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1 , followed by PKCalpha activation and stress 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 ior to undergoing myoblast fusion and muscle fiber formation.
16 ntial role for kinetic trapping in chromatin fiber formation.
17 ng with the Abeta peptide to inhibit Abeta42 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 tion with filamentous actin (F-actin) stress fiber formation.
27 imulation of ROCK, which causes actin stress-fiber formation.
28 ir effect on protein aggregation and amyloid fiber formation.
29  spreading, traction stress, and fibronectin 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 in-4 matrix deposition and thereby fibulin-4 fiber formation.
34 esult in self-association leading to amyloid fiber formation.
35 s, probably resulting from defects in xylary fiber formation.
36 res nucleating factors, which initiate actin fiber formation.
37 ha-smooth muscle actin expression and stress fiber formation.
38 like conformation does not depend on amyloid 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 rations of beta2m necessary to avoid amyloid fiber formation.
50 f full-length NET1 to stimulate actin stress fiber formation.
51 e reciprocal of the delay time that precedes fiber formation.
52 ted precocious initiation of the GA-mediated fiber formation.
53 apeutic increases in the delay time prior to fiber formation.
54 ted cell proliferation, migration and stress fiber formation.
55 omers, an active cytoskeleton can facilitate fiber formation.
56 pithelial cells, which requires actin stress fiber formation.
57 marker of the quantity and quality of muscle fiber formation.
58 nteraction and how Cu(2+) influences amyloid fiber formation.
59 llagen molecules extracellularly, disrupting fiber formation.
60 e core domain is significantly reduced after fiber formation.
61 ss of VE-cadherin, and aberrant actin stress fiber formation.
62 the myosin regulatory light chain and stress fiber formation.
63  with scAAV2.dnRhoA showed diminished stress fiber formation.
64 odify fiber-forming polymers in the stage of fiber formation.
65 hat regulates Src kinase activity and stress fiber formation.
66  beta-arrestin in RhoA activation and stress fiber formation.
67 scle actin (alpha-SMA) expression and stress fiber formation.
68 eveals where microtubules are added during K-fiber formation.
69 acids in the N terminus that is key for TasA fiber formation.
70 eta-sheet amyloid fibrils, which can trigger fiber formation.
71 exhibited a dominant negative effect on TasA fiber formation.
72 er oligomerization, which underlie chromatin fiber formation.
73 operty that is incompatible with protein/DNA fiber formation.
74 s with the bacterial inner membrane prior to fiber formation.
75 t be combined with salting-out for effective fiber formation.
76 ng kinetochores but not kinetochore fiber (K fiber) formation.
77 PKCepsilon enhances RhoA activity and stress fiber formation, a phenotype also observed in TGF-beta-t
78 ted that this BTE variant is also capable of fiber formation, albeit at a reduced persistence length.
79 ive cutis laxa and marked defects in elastic fiber formation amplifies previous observations on the m
80  HLFs, but inhibited TGF-beta-induced stress fiber formation and activation of serum response factor
81 mbly factor that is required for kinetochore fiber formation and activation of the mitotic kinase Aur
82       Treatment with AZX100 decreased stress fiber formation and altered the morphology of human derm
83 hoA inhibitor p190RhoGAP to attenuate stress fiber formation and cell contractility.
84  its downstream effector ROCK mediate stress fiber formation and cell contraction through their effec
85 ouse embryonic fibroblasts, including stress fiber formation and cell migration, it's deletion led to
86 vate RhoA and activated RhoA leads to stress fiber formation and cell spreading.
87 ding but enhances fibronectin-induced stress fiber formation and cell-mediated partial unfolding of f
88 al effect in part by preventing actin stress fiber formation and claudin 18 disorganization through s
89 N-terminally truncated Abeta will accelerate fiber formation and co-assemble into short rod-shaped fi
90  factors associated with vascularization and fiber formation and components of cellular signaling pat
91 lude that fibulin-4 is necessary for elastic fiber formation and connective tissue development.
