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1 ng with the Abeta peptide to inhibit Abeta42 fiber formation.
2 locked both TGFbeta- and FGF2-induced stress fiber formation.
3 ntation of the lipid membrane during amyloid fiber formation.
4 enting the initial association of hCT before fiber formation.
5 the tyrosine kinase c-Abl and disrupts actin fiber formation.
6 lite cell lineage causes a deficit of muscle fiber formation.
7 p accumulation, angiogenesis, and new muscle fiber formation.
8 d that adenosine inhibits HGF-induced stress fiber formation.
9 ntification and mechanistic study of amyloid fiber formation.
10 icle required for its proper growth and hair fiber formation.
11 must be highly regulated to avoid premature fiber formation.
12 hat a specific residue order is required for fiber formation.
13 istone H1 and considered important for 30-nm-fiber formation.
14 y myosin light chain kinase and actin stress fiber formation.
15 ted precocious initiation of the GA-mediated fiber formation.
16 ior to undergoing myoblast fusion and muscle fiber formation.
17 ntial role for kinetic trapping in chromatin fiber formation.
18 ation, myoblast accumulation, and new muscle fiber formation.
19 has been predicted by kinetic models of IAPP fiber formation.
20 eratocyte elongation without inducing stress fiber formation.
21 cteria, recombinant protein purification and fiber formation.
22 insight into the interactions governing Hb S fiber formation.
23 t Rac1 or Cdc42, and potently induced stress fiber formation.
24 gthens focal adhesions, and increases stress fiber formation.
25 riginal founder cell, to initiate fusion and fiber formation.
26 apeutic increases in the delay time prior to fiber formation.
27 tion with filamentous actin (F-actin) stress fiber formation.
28 imulation of ROCK, which causes actin stress-fiber formation.
29 ir effect on protein aggregation and amyloid fiber formation.
30 own to trigger signaling cascades via stress fiber formation.
31 calcium concentration and actomyosin stress fiber formation.
32 assembly pathway that may or may not lead to fiber formation.
33 esult in self-association leading to amyloid fiber formation.
34 s, probably resulting from defects in xylary fiber formation.
35 res nucleating factors, which initiate actin fiber formation.
36 ha-smooth muscle actin expression and stress fiber formation.
37 like conformation does not depend on amyloid fiber formation.
38 ted cell proliferation, migration and stress fiber formation.
39 tes to both membrane leakage and accelerated fiber formation.
40 ROCK1 and -2, which all prevent actin stress fiber formation.
41 ce to explore the details of aggregation and fiber formation.
42 lar assembly in bacteria and in vivo amyloid fiber formation.
43 naked seed mutant (N1N1) that is impaired in fiber formation.
44 ho GTPase and downstream signaling to stress fiber formation.
45 lly, an external electric field promotes saa fiber formation.
46 r the elucidation of some aspects of protein fiber formation.
47 ced and consequently there is a delay in DLM fiber formation.
48 fore either notable focal adhesion or stress fiber formation.
49 omers, an active cytoskeleton can facilitate fiber formation.
50 rations of beta2m necessary to avoid amyloid fiber formation.
51 f full-length NET1 to stimulate actin stress fiber formation.
52 e reciprocal of the delay time that precedes fiber formation.
53 pithelial cells, which requires actin stress fiber formation.
54 marker of the quantity and quality of muscle fiber formation.
55 nteraction and how Cu(2+) influences amyloid fiber formation.
56 e core domain is significantly reduced after fiber formation.
57 ss of VE-cadherin, and aberrant actin stress fiber formation.
58 the myosin regulatory light chain and stress fiber formation.
59 with scAAV2.dnRhoA showed diminished stress fiber formation.
60 odify fiber-forming polymers in the stage of fiber formation.
61 spreading, traction stress, and fibronectin fiber formation.
62 hat regulates Src kinase activity and stress fiber formation.
63 beta-arrestin in RhoA activation and stress fiber formation.
64 scle actin (alpha-SMA) expression and stress fiber formation.
65 in-4 matrix deposition and thereby fibulin-4 fiber formation.
66 eveals where microtubules are added during K-fiber formation.
67 acids in the N terminus that is key for TasA fiber formation.
68 eta-sheet amyloid fibrils, which can trigger fiber formation.
69 exhibited a dominant negative effect on TasA fiber formation.
70 er oligomerization, which underlie chromatin fiber formation.
71 operty that is incompatible with protein/DNA fiber formation.
72 s with the bacterial inner membrane prior to fiber formation.
