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1 teins, including DEB-1 (vinculin) and ATN-1 (alpha-actinin).
2 , lamellipodia (fimbrin), and stress fibers (alpha-actinin).
3 toplasmic domain of ICAM-2 binds directly to alpha-actinin.
4 t 14-3-3 binding blocks its interaction with alpha-actinin.
5 ICAM-2 with the cytoskeletal linker protein alpha-actinin.
6 nt with observations of cells overexpressing alpha-actinin.
7 ated by staining for z-line proteins such as alpha-actinin.
8 actin networks crosslinked with palladin and alpha-actinin.
9 low tract expressed the cardiomyocyte marker alpha-actinin.
10 focal adhesions and binds to both actin and alpha-actinin.
11 d in a regular pattern mainly by the protein alpha-actinin.
12 the crystallographic structures of actin and alpha-actinin.
13 itin in the Z-disk is the actin cross-linker alpha-actinin.
14 a1 activation in the presence and absence of alpha-actinin.
15 signals accumulate in the caps together with alpha-actinin.
16 erconnected Z lines and were cross-linked by alpha-actinin.
17 nd an interaction with the actin crosslinker alpha-actinin.
18 ancestor of Entamoeba and higher eukaryotic alpha-actinins.
20 We show that perturbations to formin and alpha-actinin 1 activity selectively inhibited stress fi
22 low levels of smn, cofilin 1, profilin 2 and alpha-actinin 1 did not affect smn morphant motor axon o
23 sponsive sister paralogs-myosin IIB (MYH10), alpha-actinin 1, and filamin A-had lower expression diff
24 CTN1, which encodes the cytoskeletal protein alpha-actinin 1, in 10 of 239 consecutive probands with
28 interacting with actin-cross-linking protein alpha-actinin-1 and increasing its affinity to filamento
30 1662E mutations, which impair apoCaM but not alpha-actinin-1 binding, decreased single-channel open p
31 .2 K1647A and Y1649A mutations, which impair alpha-actinin-1 but not apoCaM binding, but not the F165
32 herin EC1 ectodomain, or alternatively of an alpha-actinin-1 mutant that inhibits F-actin bundling, i
35 er leaflet of the plasma membrane, including alpha-actinin-1, moesin, 14-3-3 protein zeta/delta, anne
36 the expression and activation of moesin and alpha-actinin-1, which associate with actin filaments an
39 in which a novel disease-causing variant in alpha-actinin 2 (ACTN2) was identified by next-generatio
40 mediated regulation of Entamoeba histolytica alpha-actinin-2 (EhActn2) with features expected for the
41 ional evidence that the primary sequences of alpha-actinin-2 and alpha-actinin-3 evolved differences
42 ebrafish can be rescued by overexpression of alpha-actinin-2 but not by alpha-actinin-3 mRNAs from ze
44 n between actn2 and actn3, the phenotypes of alpha-actinin-2 deficient zebrafish can be rescued by ov
45 ete high-resolution structure of the 200 kDa alpha-actinin-2 dimer from striated muscle and explore i
46 ounts of other sarcomeric proteins including alpha-actinin-2, alpha-sarcomeric actin and tropomyosin
48 ociated with dose-dependent up-regulation of alpha-actinin-2, z-band alternatively spliced PDZ-motif
49 A premature stop codon in ACTN3 resulting in alpha-actinin-3 deficiency (the ACTN3 577XX genotype) is
50 on null polymorphism (R577X) in ACTN3 causes alpha-actinin-3 deficiency in approximately 18% of the g
51 here is no associated disease phenotype, but alpha-actinin-3 deficiency is detrimental to sprint and
56 the primary sequences of alpha-actinin-2 and alpha-actinin-3 evolved differences to optimize their fu
61 X individuals, suggesting dose-dependency of alpha-actinin-3, while others have shown no difference b
62 inin-2, which is differentially expressed in alpha-actinin-3-deficient muscle, has higher binding aff
65 t mutation (K255E) of the actin cross-linker alpha-actinin 4 (ACTN4) causes its binding kinetics to b
66 e binding affinity of the actin cross-linker alpha-actinin 4 (ACTN4) in cells modulates cytoplasmic m
70 d alpha-actinin 4, only the interaction with alpha-actinin 4 is required to promote tumor cell invasi
71 or tissue additionally reveals that elevated alpha-actinin 4 or Dyn2 expression are predictive of poo
72 nonmuscle myosin IIA (MYH9) and IIC (MYH14), alpha-actinin 4, and filamin B, were highly expressed in
73 hrough the C-terminal tails of both Dyn2 and alpha-actinin 4, and these proteins interact at invasive
74 2 binds directly to both alpha-actinin 1 and alpha-actinin 4, only the interaction with alpha-actinin
76 nd the actin-bundling protein alpha-actinin (alpha-actinin) 4 is critical for tumor cell migration an
77 n and mass spectrometric analysis identified alpha-actinin-4 (ACTN4) as an MTBP-interacting protein.
