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1 lial and alveolar epithelial cells via small Rho GTPase.
2 ivision plane, bypassing the requirement for Rho GTPase.
3 s that serve as key downstream effectors for Rho GTPases.
4 or of ECT2, a GEF required for activation of Rho GTPases.
5 a in vitro through possible interaction with Rho GTPases.
6 e formation of the active GTP-bound state of Rho GTPases.
7 ly involve spatially localized activation of Rho GTPases.
8 by monitoring the activation state of small Rho GTPases.
9 P, a disruption that does not exist in other Rho GTPases.
10 on multiple cell types and signaling through Rho GTPases.
11 G-proteins or for other G-proteins, such as Rho GTPases.
12 aspects of cell morphogenesis by turning on Rho-GTPases.
13 mitochondrial membrane protein mitochondrial Rho GTPase 1 (Miro1) is a master regulator of mitochondr
14 e used cells deficient for the mitochondrial Rho-GTPase 1 (Miro1), an essential mediator of microtubu
18 erated mechanical forces and the activity of Rho GTPases, a family of small GTP-binding proteins that
19 ad perturbations in four signaling pathways, Rho GTPases, actin, microtubule, and kinases-related pat
20 in cytoskeletal remodeling via regulation of Rho GTPases, acting as a negative regulator of ECT2, a G
23 3D spheroids of human cells, we identify the Rho GTPase activating protein ARHGAP18 as an effector of
25 ends on its presence at focal adhesions, its Rho-GTPase activating protein (Rho-GAP) function, and it
28 9, and S567) in the DLC1 tumor suppressor, a Rho GTPase-activating protein (RhoGAP) associated with f
29 ssociation of intronic variants in ARHGAP15 (Rho GTPase-activating protein 15; rs4662344-T: P=1.9 x 1
30 e 12 (MMP12)/MMP13, catenin alpha3 (CTNNA3), rho GTPase-activating protein 24 (ARHGAP24), angiopoieti
31 ll spreading through its interaction partner Rho GTPase-activating protein 29 (ArhGAP29), a GTPase ac
32 comprising the Cdc42-interactor IQGAP1, the Rho GTPase-activating protein ARHGAP10, and the integrin
33 emonstrated that selective expression of the Rho GTPase-activating protein ARHGAP42 in smooth muscle
35 otypically enriched Cadherin2 sequesters the Rho GTPase-activating protein, Gap21/23, to homotypic ju
36 r with its binding partner ARHGAP35/P190A, a RHO GTPase-activating protein, in the radial glia-like n
38 with exception of the Crossveinless-c (Cv-c) Rho GTPase-activating protein, most effectors exert litt
40 duces formation of the AKT kinase (AKT)/DLC1 Rho-GTPase-activating protein (DLC1) complex and thereby
41 neurons require Crossveinless-c, a specific Rho-GTPase-activating protein (Rho-Gap), to alter their
42 cell, which might install platforms allowing Rho-GTPase-activating protein (RhoGAP) activity to be fo
45 hat through its domain structure, SRGAP2A, a Rho-GTPase-activating protein, can co-regulate excitator
49 either the endocytic regulator TRIP10 or the Rho GTPase activator VAV2 reduces E-cadherin levels at j
50 rin, actin reorganization, localized Rac and Rho GTPase activities, and the development of strong cel
51 mics and interactions between cellular-level Rho GTPase activity and contractility and multicellular-
55 During collective cell migration, waves of Rho GTPase activity mediate mechanical contraction/exten
58 sfunction was also associated with increased Rho GTPase activity via activation of MT-bound Rho-speci
59 gnals through Abl family kinases to restrain Rho GTPase activity, support Hippo pathway suppressor fu
60 how that SLAIN2 inactivation does not affect Rho GTPase activity, trafficking, and focal adhesion for
65 pEM to experimental protein trajectories of Rho GTPases, an integral regulator of cytoskeletal dynam
66 on of Y256 of N-WASP via activation of small Rho GTPase and focal adhesion kinase mediates TGF-beta1-
68 osyltransferase domain for inactivating host Rho GTPases and a cysteine protease domain for the deliv
69 n as effectors that specifically target host Rho GTPases and heterotrimeric G proteins, respectively.