73 ng kinetochores but not kinetochore fiber (K fiber) formation.
74 ted that this BTE variant is also capable of fiber formation, albeit at a reduced persistence length.
75 ive cutis laxa and marked defects in elastic fiber formation amplifies previous observations on the m
76 HLFs, but inhibited TGF-beta-induced stress fiber formation and activation of serum response factor
77 mbly factor that is required for kinetochore fiber formation and activation of the mitotic kinase Aur
81 its downstream effector ROCK mediate stress fiber formation and cell contraction through their effec
82 ouse embryonic fibroblasts, including stress fiber formation and cell migration, it's deletion led to
84 ding but enhances fibronectin-induced stress fiber formation and cell-mediated partial unfolding of f
85 al effect in part by preventing actin stress fiber formation and claudin 18 disorganization through s
86 N-terminally truncated Abeta will accelerate fiber formation and co-assemble into short rod-shaped fi
87 factors associated with vascularization and fiber formation and components of cellular signaling pat
90 utflow facility, whereas S1P promotes stress fiber formation and contractility in cultured trabecular
92 Eg5 interaction was required for kinetochore fiber formation and contributed to Eg5 localization to s
94 gnaling was associated with a loss of stress fiber formation and decreased expression of SMC differen
96 tion, tissue edema led to significant stress fiber formation and decreased numbers of focal contacts.
97 brillogenesis: it increases the lag-time for fiber formation and decreases the rate of addition of hI
98 e migratory response through enhanced stress fiber formation and disruption of endothelial cell-cell
99 of proteotoxicity and the dynamic changes in fiber formation and dissemination remain unclear, preven
101 microfibrils have essential roles in elastic fiber formation and elastic tissue homeostasis, as well
103 239 is accompanied by increased actin stress fiber formation and enhanced endothelial tube formation.
104 Larger nucleation domains result in rapid fiber formation and eventual precipitation or gelation w
105 IGPR-1 activity also modulates actin stress fiber formation and focal adhesion and reduces cell migr
106 ouse podocytes with Bis-T-23 promoted stress fiber formation and focal adhesion maturation in a dynam
107 e examined the effect of adenosine on stress fiber formation and found that adenosine inhibits HGF-in
108 ly inform reaction-based theories of amyloid fiber formation and have implications for neurodegenerat
109 ells display substantial decreases of stress fiber formation and impaired cell migration and spreadin
110 e signaling events result in enhanced stress fiber formation and increased actomyosin contractility,
112 t limits Rho-dependent events such as stress fiber formation and it maintains the association of beta
113 tocyte contractility, as indicated by stress fiber formation and matrix compaction and alignment.
117 I formin homology 2 domain, inhibited stress fiber formation and myofibroblast differentiation induce
118 n stress fibers, which further drives stress fiber formation and myofibroblast differentiation, and (
120 myosin L chain (MLC) phosphorylation, stress fiber formation and permeability increases during inflam
122 in Nf1(-/-) astrocytes rescued actin stress fiber formation and restored cell motility and prolifera
124 r its proposed non-classical roles in muscle fiber formation and sensory neuron development, but is c
125 l the central importance of BMP in secondary fiber formation and show that although FGF may be necess
126 nteraction inhibited thrombin-induced stress fiber formation and SRE activation supports this hypothe
127 iRNA inhibited thrombin-induced actin stress fiber formation and SRE-dependent gene transcription.
128 anical model provides a mechanism for stress fiber formation and stiffness sensing in cells adhered t
129 esponse to genotoxic stress maintains stress fiber formation and strikingly increases apoptosis, impl
130 ntensity (1680 s), are attributed to initial fiber formation and subsequent formation of larger assem
131 t required for mouse development and elastic fiber formation and suggest possible functional redundan
132 ation include the disruption of actin stress fiber formation and the decreased expression of lateral
135 d NO bioavailability, increased actin stress fiber formation, and a lack of distinct cell polarity co
136 n by preventing cell spreading, actin stress fiber formation, and activation of focal adhesion kinase
137 cells enhanced cell spreading, actin stress fiber formation, and adhesion to extracellular matrix, a
138 al resistance, increased actinomyosin stress fiber formation, and alterations in tight junction molec
139 tion, cell spreading, focal adhesion, stress fiber formation, and compaction, whereas Par1b depletion
141 cted the migration defect, diminished stress fiber formation, and enhanced pseudopod and uropod forma
144 with CTGF for 24 hours induced actin stress fiber formation, and increased MLC phosphorylation, fibr
145 of interendothelial junctions, actin stress fiber formation, and increased permeability in complemen
149 ncreased RhoA activity, induced actin stress fiber formation, and produced an amplified and protracte
150 ncreased RhoA activity, induced actin stress fiber formation, and produced an irreversible increase i
152 in light chain phosphorylation, actin stress fiber formation, and the increased endothelial permeabil
153 preserved tissue stiffness, prevented stress fiber formation, and was associated with improved intest
155 ly, FN075 stimulates alpha-synuclein amyloid fiber formation as measured by thioflavin T emission, el
156 pilus-associated sortases are essential for fiber formation as they create covalent isopeptide bonds
157 ight chain phosphorylation, and actin stress fiber formation as well as inter-endothelial junctional
158 ctile apparatus, including Z-disc and stress fiber formation, as well as mislocalization and/or atten
159 phorylation of myosin light chain and stress fiber formation, both of which occur in a ROCK-dependent
160 increases of NO production and actin stress fiber formation, both of which were markedly reduced upo
161 cause it is the rate-determining step toward fiber formation but also because early, soluble aggregat