78 hat occur within the actin binding domain of alpha-actinin-4 (ACTN4) cause an autosomal dominant form
79 the homodimeric actin cross-linking protein alpha-actinin-4 (ACTN4) during cell migration involves s
81 lin further increased binding of MICAL-L2 to alpha-actinin-4 (ACTN4), a protein involved in GLUT4 tra
84 ge of cortical mechanical tension, rendering alpha-actinin-4 a catch bond in physiological tension ra
87 n actin-binding proteins alpha-actinin-1 and alpha-actinin-4 and actin-related protein 2/3 complex su
89 apply our approach to the actin cross-linker alpha-actinin-4 and show that the cross-linking time of
90 eling by metabotropic signaling and identify alpha-actinin-4 as a critical effector of structural pla
93 FSGS3/CD2AP colocalizes with E-cadherin and alpha-actinin-4 at the apical junction in polarized Madi
94 Degradation of the podocyte-specific protein alpha-actinin-4 by the UPS depended on oxidative modific
95 and coimmunoprecipitation studies showed the alpha-actinin-4 carboxyl-terminal region specifically in
98 have shown that actin cross-linkers such as alpha-actinin-4 exhibit mechanosensitive properties in t
99 ltured podocytes, treatment with C3a reduced alpha-actinin-4 expression and promoted ILK-dependent nu
101 ence supporting mechanisms involving loss-of-alpha-actinin-4 function in human glomerular diseases re
103 in-4 and show that the cross-linking time of alpha-actinin-4 homodimers increases approximately twofo
111 al change requiring the C-terminal domain of alpha-actinin-4 that binds to CaMKII, an interaction we
112 A point mutation at lysine 255 in human alpha-actinin-4 to glutamate increases the binding affin
113 NHERF1/alpha-actinin-4 interaction increased alpha-actinin-4 ubiquitination and decreased its express
115 d by NHERF3 and another ligand such as NHE3, alpha-actinin-4, and PKCalpha, promoting formation of NH
117 TN4 gene, encoding the actin-binding protein alpha-actinin-4, are a rare cause of autosomal dominant
118 fy a Ca(2+)-sensitive actin-binding protein, alpha-actinin-4, as a novel group 1 mGluR-interacting pa
124 the in vitro actin assembly assay identified alpha-actinin-4/focal segmental glomerulosclerosis 1 (FS
125 , we reported that an actin-binding protein, alpha-actinin (ACTN)4, was dysregulated in placentas fro
128 By mutating or titrating actin cross-linkers alpha-actinin Ain1 and fimbrin Fim1 in live cells, we re
130 between Dyn2 and the actin-bundling protein alpha-actinin (alpha-actinin) 4 is critical for tumor ce
133 organized accumulation of actin, myosin, and alpha-actinin and a complete loss of myofibrillar organi
134 otion, PLM synaptogenesis was independent of alpha-actinin and ENA-VASP, both of which bind to the N-
136 radation of key sarcomeric proteins, such as alpha-actinin and filamin C, and is essential for mainte
139 integrin, other cytoplasmic proteins such as alpha-actinin and filamin can directly interfere with ta
141 g, we successfully predicted which mammalian alpha-actinin and filamin paralogs would be mechanoaccum
142 in II motors and actin cross-linkers such as alpha-actinin and filamin, accumulate in response to int
144 y regulates neuronal migration by binding to alpha-actinin and influencing phosphorylation of both FA
145 ghly seropositive in response to trichomonad alpha-actinin and its truncated protein (ACT-P2) (positi
149 ely controlled by zyxin and binding partners alpha-actinin and p130Cas, but not vasodilator-stimulate