92 zation results in Rho-dependent actin stress fiber formation and contractile cell morphology.
93 utflow facility, whereas S1P promotes stress fiber formation and contractility in cultured trabecular
94 hat Cdk5 is strongly activated during stress fiber formation and contraction in spreading cells.
95 Eg5 interaction was required for kinetochore fiber formation and contributed to Eg5 localization to s
96  GTPase, RhoA, which is necessary for stress fiber formation and cytoskeleton integrity.
97 d by changes in stiffness, leading to stress fiber formation and decreased intestinal transit.
98 tion, tissue edema led to significant stress fiber formation and decreased numbers of focal contacts.
99 brillogenesis: it increases the lag-time for fiber formation and decreases the rate of addition of hI
100 e migratory response through enhanced stress fiber formation and disruption of endothelial cell-cell
101 of proteotoxicity and the dynamic changes in fiber formation and dissemination remain unclear, preven
102                                              Fiber formation and domain formation from deoxy-HbS as w
103 microfibrils have essential roles in elastic fiber formation and elastic tissue homeostasis, as well
104               Moreover, C4a increased stress fiber formation and enhanced endothelial permeability, b
105 239 is accompanied by increased actin stress fiber formation and enhanced endothelial tube formation.
106    Larger nucleation domains result in rapid fiber formation and eventual precipitation or gelation w
107 gn considerations to tune the propensity for fiber formation and fiber mechanical properties, includi
108  IGPR-1 activity also modulates actin stress fiber formation and focal adhesion and reduces cell migr
109 ouse podocytes with Bis-T-23 promoted stress fiber formation and focal adhesion maturation in a dynam
110 e examined the effect of adenosine on stress fiber formation and found that adenosine inhibits HGF-in
111 ly inform reaction-based theories of amyloid fiber formation and have implications for neurodegenerat
112 ells display substantial decreases of stress fiber formation and impaired cell migration and spreadin
113 e signaling events result in enhanced stress fiber formation and increased actomyosin contractility,
114 effects in P aeruginosa-induced actin stress fiber formation and increased paracellular permeability.
115 otein (Radil) to inhibit Rho-mediated stress fiber formation and induces junctional tightening.
116 t limits Rho-dependent events such as stress fiber formation and it maintains the association of beta
117 tocyte contractility, as indicated by stress fiber formation and matrix compaction and alignment.
118 d PAK1 stimulation in VSMCs and their stress fiber formation and migration.
119                                         Lens fiber formation and morphogenesis requires a precise orc
120 ches attenuated thrombin-induced VSMC stress fiber formation and motility.
121 I formin homology 2 domain, inhibited stress fiber formation and myofibroblast differentiation induce
122 n stress fibers, which further drives stress fiber formation and myofibroblast differentiation, and (
123 myosin L chain (MLC) phosphorylation, stress fiber formation and permeability increases during inflam
124 attenuated P aeruginosa-induced actin stress fiber formation and prevented paracellular permeability.
125  integrin beta1 is required for actin stress fiber formation and proliferative growth.
126  in Nf1(-/-) astrocytes rescued actin stress fiber formation and restored cell motility and prolifera
127          Acute hypoxia enhanced actin stress fiber formation and RhoA activity in both inner and oute
128 r its proposed non-classical roles in muscle fiber formation and sensory neuron development, but is c
129 l the central importance of BMP in secondary fiber formation and show that although FGF may be necess
130 nteraction inhibited thrombin-induced stress fiber formation and SRE activation supports this hypothe
131 iRNA inhibited thrombin-induced actin stress fiber formation and SRE-dependent gene transcription.
132 anical model provides a mechanism for stress fiber formation and stiffness sensing in cells adhered t
133 esponse to genotoxic stress maintains stress fiber formation and strikingly increases apoptosis, impl
134 ntensity (1680 s), are attributed to initial fiber formation and subsequent formation of larger assem
135 t required for mouse development and elastic fiber formation and suggest possible functional redundan
136 sal relation between the delay time prior to fiber formation and supersaturation, show that in vivo f
137 ation include the disruption of actin stress fiber formation and the decreased expression of lateral
138 nknown, several theories account for amyloid fiber formation and their toxic significance.