162 NG-finger domain almost completely abolishes fiber formation but not cellulose biosynthetic activity.
163 F1F2Delta1, respectively) suppressed stress fiber formation, but fibers appeared after 10% cyclic un
164 ylation leading to RhoA-ROCK-mediated stress fiber formation, but membrane dynamics is reliant on LKB
165 ter formation is independent of actin stress fiber formation, but requires active (high-affinity) int
166 important role in the elucidation of amyloid fiber formation, but the coupling models that link spect
168 esis that fibulin-5 is necessary for elastic fiber formation by facilitating the deposition of elasti
170 med in dilute SDS (2 mM) promote Abeta(1-40) fiber formation by supporting peptide interaction on the
171 rease in the E-cadherin abundance and stress fiber formation by TGF-beta, gene ontology analysis show
175 001) and was accompanied by greater collagen fiber formation, capillary density, smooth muscle-contai
176 nd RhoB maximized the hypoxia-induced stress fiber formation caused by RhoB/mammalian homolog of Dros
177 effect was associated with increased stress fiber formation, cell-matrix, and cell-cell adhesion in
178 uding Ras activation, cell spreading, stress fiber formation, chemotaxis, and membrane vesicle traffi
180 contrast, active V14RhoA promoted EC stress fiber formation, contractility, and organization into co
181 nstitutive alphaSMA expression, actin stress fiber formation, contraction, and nuclear Smad2/3, indic
184 he ability of NET1 to stimulate actin stress fiber formation does not correlate with its transforming
188 e as a quantitative measure of the degree of fiber formation during differentiation of muscle precurs
189 64), play a crucial role in transient stress fiber formation during osteoblast mechanotransduction, m
190 rum response factor response element, stress fiber formation, ERK1/2 phosphorylation, and beta-arrest
191 tiffening including cell spread area, stress fiber formation, focal adhesion maturation, and intracel
192 ed FlnB loss, however, promotes actin-stress fiber formation following plating onto an integrin activ
193 d cytoskeleton re-organization (actin stress fiber formation) following LPA stimulation, but does not
195 ing, sticky particles, we demonstrate robust fiber formation for a variety of particle shapes and agg
198 d Rho-mediated neurite retraction and stress fiber formation; G(q) protein and pertussis toxin-sensit
199 e discovery of additional drugs that inhibit fiber formation has been hampered by the lack of a sensi
201 l resistance changes and cytoskeletal stress fiber formation in both human umbilical vein endothelial
204 , zebrafish Arhgef11 stimulated actin stress fiber formation in cultured cells, whereas overexpressio
205 s induced by PMA, and increased actin stress fiber formation in epithelial and endothelial cells.
206 d to induce RhoA activation and actin stress fiber formation in human pulmonary arterial endothelial
207 n paracellular permeability and actin stress fiber formation in lung microvascular endothelial and al
208 itutively active EhRho1 induces actin stress fiber formation in mammalian fibroblasts, thereby identi
209 190RhoAGAP restored RhoA activity and stress fiber formation in Nef-infected podocytes, whereas siRNA
211 exogenous VEGF significantly induces stress fiber formation in osteoblasts that is comparable with P
212 the molecular mechanisms of impaired elastic fiber formation in recessive cutis laxa, we have investi
213 small globular protein implicated in amyloid fiber formation in renal patients on long-term hemodialy
216 Gene silencing of Synpo-T abrogates stress-fiber formation in synpo(-/-) podocytes, demonstrating t
218 to their ability to interfere with adhesive fiber formation in uropathogenic Escherichia coli and ol
219 phalloidin staining revealed increase stress fiber formation in vascular smooth muscle cells of profi
221 esults are not compatible with a model for K-fiber formation in which microtubules are added to nasce
223 ules by treatment with brassinazole inhibits fiber formation, indicating that BR plays an important r
224 ion, depletion of Profilin1 inhibited stress fiber formation induced by non-canonical Wnt signaling.
