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1 GTPase activity was essential only for turnover of FtsZ2
2 GTPase-activating proteins (GAPs) and guanine exchange f
4 anine nucleotide exchange factor (GEF) and a GTPase activating protein (GAP) is an efficient method f
5 al homologue, LRRK2 was proposed to act as a GTPase activated by dimerization (GAD), while recent rep
6 sensitivity to mutation when regulated by a GTPase activating protein and a nucleotide exchange fact
9 response to amino acids, including GATOR1, a GTPase activating protein for RAGA, and GATOR2, a positi
13 tion-based nucleotide binding, intrinsic and GTPase-activating protein-stimulated GTPase, and ARL3 gu
14 od pathways, involving ubiquitin ligases and GTPase exchange factors/GTPase-activating proteins (GEF/
18 ynthetic sorting center of the cell, the Arf GTPases are responsible for coordinating vesicle formati
20 we focused on ADP ribosylation factor (Arf) GTPases, which orchestrate a variety of regulatory funct
21 the role of ADP-ribosylation factor 1 (ARF1)-GTPase and its effector ARF-guanine-exchange factors (GE
22 Unlike the ubiquitously expressed human Arf6 GTPase, PSD3 localization is restricted to the brain, pa
24 ospholipase Dalpha1 (PLDalpha1), both act as GTPase-activity accelerating proteins (GAPs) for the Gal
28 echanism involves trans-dimerization between GTPase heads and a favorable crossover conformational sh
29 conformation that functions as a GTP-binding GTPase and is required for cancer stem cell survival.
30 , as the closed conformation has GTP binding/GTPase activity, and the open conformation transamidase
32 experiments were accompanied by biochemical GTPase activity assays and transendothelial resistance m
33 ntifiers are phosphoinositides and GTP-bound GTPases, which provide well-defined but mutable labels.
37 ator of cell polarity, the activity of CDC42 GTPase is tightly controlled in maintaining normal hemat
38 eta-Arrestin1 binds and suppresses the Cdc42 GTPase-activating protein ARHGAP21, we hypothesize that
41 rotein 1 (IQGAP1), an effector of Rac1/CDC42 GTPases, in the regulation of actin cytoskeleton dynamic
42 ins that belong to the subgroup of centaurin GTPase family, encoded by CENTG1 located in CDK4 amplico
45 tion following the selective loss of ciliary GTPase Arl13b in interneurons impairs interneuronal morp
46 Here, we identify a universally conserved GTPase (HflX) as a bona fide dissociation factor of the
47 affold proteins, such as IQ motif containing GTPase activating protein 1 (IQGAP1), are promising targ
49 egion mapping to Iqgap2 (IQ motif-containing GTPase activating protein 2) and F2rl2 (proteinase-activ
50 that LGR5 interacts with IQ motif-containing GTPase-activating protein 1 (IQGAP1), an effector of Rac
51 OK2 directly phosphorylates the cytoskeletal GTPase Septin7, at an evolutionary conserved residue.
54 ing through Rag GTPases, and GATOR1 displays GTPase activating protein (GAP) activity for RAGA and RA
55 hosphorylation of the mitochondrial division GTPase dynamin-related protein 1 promoted mitochondrial
59 SGK1 promotes expression of the Rho family GTPase Cdc42, a positive regulator of actin assembly, ce
60 ling through sequestration of Rac/Rho family GTPases and by using monomeric actin as bait to recruit
63 ts, Gbetagamma subunits, and some Rho family GTPases, phospholipase C-beta (PLC-beta) isoforms hydrol
67 cific isoform of the large, membrane fission GTPase, can be activated in nonneuronal cells downstream
71 e nucleotide dissociation inhibitors (GDIs), GTPase-activating proteins (GAPs), or the chaperone/GEF
74 e we demonstrate that the interferon-induced GTPase family of guanylate-binding proteins (GBPs) coats
75 nce protein 1 (MX1) is an interferon-induced GTPase that plays an important role in the defense of ma
76 ich led to formation of interferon-inducible GTPase-containing aggregates and hampered recruitment of
77 tion of autophagy proteins and IFN-inducible GTPases to inhibit replication of positive-sense RNA vir
78 LC3 conjugation system and the IFN-inducible GTPases were necessary to inhibit MNV replication in mic
79 proteins and the induction of IFN-inducible GTPases, which are known to destroy the membrane of vacu
82 rms of Ras alter effector binding and innate GTPase activity, leading to deregulation of downstream s
83 equence of hypotheses for how intracellular (GTPase) and ECM signaling jointly regulate lamellipodial
85 and promoting vascular relaxation due to its GTPase accelerating protein activity toward Galphaq.