70 viduals with SRNS abrogated interaction with RHO GTPases and increased active GTP-bound RAC1 and CDC4
73 By regulating actin cytoskeleton dynamics, Rho GTPases and their activators RhoGEFs are implicated
74 is intrinsically linked to the activation of Rho GTPases and their cytoskeletal-remodeling effectors.
78 of paxillin and activated p42/44-MAP kinase, Rho GTPase, and paxillin/GEF-H1/p42/44-MAPK association.
79 patiotemporal dynamics of F-actin and active Rho GTPase, and that Cdh6 is required for accumulation o
80 , likely secondary to elevated activation of RHO GTPases, and 2) increased salivary cell proliferatio
81 signaling molecules, including MAP kinases, Rho GTPases, and components of the Wnt signaling pathway
83 mouse mutagenesis screen and identified the Rho GTPase antagonist p190RhoGAP as a critical regulator
85 found in cancer and developmental disorders, Rho GTPases are activated most commonly in disease by in
86 e nucleotide exchange factors (Rho GEFs) and Rho GTPases are among the key regulators of cytokinesis.
88 remains unknown how activities of different Rho GTPases are coordinated by Rasip1 to direct tubuloge
101 cular pathways downstream of Cdc42, Rac, and Rho GTPases are well documented, but we know surprisingl
102 sophila melanogaster cell wound repair model Rho GTPase arrays form in response to prepatterning by R
103 F7, a guanine nucleotide exchange factor for Rho GTPases, as one novel TIP-1-interacting protein in h
104 f CDC42 (cell division cycle 42), one of the Rho-GTPases associated with Th-cell differentiation, was
108 gy (DH) domain in a manner that occludes the Rho GTPase binding site, thereby suggesting the molecula
110 ease-like catalytic triad, which inactivates Rho GTPases by deamidating a conserved asparagine in the
111 that medium folate regulates the function of Rho GTPases by enabling their carboxyl methylation and t
113 Herein, we demonstrate that AMPylation of Rho GTPases by VopS is a multifaceted virulence mechanis
114 e factors (GEFs), the enzymes that stimulate Rho GTPases, can be a valuable therapeutic strategy to t
116 forts that investigate how PARs regulate the Rho GTPase CDC-42, which in turn regulates the actin-myo
118 in part mediated by down-regulation of small Rho GTPase CdC42 and the protein target PAK1, but not by
122 a adenosine A1 receptor (A1R) induction of a Rho GTPase CDC42-dependent conformational change of the
124 a guanine nucleotide exchange factor for the Rho-GTPase CDC42, which is known for its role in the ass
125 sion yeast Schizosaccharomyces pombe has six Rho GTPases (Cdc42 and Rho1-Rho5) and seven Rho GEFs (Sc
130 significantly greater proportion of the two Rho GTPases cell division cycle 42 (CDC42) and Rac famil
133 ases mesenchymal proliferation and modulates Rho-GTPase-dependent actin cytoskeletal signaling in fet
134 es revealed a smoke-induced up-regulation of Rho-GTPase-dependent actin cytoskeletal signaling that c
135 -bound form of the conserved small G protein Rho GTPase directly activates mTORC2 in AKT phosphorylat
136 e Salmonella effector SopE, we recapitulated Rho GTPase-driven actin polymerization at model phosphol
137 rlying this process, we examined the role of Rho GTPases during cardiac migration using inhibitory an
139 Rho-associated kinases 1 and 2 (ROCK1/2) are Rho-GTPase effectors that control key aspects of the act
140 We performed two siRNA screens targeting Rho-GTPases effectors and guanine nucleotide exchange fa
143 he Galpha(s) subfamily regulates activity of Rho GTPases extends our understanding of Galpha(s) activ
144 Network analyses identified enrichment of Rho GTPase, extracellular matrix, focal adhesion and cyt
145 membrane dynamics; however, the roles of the Rho GTPase family are not limited to cell adhesion and m
146 molecular targets in PCa cells including the Rho GTPase family members (for example, CDC42, CDC42EP3,
150 , and YAP-TRIO-Merlin mediated regulation of Rho GTPase family proteins, enhancing cell migration.