226 ntegrin alpha9beta1, abolishing actin stress fiber formation, inhibiting YAP and its target gene expr
228 embly, whereas for the two-component system, fiber formation is always accompanied by chiral ordering
231 ast, its effect on bivalent stretching and K-fiber formation is independent of PP2A and mediated by r
235 hese results suggest a new model where curli fiber formation is spatially coordinated with the CsgG a
236 A key mediator of steady flow-induced stress fiber formation is Src that regulates downstream signali
238 g 2D-IR spectra that allows us to follow the fiber formation kinetics of the human islet amyloid poly
239 The skeletal muscle ECM substrates enhanced fiber formation leading to the expression of the main sk
240 rombin, exaggerated AJ disruption and stress fiber formation, leading to an irreversible increase in
241 leads to prevention of signaling via stress fiber formation, leading to preserved intestinal functio
242 y revealed a time-dependent defect in stress fiber formation, membrane protrusions, cell motility, an
243 d an increase in cell motility, actin stress fiber formation, metalloprotease activity, and extracell
245 We hypothesized that inhibition of stress fiber formation might allow myocyte maturation on stiffe
249 at mTOR-dependent regulation of actin stress fiber formation, motility, and proliferation requires ra
250 t form amyloid fibers, our results show that fiber formation need not be directly coupled to toxicity
252 g extension of cellular processes and stress fiber formation, occurred predominantly in the stretch d
257 containing 14 repeats can readily cross-seed fiber formation of proteins that have the wild type numb
261 system, are likely to be applicable to other fiber formation processes in a variety of Gram-positive
265 t the cytoskeletal reorganization and stress fiber formation required for migration in IEC-6 enterocy
268 udil, an inhibitor of RhoA kinase and stress fiber-formation, resulted in enhanced force generation o
269 t literature, analyzes the processes of club fiber formation, retention, and release, which may influ
270 cause the small GTPase Rho stimulates stress fiber formation, Rho inactivation by Src has been though
272 dia, DeltaN-Ect2 DH/PH enhanced actin stress fiber formation, suggesting that C-terminal sequences in
273 has no apparent effect on Rho-induced stress fiber formation, suggesting that it acts as a specific e
274 d shear stress-mediated mechanism for stress fiber formation that involves a TXNIP-dependent vascular
275 -galactosidase resulted in pronounced stress fiber formation that was exacerbated by S1P2 overexpress
276 n a decrease of G-actin and the actin stress fiber formation, the effects seen upon FDH expression.
277 lications for the mechanism of hIAPP amyloid fiber formation, the inhibitory action of IAPP variants,
280 regulator of RhoA activity and actin stress fiber formation through phosphorylation of rhotekin.
281 ith RhoA and switch Rho function from stress fiber formation to membrane ruffling to confer an invasi
282 lly, LPP increased focal adhesion and stress fiber formation to promote endothelial cell motility and
283 maturation, causes smooth muscle alpha-actin fiber formation, up-regulation of collagen I, and down-r
284 protein additionally showed reduced elastic fiber formation upon addition to human retinal pigmented
288 mparing the rates of monomer consumption and fiber formation, we are able to show that EGCG stabilize
289 r insight into the nature of the HbS polymer fiber formation, we develop a particle model-resembling
292 5E rhotekin mutant displayed enhanced stress fiber formation when expressed in serum-starved fibrobla
293 teady flow increased Src activity and stress fiber formation, whereas it decreased TXNIP expression.
294 Ectopic expression of hCDC14A induced stress fiber formation, whereas stress fibers were diminished i
295 that is comparable with PFSS-induced stress fiber formation, whereas VEGF knockdown abrogates this r
296 myoblast pool have the capacity to initiate fiber formation, which is normally inhibited by the orga
297 ed in transcription-independent actin stress fiber formation, which needs also the activity of ROCK.
298 erved cytoskeletal reorganization and stress-fiber formation while measuring the contractile force of
299 : a' interactions dominate the first step in fiber formation, while the analogous 'B: b' interactions
300 these effects and induced significant stress fiber formation, without a detectable shift in actin poo
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