86 mplex signaling network composed of kinases, GTPases, and lipids, such as phosphoinositides, helps to
88 OPA1, a gene encoding a mitochondrial large GTPase involved in cristae structure and mitochondrial n
90 at PI(4)P is needed to anchor Arl8 (Arf-like GTPase 8) and its effector homotypic fusion/vacuole prot
92 ted the protein ADP-ribosylation factor-like GTPase 13b (ARL13b) as a model palmitoylated ciliary pro
93 erial division, polymers of the tubulin-like GTPase FtsZ assemble at midcell to form the cytokinetic
96 nfluences their ability to control localized GTPase activity in the context of migration and invasion
97 orosarcina pasteurii UreG (SpUreG), a P-loop GTPase and the first discovered native ID enzyme, involv
98 ue GTP-specific antibody fragment to monitor GTPase cycling in the presence of a guanine nucleotide e
99 n this work, we show that RabA2, a monomeric GTPase from common bean, is required for the progression
100 Dynamins are a family of large, multidomain GTPases involved in key cellular processes in eukaryotes
101 model whereby RAPGEF5 activates the nuclear GTPases, Rap1a/b, to facilitate the nuclear transport of
104 n mechanism that regulates the Ras family of GTPases and provides an important mechanism by which SIR
105 s critical actions of the atlastin family of GTPases in maintaining the morphology of the endoplasmic
106 tivated downstream of the Ras superfamily of GTPases, and Ras-PI3K interaction plays a key role in pr
107 ad only modest effects on GTP binding and on GTPase activity and did not perturb stability of the MCM
108 ith CDR formation, whereas the role of other GTPases in this process is either lacking or inconclusiv
109 n XLRP.Mutations in the Retinitis Pigmentosa GTPase Regulator (RPGR) cause retinal dystrophy, but how
113 ng induces conformational changes to promote GTPase domain dimerization in the transition state.
115 g LRRK2 kinase phosphorylates a group of Rab GTPase proteins including Rab29, within the effector-bin
116 Overexpression of a specific subset of Rab GTPase-activating proteins (RabGAPs) inhibited histamine
117 understanding of the molecular basis of Rab GTPase-regulated membrane trafficking in eukaryotic cell
119 ers of functional diversification in the Rab GTPase gene family in three Paramecium aurelia species.
125 ost-translational geranylgeranylation of Rab GTPases represents one way to control the activity of th
127 cts of C-terminal carboxylmethylation on RAB GTPases and provide a rationale for targeting ICMT in th
128 ncrease in the activated levels of small Rab GTPases such as Rab5 and Rab7, both key regulators of en
131 Zerial was the first to discover that Rab GTPases represent identity markers for different membran
132 e of the established players include the Rab GTPases, the SNARE complex proteins, and others, which f
134 pH-sensitive machinery downstream of the Rab-GTPase Ypt7 needed for SNARE-mediated lipid bilayer merg
135 e-nucleotide exchange factor activating Rab5 GTPases, is required for both pre- and postinvasive immu
137 e molecular level, RIN1 signals through Rab5 GTPases that control endocytosis of cell-surface recepto
139 P19, we identify CEP350, FOP, and the RABL2B GTPase as proteins organizing the first known mechanism
140 ar superoxide scavenger) or NSC 23766 (a Rac GTPase inhibitor) completely inhibited Siglec-8-mediated
142 he unexpected pro-oncogenic functions of Rac GTPase-activating proteins also challenged the dogma tha
143 o to stimulate the signaling activity of Rac GTPase: Abl gates the activity of the spectrin repeats o
147 e study was to characterize the role of Rac1 GTPase for the mineralocorticoid receptor (MR)-mediated
148 tive effects of PGA2 by activating Rap1/Rac1 GTPase and protein kinase A targets at cell adhesions an
151 Multiple protein complexes regulate the Rag GTPases in response to amino acids, including GATOR1, a
152 nput to this system, and act through the Rag GTPases to promote the translocation of mTORC1 to the ly
153 through a pathway that converges on the Rag GTPases, an obligate heterodimer of two related GTPases.
