 and suggest that laminin alpha1 LG4-5 may also
84 which involves the cell-binding domain(s) of laminin-1 and tumor cell surface heparan sulfate (HS).
86 ation in C2C12 myotubes, which suggests that laminin-1 and V. villosa agglutinin do not compete for t
91 upportive if III(7-10), supportive if pFN or laminin-1) and suggest that efficient interaction of fre
94 fically laminin-1), 2) the "cross-region" of laminin-1, and 3) the alpha6 moiety of the integrin rece
95 RNA-7 decreased Caco2-BBE cell attachment on laminin-1, and CD98 overexpression recovered this inhibi
96 s were considerably more spread on Matrigel, laminin-1, and collagen I than the mock transfectants an
98 f fibronectin, heparan sulfate proteoglycan, laminin-1, and entactin was observed in the GBM of the a
99 local loss of beta1C integrin, of its ligand Laminin-1, and of IGF-II in the tumor microenvironment m
100 hesion to the matrix components fibronectin, laminin-1, and thrombospondin-1 differentially regulates
101 DWS repeats, is involved in cell adhesion to laminin-1, and we specifically implicate the repeat sequ
106 idly phosphorylated on S518 by Pak following laminin-1 binding to beta1 integrin, and by protein kina
108 solid phase microtiter assay, 125I-laminin (laminin-1) bound to purified alpha-dystroglycan in a spe
111 These peptides inhibited cell attachment to laminin-1 but not to collagen I, suggesting these active
113 the same low concentrations, only Drosophila laminin-1, but neither recalphaL nor recalphaS supported
115 )-neutralizing Ab 6A11 inhibited adhesion to laminin-1 by 98% (p < 0.05), demonstrating a novel role
117 e regeneration occurred within 6 h after the laminin-1 chase by forming a morphologically complete ba
118 agated in 3-dimensional cultures composed of laminin-1, collagen I, or mixtures of the two, and analy
119 es and to E3, an elastase digest fragment of laminin-1 containing AG73, is specific, since other lami
121 hypothesis that the increased expression of laminin-1 contributes to the failure of crest-derived ce
122 tained in muscle; however, in pathway cells, laminin 1 declined modestly, and laminin beta2 decreased
124 trength of alpha6beta1-dependent adhesion to laminin-1, defined forces (0-1.5 nN) were applied to mag
125 in neurite outgrowth and also suggests that laminin-1 degradation by plasmin contributes to the proc
126 ull lens capsules exhibited higher levels of laminin-1 deposition relative to their wild-type counter
131 ainst alpha6 integrin, beta1 integrin or the laminin-1/E8 domain recognized by alpha6beta1 integrin,
134 nents (type IV, collagen, perlecan, bamacan, laminin-1, entactin-nidogen, fibronectin) in SEF areas a
139 cells cultured with and without TGF-beta1 to laminin-1, fibronectin, and vitronectin along with expre
140 e ability of an LCMV isolate to compete with laminin-1 for receptor binding is determined by its bind
143 east partially due to the interaction of the laminin-1 gamma1 chain with endogenous laminin-10, becau
144 protein because infusion of plasmin-digested laminin-1 gave similar results; 2) was posttranscription
145 ere we demonstrate that elastase cleavage of laminin-1 generates fragments, which stimulate proteinas
146 1-chain (SRARKQAASIKVAVSADR), whereas intact laminin-1 has no effect on proteinase expression by macr
148 and hence other isoforms, act redundantly to laminin 1 in posterior notochord and ISV development.
150 lular beta1 integrin ligands fibronectin and laminin-1 in a cohort of 249 breast cancer patients who
153 nces between the functions of collagen I and laminin-1 in regulating endothelial cell morphogenesis.
157 larger acinar-like structures on exposure to laminin-1 in vitro and smaller, more differentiated tumo
159 ion of PMA-stimulated cultured mast cells to laminin-1 increased from 5.3 +/- 3.6% (mean +/- SEM) in
161 src and fyn and found that neural agrin and laminin-1 induced normal clustering of AChRs and that ag
164 nhibited agrin-, V. villosa agglutinin-, and laminin-1-induced acetylcholine receptor clustering in C
172 -dimensional model, we present evidence that laminin-1 is capable of inducing epigenetic change by in
176 ryonic pancreas supports the conclusion that laminin-1 is important in the induction of exocrine (duc
180 on proteoglycans and was more effective than laminin-1, L1-Fc, or intact tenascin-C, thus demonstrati
181 eptide for blocking adhesion to fibronectin, laminin 1, laminin 5, and collagen IV was 2.4 microg, 1.
182 eptide for blocking adhesion to fibronectin, laminin 1, laminin 5, and collagen IV was 6.9 microg, 5.