150 ge-independent growth, co-precipitation with alpha-actinin and production of localized and disseminat
151 tes of Cas and two other adhesion molecules, alpha-actinin and talin, were also significantly slower
156 proteins), adherens junctions (VE-cadherin, alpha-Actinin), and the basement membrane (Collagen IV),
157 s via its C-terminal SH3 domains in an ATN-1(alpha-actinin)- and ALP-1(ALP/Enigma)-dependent manner,
158 Here, we show that non-muscle myosin II, alpha-actinin, and filamin accumulate to mechanically st
159 ents separated by the actin bundling protein alpha-actinin, and is mechanically coupled to noncontrac
161 d by overexpression of the actin crosslinker alpha-actinin, and rheology measurements reveal that cha
162 by pulling VBS peptides derived from talin, alpha-actinin, and Shigella IpaA out of the vinculin hea
163 on simulations with the K237E mutant chicken alpha-actinin--and evaluate the mechanism of alpha-actin
165 Immunofluorescence staining with the anti-alpha-actinin antibody (a z-line marker) showed that nea
173 afish embryos results in the accumulation of alpha-actinin associated with severely impaired contract
174 filaments and the muscle-specific isoform of alpha-actinin at the PM of differentiated myotubes.
175 anization, changing spacing and alignment of alpha-actinin bands due to increase in proteolytic activ
178 presented here was to evaluate the impact of alpha-actinin binding to ICAM-2 on the phenotype of NB t
181 lls expressing ICAM-2 variants with modified alpha-actinin-binding domains differed from cells expres
182 en expressed variants of ICAM-2 with mutated alpha-actinin-binding domains, and compared the impact o
187 n was soluble and interacted with sarcomeric alpha-actinin by coimmunoprecipitation, while alpha-syne
189 icant reduction of cardiac myocyte proteins (alpha-actinin, cardiac myosin-binding protein C, and car
191 ids with high seeding density exhibited more alpha-actinin(+) cells and less nuclear YAP expression.
193 we show in an in vitro assay that talin and alpha-actinin compete for binding to beta3 integrins, bu
195 to the actin cytoskeleton by talin, and then alpha-actinin competes with talin to bind beta3 integrin
196 epletion of CLP36 or disruption of the CLP36-alpha-actinin complex in breast cancer cells substantial
198 (actin, tropomyosin, troponins) and Z-band (alpha-actinin) components and promotes their degradation
199 g activity with robust expression of cardiac alpha-actinin, connexin 43, myosin light chain 2a, alpha
200 n adapter protein, ArgBP2, is a component of alpha-actinin containing stress fibers and inhibits migr
201 yosin network consisting of actin filaments, alpha-actinin cross-linking proteins, and non-muscle myo
203 interactions with the actin cytoskeleton via alpha-actinin (DeltaABD) abrogated migratory responses t
205 Consistently, we find opposite effects of alpha-actinin depletion and expression of mutants on sub
207 t fascin domains are densely packed, whereas alpha-actinin domains consist of widely spaced parallel
208 that depletion of the focal adhesion protein alpha-actinin enhances force generation in initial adhes
212 f actin cytoskeleton, bundle-like sarcomeric alpha-actinin expression, higher pacing beat rate at low
213 ed by disrupting nonfocal adhesion proteins (alpha-actinin, F-actin, and myosin II) and subcellular o