139 al resistance, increased actinomyosin stress fiber formation, and alterations in tight junction molec
140 tion, cell spreading, focal adhesion, stress fiber formation, and compaction, whereas Par1b depletion
141 induced VASP Ser-239 phosphorylation, stress fiber formation, and endothelial tube formation.
142 tion, G-actin polymerization, F-actin stress fiber formation, and HASMC migration.
143 cting G-actin polymerization, F-actin stress fiber formation, and HASMC migration.
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
146 HASMC G-actin polymerization, F-actin stress fiber formation, and migration.
147  is linked to defective Rho activity, stress fiber formation, and MLC phosphorylation.
148 ein known to influence contractility, stress fiber formation, and motility.
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
151 s showed increased cellular adhesion, stress fiber formation, and reduced cellular migration.
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
154                      The kinetics of amyloid fiber formation are of particular interest because evide
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 r understanding on the allosteric control of fiber formation at equilibrium by showing how the simple
160 phorylation of myosin light chain and stress fiber formation, both of which occur in a ROCK-dependent
161  increases of NO production and actin stress fiber formation, both of which were markedly reduced upo
162 cause it is the rate-determining step toward fiber formation but also because early, soluble aggregat
163 NG-finger domain almost completely abolishes fiber formation but not cellulose biosynthetic activity.
164  F1F2Delta1, respectively) suppressed stress fiber formation, but fibers appeared after 10% cyclic un
165 ylation leading to RhoA-ROCK-mediated stress fiber formation, but membrane dynamics is reliant on LKB
166 ter formation is independent of actin stress fiber formation, but requires active (high-affinity) int
167 important role in the elucidation of amyloid fiber formation, but the coupling models that link spect
168                   The molecular mechanism of fiber formation by calcitonin is not well understood.
169 esis that fibulin-5 is necessary for elastic fiber formation by facilitating the deposition of elasti
170                                              Fiber formation by human IAPP (hIAPP) is markedly accele
171 med in dilute SDS (2 mM) promote Abeta(1-40) fiber formation by supporting peptide interaction on the
172 rease in the E-cadherin abundance and stress fiber formation by TGF-beta, gene ontology analysis show
173                      VCAM-1 inhibited stress fiber formation by TGFbeta1, TGFbeta2, TGFbeta3 and lyso
174  investigation of the multiple ways in which fiber formation can be inhibited.
175                               Because stress fiber formation can be modified by substrate stiffness,
176 001) and was accompanied by greater collagen fiber formation, capillary density, smooth muscle-contai
177 nd RhoB maximized the hypoxia-induced stress fiber formation caused by RhoB/mammalian homolog of Dros
178  effect was associated with increased stress fiber formation, cell-matrix, and cell-cell adhesion in
179 uding Ras activation, cell spreading, stress fiber formation, chemotaxis, and membrane vesicle traffi
180 ldtype strongly induced RhoA-mediated stress fiber formation compared with mutant receptor.
181 nstitutive alphaSMA expression, actin stress fiber formation, contraction, and nuclear Smad2/3, indic
182 regation propensity and that the kinetics of fiber formation depends on the number of repeats.
183 NET1 proteins that potently stimulate stress fiber formation do not transform cells.
184 he ability of NET1 to stimulate actin stress fiber formation does not correlate with its transforming
185 ight chain phosphorylation, and actin stress fiber formation due to JAM-C knockdown.
186 sing stiffness raised mDia1-nucleated stress fiber formation due to Rho activation.
187 een shown to play essential roles in elastic fiber formation during development.