155 quires intersubunit communication by the Rag GTPases, providing a rationale for why they exist as a d
156 plex regulates mTORC1 signalling through Rag GTPases, and GATOR1 displays GTPase activating protein (
157 cilitates mTORC1 activation by inducing RagA GTPase recruitment of mTORC1 to the lysosomal outer surf
158 n for TRPM8 that unexpectedly acts as a Rap1 GTPase inhibitor, thereby inhibiting endothelial cell mo
160 key regulator of this cascade is the Nf1 Ras GTPase activating protein (RasGAP), which attenuates Ras
162 f-assembly of plasma membrane-associated Ras GTPases has major implications to the regulation of cell
163 ond system is driven by interferon-regulated GTPases that promote rupture of pathogen-containing vacu
164 of the small GTPase Arl3 and its regulatory GTPase activating protein (GAP) Retinitis Pigmentosa 2 (
165 ADP ribosylation factor family of regulatory GTPases, but is atypical in having a non-homologous, C-t
172 iation of intronic variants in ARHGAP15 (Rho GTPase-activating protein 15; rs4662344-T: P=1.9 x 10(-1
173 and have elucidated the role of atypical Rho GTPase RhoBTB in Drosophila neurological function and po
175 (MMP12)/MMP13, catenin alpha3 (CTNNA3), rho GTPase-activating protein 24 (ARHGAP24), angiopoietin 4
178 chondrial membrane protein mitochondrial Rho GTPase 1 (Miro1) is a master regulator of mitochondrial
179 90RhoGAP-A and -B, are key regulators of Rho GTPase signaling and are essential for actin cytoskeleta
180 cations in the design and application of Rho GTPase targeting strategies in future cancer therapies.
181 lmonella effector SopE, we recapitulated Rho GTPase-driven actin polymerization at model phospholipid
182 tegrating guidance signals with the ROP1 Rho GTPase signaling and coordinating intracellular signalin
183 cient mice, we define the poorly studied Rho GTPase TC10 as an immunomodulatory molecule playing a ro
184 cular targets in PCa cells including the Rho GTPase family members (for example, CDC42, CDC42EP3, RAC
187 r pathways downstream of Cdc42, Rac, and Rho GTPases are well documented, but we know surprisingly li
188 idely acknowledged, the role of atypical Rho GTPases (such as RHOBTB2) in neurodevelopment has barely
189 erturbations in four signaling pathways, Rho GTPases, actin, microtubule, and kinases-related pathway
190 titioning of charged polarity-regulating Rho GTPases like Rho1 or Cdc42 in a protein charge-dependent
191 in caused the translocation of the small Rho GTPases RhoA, Cdc42, and Rac1/2/3 from cell membranes to
195 ed cells deficient for the mitochondrial Rho-GTPase 1 (Miro1), an essential mediator of microtubule-b
196 mesenchymal proliferation and modulates Rho-GTPase-dependent actin cytoskeletal signaling in fetal l
197 evealed a smoke-induced up-regulation of Rho-GTPase-dependent actin cytoskeletal signaling that can l
198 r mechanism by which cell spreading and RhoA GTPase activity control FA formation through YAP to stab
200 sin RLC phosphorylation is regulated by RhoA GTPase during ACh stimulation, and NM RLC phosphorylatio
204 Arf-like protein 13b (ARL13b) is a small GTPase that functions as a guanosine nucleotide exchange
205 a guanine exchange factor for Rab26, a small GTPase that specifically directs synaptic vesicles to pr
208 an endosomal budding, upstream of ARF6 small GTPase and its effector phospholipase D2, directly phosp
210 showed that the ubiquitously expressed small GTPase Arf6 is required for normal ethanol-induced sedat
211 ic oncogenic phenotypes.The Ras-family small GTPase RAB25 can exert both pro- and anti-oncogenic func
214 nipulation, permeability measurements, small GTPase activity, luciferase assays, chromatin immunoprec
216 ormation on the new functional role of small GTPase, NOG1, in guard cell signaling and early plant de
217 e signaling events linking JAKs to rho small GTPase activation by chemokines is still incompletely de
220 nanoscopy, we explore the role of the small GTPase ARF1 in mediating transport steps at the Golgi.