218 We demonstrate that calmodulin displaces alpha-actinin from their shared binding site on alpha11.
220 e, which contains orthologoues of each human alpha-actinin gene, including duplicated copies of actn3
221 lamin that shares actin-binding domains with alpha-actinin had a strong inhibitory effect on PC2(iv)
225 nor component of the Z-disc (about 1 per 400 alpha-actinin) important for myofibrillar development an
226 These results may shed light on the role of alpha-actinin in cellular mechanotransduction and focal
228 ides a detailed understanding of the role of alpha-actinin in transmitting tension between actin fila
232 the presence of alpha-actinin-dependent and alpha-actinin-independent mechanisms, and indicate that
233 king model for NA assembly whereby transient alpha-actinin-integrin complexes help nucleate NAs withi
234 Here we directly observe that fascin and alpha-actinin intrinsically segregate to discrete bundle
238 indicate that the interaction of ICAM-2 with alpha-actinin is critical to conferring an ICAM-2-mediat
240 lates with force generation, suggesting that alpha-actinin is the main link transmitting force betwee
241 e of alpha actinin-1 (ACTN1), one of the two alpha actinin isoforms expressed in keratinocytes, in sk
243 ly, disordered actomyosin bundles induced by alpha-actinin knockdown led to higher than normal tensio
244 ises four to six layers of links, presumably alpha-actinin, linking antiparallel overlapping ends of
245 lex formation with the actin-binding protein alpha-actinin, linking membrane-bound CD13 to the cytosk
246 filaments within the Z-band is devoid of any alpha-actinin links and is likely to be the location of
249 taining protein (ZASP)/Cypher interacts with alpha-actinin, myotilin, and other Z-disc proteins via t
250 from women and men that were unreactive with alpha-actinin (negative control sera) failed to detect a
251 and caveolin, Rab5a in early endosomes, and alpha-actinin, often in relationship to cortical actin.
252 tituted with zyxin variants that lack either alpha-actinin or Ena/VASP-binding capacity display compr
253 ell polarization on soft substrates, whereas alpha-actinin overexpression prevented polarization on s
254 's canal cells with dexamethasone treatment, alpha-actinin overexpression, or RhoA overexpression cau
255 These results also suggest that the zyxin/alpha-actinin/p130Cas module may ensure that motile cell
256 udies also showed that composite networks of alpha-actinin/palladin/actin behave very similar to pure
257 on, we have demonstrated that the sarcomeric alpha-actinins play a role in the regulation of calcineu
262 othelial ABPs, such as cortactin, myosin, or alpha-actinin, regulate leukocyte extravasation by contr
263 showed that the interplay between talin and alpha-actinin regulates signal transmission via controll
266 n elicit distinct responses, with myosin and alpha-actinin responding to dilation, and filamin mainly
270 activation trajectory is generated in which alpha-actinin's vinculin-binding site swings out of the
271 CHC in myotubes induced a loss of actin and alpha-actinin sarcomeric organization, whereas CHC deple
273 tin binding proteins, including spectrin and alpha-actinin, serve as molecular linkages between the a
274 es pombe, in which the cross-linking protein alpha-actinin SpAin1 bundles the actin filament network.
275 actin filaments of mixed polarity like other alpha-actinins, SpAin1 has lower bundling activity and i
278 embrane AMPAR regulatory protein) binding to alpha-actinin-stabilized PSD-95, and extracellular inter
281 However, we found evidence that palladin and alpha-actinin synergistically modify network viscoelasti
282 binding of vinculin and, to a lesser extent, alpha-actinin, talin, and filamin, to phosphomimetic Cav
283 ere we show that the F-actin-binding protein alpha-actinin targets CaMKIIalpha to F-actin in cells by
284 just forces on matrices, unveiling a role of alpha-actinin that is different from its well-studied fu
285 oleus muscles exhibit normal localization of alpha-actinin, the nebulin M1M2M3 domain, Tmod3, and cyt
287 tion of EWI-2 with the actin-binding protein alpha-actinin; this association was regulated by PIP2.
290 data show that Ca(2+)-independent binding of alpha-actinin to CaMKII differentially modulates the pho
292 prominent actin-bundling proteins fascin and alpha-actinin to distinct networks is an intrinsic behav
293 ents interlace with perijunctional actin and alpha-actinin to form a continuous belt of muscle-like s
295 te a major mechanosensitive pathway in which alpha-actinin triggers adhesion maturation by linking in
297 reducing myosin II activity or knocking down alpha-actinin, we found that both promoted cell polariza
298 n flow is correlated with a third component, alpha-actinin, which upon CRISPR knockout led to reduced
300 at Zasp52 is required for the association of alpha-actinin with the flight muscle Z-disc, and for nor
301 Our results suggest a model where multiple alpha-actinin/Z-repeat interactions cooperate to ensure