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
194        RKI-18 suppresses ROCK-mediated actin fiber formation, following stimulation with LPA as well
195 ing, sticky particles, we demonstrate robust fiber formation for a variety of particle shapes and agg
196                                              Fiber formation from murine serum amyloid A1 (SAA) was c
197                        We propose a model of fiber formation from sheets and compare it with current
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
200          MCP1 also stimulated F-actin stress fiber formation in a delayed manner in HASMCs, as well a
201  substantially reduced IL-17A-induced stress fiber formation in ASMCs and attenuated IL-17A-enhanced,
202 l resistance changes and cytoskeletal stress fiber formation in both human umbilical vein endothelial
203 ro and its ability to stimulate actin stress fiber formation in cells.
204 sed myosin phosphorylation as well as stress fiber formation in cells.
205 , zebrafish Arhgef11 stimulated actin stress fiber formation in cultured cells, whereas overexpressio
206 ranscriptional regulator HuR promotes muscle fiber formation in cultured muscle cells.
207 s induced by PMA, and increased actin stress fiber formation in epithelial and endothelial cells.
208 d to induce RhoA activation and actin stress fiber formation in human pulmonary arterial endothelial
209 n paracellular permeability and actin stress fiber formation in lung microvascular endothelial and al
210 itutively active EhRho1 induces actin stress fiber formation in mammalian fibroblasts, thereby identi
211 190RhoAGAP restored RhoA activity and stress fiber formation in Nef-infected podocytes, whereas siRNA
212 hanges in lipid metabolism could induce IAPP fiber formation in NIDDM.
213  exogenous VEGF significantly induces stress fiber formation in osteoblasts that is comparable with P
214 the molecular mechanisms of impaired elastic fiber formation in recessive cutis laxa, we have investi
215 small globular protein implicated in amyloid fiber formation in renal patients on long-term hemodialy
216 ) promotes mitochondrial biogenesis and slow fiber formation in skeletal muscle.
217 and help explain the origins of aggregate or fiber formation in solution.
218   Gene silencing of Synpo-T abrogates stress-fiber formation in synpo(-/-) podocytes, demonstrating t
219 filamentous/globular actin ratio, and stress fiber formation in TM cells.
220  to their ability to interfere with adhesive fiber formation in uropathogenic Escherichia coli and ol
221 phalloidin staining revealed increase stress fiber formation in vascular smooth muscle cells of profi
222 nd suggest that MCP-1 may influence collagen fiber formation in vivo.
223 esults are not compatible with a model for K-fiber formation in which microtubules are added to nasce
224                            The mechanisms of fiber formation, in particular the role that hydration w
225 ules by treatment with brassinazole inhibits fiber formation, indicating that BR plays an important r
226 ion, depletion of Profilin1 inhibited stress fiber formation induced by non-canonical Wnt signaling.
227                      Mechanistically, stress fiber formation induced by Rnd3 knockdown required the s
228 ntegrin alpha9beta1, abolishing actin stress fiber formation, inhibiting YAP and its target gene expr
229                                Additionally, fiber formation is accelerated by constructs that mimic
230 embly, whereas for the two-component system, fiber formation is always accompanied by chiral ordering
231                                 Since stress fiber formation is associated with loss of cell mobility
232                         We also show that if fiber formation is at equilibrium in vivo, the vast majo
233                                      Amyloid fiber formation is correlated with pathology in many dis
234 ast, its effect on bivalent stretching and K-fiber formation is independent of PP2A and mediated by r
235                                 For example, fiber formation is more strongly suppressed in cell cult
236 the properties of a trace protein capable of fiber formation is presented.
237   Despite the presence of founder cells, DVM fiber formation is rarely observed.
238                                      Amyloid fiber formation is responsible for several human disease
239 hese results suggest a new model where curli fiber formation is spatially coordinated with the CsgG a
240 A key mediator of steady flow-induced stress fiber formation is Src that regulates downstream signali
241 ation and supersaturation, show that in vivo fiber formation is very far from equilibrium.
242 ber of fibers, but they are not required for fiber formation itself.