151 tic-specific, GTPase-deficient member of the Rho GTPase family that was first identified as a hypermu
152 are linked to cell migration such as p38 and rho GTPase-family activation, F-actin polymerization, ad
153 ng experimental data of mechanically-induced Rho GTPase FilGAP release from actin-filamin crosslinks.
155 ight the importance of CirA in coopting host Rho GTPases for establishment of Coxiella burnetii infec
156 Collectively, these findings identify a Rho GTPase-formin network that is critically involved in
162 es our current understanding of the roles of Rho GTPases in early erythropoiesis, downstream of cytok
163 o suggest that the targeting action of other Rho GTPases in other organ cells, such as RhoA in vascul
164 nteracted with ARHGDIA, a known regulator of RHO GTPases in podocytes that is dysfunctional in some t
165 Our findings reveal a critical role for Rho GTPases in positioning Ras activation and thereby es
166 We have analysed the expression levels of Rho GTPases in primary T-ALL samples compared with norma
168 hRNA library screen of all human kinases and Rho-GTPases in a patient-derived NF1 (-/-) Schwann cell
169 hRNA library screen of all human kinases and Rho-GTPases in a patient-derived NF1(-/-) Schwann cell l
174 This original mechanism of regulation of a Rho-GTPase-independent formin, recruited by Spire at Rab
178 ystematic RNA interference perturbation of a Rho GTPase interactome consisting of 219 proteins reveal
182 is" that consists of Wnt-FZD/ROR-Galpha12/13-Rho GTPases-Lats1/2 to promote YAP/TAZ activation and TE
183 nucleotide exchange factors (GEFs) activates Rho GTPases, leading to important roles for PREX protein
184 partitioning of charged polarity-regulating Rho GTPases like Rho1 or Cdc42 in a protein charge-depen
187 n certain instances inhibition of individual Rho GTPases may paradoxically result in pro-neoplastic e
188 t cell migrations require cell polarization, Rho GTPase-mediated cytoskeletal rearrangements, and myo
189 has been suggested to code signals to induce Rho GTPase-mediated fibrosis, but it is obscure how the
193 regulated by three evolutionarily conserved Rho GTPases, notably, Rac1 activation is sufficient and
194 GLOSS2 (PAN2) and PAN1, and the small GTPase RHO GTPASE OF PLANTS (ROP) promote mother cell polarity
196 h asthma.Conclusions: We found enrichment of Rho-GTPase pathways in obese asthmatic Th cells, identif
199 tenin mutants influenced p120(ctn)-dependent Rho GTPase phosphorylation and shifted cells towards dif
201 pression of RhoGDIalpha that in turn affects Rho GTPase protein levels, and thereby, controls cellula
208 Increased tension directly altered the small Rho GTPase Rac1, 3'-phosphoinositide, and cytoskeletal o
209 Since VAV2 serves as a GEF for the small Rho GTPase Rac1, a key player in cell motility and adhes
210 TKs), Src family PTK, focal adhesion kinase, Rho GTPase Rac1, and neural Wiskott-Aldrich syndrome pro
213 gnaling pathway and involves the PAR-1/c-Src/Rho GTPases Rac1 and Cdc42/c-Jun N-terminal kinase axis
216 indirectly, through activation of the small Rho GTPase Ras-related C3 botulinum toxin substrate 1 (R
217 toma-associated protein and increases in the Rho GTPases Ras-related C3 botulinum toxin substrate 1 (
219 multitude of RhoGEFs that activate a single Rho GTPase reflects the very specific role of each RhoGE
223 vertebrate species, TRIO is a well-conserved Rho GTPase regulator that is highly expressed in the dev
226 croscopy and RT-PCR expression of Rac1/CdC42 Rho GTPases, responsible for actin remodeling, we show t
229 a-catenin) and RHO guanosine triphosphatase [RHO GTPase, RHO], two signaling pathways previously show
233 statin caused the translocation of the small Rho GTPases RhoA, Cdc42, and Rac1/2/3 from cell membrane
234 ugh a wealth of data exists on the canonical Rho GTPases RhoA, Rac1, and Cdc42, several other family
236 e spatiotemporally coordinated activation of Rho GTPases (RhoA, Cdc42 and Rac1) in migrating glioblas
240 c Ca(2+) pools, which leads to a decrease in Rho-GTPases, RhoA and Rac1, and Ca(2+)-dependent Calpain
241 thy and have elucidated the role of atypical Rho GTPase RhoBTB in Drosophila neurological function an
243 s dependent on the expression of an atypical RHO-GTPase, RND3/RHOE, together with its binding partner
244 hange factor (PIX; Arhgef6), an activator of Rho GTPases, showed greatly increased motility and alter
245 To test the hypothesis that dysregulated Rho GTPase signaling and a resulting fibrotic activity w
246 , p190RhoGAP-A and -B, are key regulators of Rho GTPase signaling and are essential for actin cytoske
247 ession of the ADFH domain of mAbp1 increased Rho GTPase signaling and breast cancer cell invasion.