183 ound to laminin-5 and laminin-10, but not to laminin-1, laminin-2, fibronectin, various collagens, ni
184 ttach to and extend neurites on substrata of laminin-1 (LN-1) during late embryogenesis, in a time fr
185 minins' functions, we examined the motion of laminin-1 (Ln-1) in physiological buffers using atomic f
186 urons lose the ability to extend neurites on laminin-1 (LN-1) with increasing developmental age yet s
187 eurites on the extracellular matrix molecule laminin-1 (LN-1), despite the fact that they retain expr
189 ases the adhesive strength of these cells on laminin-1 matrices, although it does not increase their
192 he most potent gamma1 chain peptide, blocked laminin-1-mediated adhesion and was the only gamma1 chai
194 aring the distribution of agrin with that of laminin-1, merosin (laminin-2), neurofilament, and neura
195 (KQNCLSSRASFRGCVRNLRLSR) in the G domain of laminin-1, modeled as a right-handed alpha-helix, carrie
197 hR clustering in C2 myotubes is specific for laminin-1; neither laminin-2 (merosin) nor laminin-11 (a
200 lamina proteins from chick embryos, such as laminin-1, nidogen-1, collagens IV and XVIII, perlecan,
203 isruption of the endogenous laminin layer by laminin-1 or anti-laminin gamma1 antibody renders the tP
204 forces exerted through alpha6beta4 on either laminin-1 or on an anti-alpha6 antibody, demonstrating t
206 ivation of integrin receptors by adhesion to laminin-1 or Semaphorin 7A also promotes neurite branchi
207 ue for carcinoma cells migrating randomly on laminin-1 or stimulated to migrate on collagen I with ly
208 ophin is increased by the addition of either laminin-1 or the isolated laminin alpha1 globular domain
209 amount of cAMP decreases in the presence of laminin-1 or YIGSR, suggesting a possible mechanism for
210 nhibited adhesion of MDA-MB-435 cells to the laminin-1 peptide GD6, which contains a potential integr
213 is revealed increased sinusoidal PECAM-1 and laminin-1 protein expression, suggesting gain of adheren
215 An uneven and aggregated distribution of laminin-1 protein was apparent in the anterior region of
216 nt membrane and, in particular, contact with laminin-1 provides a potent signal to down-regulate MMP-
217 , the chemotactic migration of A431 cells on laminin-1 requires not only the formation of F-actin-ric
218 trimers exert distinct effects on subsets of laminin-1-responsive cells, suggesting that isoform dive
219 me-lapse videomicroscopy of clone A cells on laminin-1 revealed that their migration is characterized
222 ses, epithelial cells in direct contact with laminin-1 seem to differentiate into ducts and acini, wh
223 all three proteins was inhibited by EDTA and laminin-1 short arm fragments, (b) polymerization of lam
224 either chain results in the dramatic loss of laminin 1 staining throughout the embryo and prevents fo
230 components (e.g., growth factors) other than laminin-1 that can sustain both carbonic anhydrase II ex
231 trate that plasminogen specifically bound to laminin-1, the interaction resulted in increased plasmin
232 integrin functions in carcinoma migration on laminin-1 through its ability to promote the formation a
234 th alpha1:SRARKQAASIKVAVSADR, but not intact laminin-1, triggers protein kinase C-dependent activatio
235 , a peptide derived from the alpha1-chain of laminin-1, triggers protein kinase C-dependent activatio
236 espite such differences in binding, LCMV and laminin-1 use, in part, an overlapping binding site on a
237 anism that locally supports cell adhesion to Laminin-1 via IGF-II is selectively regulated by the bet
238 ion and survival of HPPL in culture, whereas laminin-1 was a crucial component of Matrigel for induci
239 Increased adhesion of MMC homologues to laminin-1 was also stimulated by FcepsilonRI cross-linki
240 Moreover, during NGF-induced neuritogenesis, laminin-1 was degraded, and this cleavage was catalyzed
243 1 short arm fragments, (b) polymerization of laminin-1 was inhibited by fragments of laminins-2 and -
244 ng at the marginal edges of clone A cells on laminin-1 was resistant to solubilization with Triton X-
246 e alpha-, beta-, and gamma-chain subunits of laminin-1 were expressed in all combinations, transientl
247 concentrations of V. villosa agglutinin and laminin-1 were strictly additive with respect to acetylc
248 ast carcinoma cells, normally nonadherent to laminin 1, were stably transfected with cDNA for mouse a
249 ng the alpha 7-X2 variant adhered rapidly to laminin 1, whereas those expressing alpha 7-X1 failed to
250 a7X1 coupled with beta1A failed to adhere to laminin-1, whereas cotransfectants expressing alpha7X1 a
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