243 g 2D-IR spectra that allows us to follow the fiber formation kinetics of the human islet amyloid poly
244  The skeletal muscle ECM substrates enhanced fiber formation leading to the expression of the main sk
245 rombin, exaggerated AJ disruption and stress fiber formation, leading to an irreversible increase in
246  leads to prevention of signaling via stress fiber formation, leading to preserved intestinal functio
247 y revealed a time-dependent defect in stress fiber formation, membrane protrusions, cell motility, an
248 d an increase in cell motility, actin stress fiber formation, metalloprotease activity, and extracell
249                                          The fiber formation method presented in this study can be ex
250    We hypothesized that inhibition of stress fiber formation might allow myocyte maturation on stiffe
251 suppressed MCP1-induced HASMC F-actin stress fiber formation, migration, and proliferation.
252 and, thereby, decreased HASMC F-actin stress fiber formation, migration, and proliferation.
253 d resulted in decreased HASMC F-actin stress fiber formation, migration, and proliferation.
254 at mTOR-dependent regulation of actin stress fiber formation, motility, and proliferation requires ra
255 t form amyloid fibers, our results show that fiber formation need not be directly coupled to toxicity
256         Methylene blue-mediated promotion of fiber formation occurred via a dose-dependent decrease i
257 g extension of cellular processes and stress fiber formation, occurred predominantly in the stretch d
258                                              Fiber formation occurs at low mum concentrations of Dnmt
259 nds bind to Abeta fibers, they do not reduce fiber formation of Abeta.
260 ) was compared to the linear aggregation and fiber formation of colloidal gold particles.
261 CDR3 (position 91) affects the stability and fiber formation of human lambda3r light chains.
262 containing 14 repeats can readily cross-seed fiber formation of proteins that have the wild type numb
263 del for how E. coli guides efficient amyloid fiber formation on the cell surface.
264              By contrast, subsequent amyloid fiber formation on the surface of the membrane fragments
265 within 3-D matrices, without inducing stress fiber formation or collagen reorganization.
266 system, are likely to be applicable to other fiber formation processes in a variety of Gram-positive
267                            In this scenario, fiber formation propensity and toxicity of oligomeric st
268                                          The fiber formation reactions are promiscuous in that the ch
269 t the cytoskeletal reorganization and stress fiber formation required for migration in IEC-6 enterocy
270                         We found that stress fiber formation requires de novo protein synthesis, p38M
271 ic CsgA peptides proficient and deficient in fiber formation, respectively.
272 udil, an inhibitor of RhoA kinase and stress fiber-formation, resulted in enhanced force generation o
273 t literature, analyzes the processes of club fiber formation, retention, and release, which may influ
274 cause the small GTPase Rho stimulates stress fiber formation, Rho inactivation by Src has been though
275 res Zn(2+) as a catalyst that drives amyloid fiber formation, similar to many mammalian amyloid-formi
276 static and cation-pi interactions in driving fiber formation, stability and thickening.
277 d shear stress-mediated mechanism for stress fiber formation that involves a TXNIP-dependent vascular
278 -galactosidase resulted in pronounced stress fiber formation that was exacerbated by S1P2 overexpress
279 n a decrease of G-actin and the actin stress fiber formation, the effects seen upon FDH expression.
280 lications for the mechanism of hIAPP amyloid fiber formation, the inhibitory action of IAPP variants,
281 I domain mediating cell spreading and stress fiber formation through alpha4beta1 integrin.
282 ation water dynamics is suggested to promote fiber formation through entropic effects.
283  regulator of RhoA activity and actin stress fiber formation through phosphorylation of rhotekin.
284 tches its function from a promoter of muscle fiber formation to become an inducer of muscle loss.
285 ith RhoA and switch Rho function from stress fiber formation to membrane ruffling to confer an invasi
286 lly, LPP increased focal adhesion and stress fiber formation to promote endothelial cell motility and
287 maturation, causes smooth muscle alpha-actin fiber formation, up-regulation of collagen I, and down-r
288  protein additionally showed reduced elastic fiber formation upon addition to human retinal pigmented
289                                              Fiber formation was much faster than in the absence of a
290 mparing the rates of monomer consumption and fiber formation, we are able to show that EGCG stabilize
291 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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