248 y integrating guidance signals with the ROP1 Rho GTPase signaling and coordinating intracellular sign
249 inding partners that differentially regulate Rho GTPase signaling and MTLn3 breast cancer cell invasi
250 hat LLG1 is a component of the FER-regulated RHO GTPase signaling complex and that fer and llg1 mutan
251 IPs in mutant HTT toxicity, we show that the Rho GTPase signaling components, BAIAP2, EZR, PIK3R1, PA
253 e a starting point to dissect spatiotemporal Rho GTPase signaling networks that regulate neurite outg
256 HD, including mammalian target of rapamycin, Rho GTPase signaling, and oxidative stress response.
261 1beta altered the cell cycle (108 genes) and Rho GTPases signaling (72 genes) in chondrocytes, while
262 ulator of filopodia formation, which couples Rho-GTPase signaling to actin cytoskeleton and membrane
263 regulator of filopodia dynamics that couples Rho-GTPase signaling to cytoskeleton and membrane remode
264 dermal growth factor receptor signaling, and Rho-GTPase signaling, commonly active in tumorigenesis a
265 Activation of c-Jun downstream of oncogenic Rho GTPase signalling leads to elevated GLS gene express
266 rin receptors sense these changes triggering Rho GTPase signals that modulate RPE tight junctions and
267 enous Yap activation by lats1/2 knockdown or Rho-GTPase stimulation mimicked Yap overexpression and i
269 is widely acknowledged, the role of atypical Rho GTPases (such as RHOBTB2) in neurodevelopment has ba
272 mplications in the design and application of Rho GTPase targeting strategies in future cancer therapi
273 deficient mice, we define the poorly studied Rho GTPase TC10 as an immunomodulatory molecule playing
274 Wounding triggers the formation of arrays of Rho GTPases that act as signaling centers that modulate
275 pathway involving SWIP-13/ERK8 activation of Rho GTPases that dictates DAT surface expression and fun
276 guanine-nucleotide-exchange factor (GEF) for Rho GTPases that is characterized by its localization at
277 is a guanine nucleotide exchange factor for Rho GTPases that is overexpressed in many cancers and in
278 anine nucleotide exchange factors (GEFs) for RHO GTPases that regulate intracellular actin dynamics.
279 rhotekin, as well as abnormal activation of Rho GTPases that was accompanied with impaired motility
280 dent on the levels of Miro1, a mitochondrial Rho-GTPase that regulates intercellular mitochondrial mo
281 In turn, coordinated crosstalk among the Rho GTPases themselves, as well as with the cytoskeleton
282 ors that alter the activation state of small Rho GTPases, thereby manipulating the host cell cytoskel
283 tracellular redistribution and activation of Rho GTPases, this study suggests that TIP-1 holds potent
285 dispensable for uptake and instead recruits Rho GTPase to promote biogenesis of the bacterial vacuol
288 Unlike other effector proteins that subvert Rho GTPases to modulate uptake, CirA is the first effect
289 ormed by oncogenic Dbl, which hyperactivates Rho GTPases, together with (13)C-labeled glutamine and s
290 f plasma membrane cholesterol and disrupting Rho GTPase trafficking-a process required for cell adhes
291 K, MAPK, and PI3K); and (c) association with Rho GTPases, tyrosine kinase receptors, Toll-like recept
293 protein 42) and its effector Borg (binder of Rho GTPases), which act as up-stream regulators of septi
294 iated actin polymerization and activation of Rho GTPase, which appear to be essential for EMyT induct