221 OPI coated vesicle is initiated by the small GTPase Arf1 that recruits the coatomer complex to the me
222 ycling between both sites requires the small GTPase Arf6 but neither caveolin1 (Cav1) nor Cavin1.
223 terestingly, a known ACAP2 target, the small GTPase Arf6, supported histamine-evoked WPB exocytosis,
225 7 as novel interaction partners of the small GTPase Arl3 and its regulatory GTPase activating protein
227 sitively regulated the activity of the small GTPase CDC42, deletion of which caused severe defects in
229 grin-dependent local activation of the small GTPase RAC1 at the plasma membrane to control the activi
230 s well as signaling via ERK1/2 and the small GTPase Rac1); however, CXCL14 bound to CXCR4 with high a
233 s been linked to the activation of the small GTPase Ras homolog family member A (RhoA) by the Galpha1
234 The activation of Raf kinases by the small GTPase Ras requires two major sets of phosphorylations.
237 ivator-inhibitor network, in which the small GTPase Rho amplifies its activity by recruiting its acti
238 and ROCK2) function downstream of the small GTPase RhoA to drive actomyosin cytoskeletal remodeling.
241 The roles of protein kinase C and the small GTPase, Rab9, in alpha1B-AR vesicular traffic were inves
243 ed that NUMB and NUMBL interacted with small GTPase Rab7 to transition ERBB2 from early to late endos
245 expressing DiRas1 or DiRas2, which are small GTPases that bind SmgGDS and act as tumor suppressors.
248 ous GEFs and also a host of Ras family small GTPases, it is important to know which specific GEF-smal
249 ed activation of downstream Ras family small GTPases, which ultimately lead to ERK, JNK, and p38 phos
251 by several paralog families, including small GTPases, coiled-bundle proteins, and proteins with beta-
253 the post-translational prenylation of small GTPases that perform a plethora of cellular functions.
257 e the signaling between RABs and other small GTPases, some of which have a crucial role in the traffi
258 d the membrane localization of several small GTPases and this was potentiated by zoledronic acid.
259 es, which act as effectors for several small GTPases, and has been specifically identified to functio
260 e trans-Golgi and was regulated by the small GTPases Arl1 and Arl8, suggesting a role in trans-Golgi
263 regulation, and that expression of the small GTPases was markedly increased in miR-142(-/-) neutrophi
265 sic and GTPase-activating protein-stimulated GTPase, and ARL3 guanine nucleotide exchange factor acti
266 on assays and light microscopy, we find that GTPase activation and trans-SNARE complex zippering have
270 oth the WASP homology 1 (WH1) domain and the GTPase binding domain (GBD) of N-WASP and no binding to
271 phosphatidylinositol-3,4-biphosphate and the GTPase Rab5 then appear and remain as the uncoating vesi
272 ation of both protein kinase A (PKA) and the GTPase Ras, and is induced upon the activation of beta-a
274 ich lipid droplets (LDs) in the liver by the GTPase ARF1, which is a key activator of lipolysis.
275 we cloned, expressed, and characterized the GTPase LdSar1 and other COPII components like LdSec23, L
276 ures of engineered human MFN1 containing the GTPase domain and a helical domain during different stag
279 ct activator of mTOR, and its inhibitor, the GTPase-activating protein tuberin (TSC2), may play a rol
281 Here, the authors identify inhibitors of the GTPase activating function of LRS, not affecting its cat
282 e analyses reveal enhanced expression of the GTPase RAC1 and cholesterol-biosynthesis-associated gene
289 tion can rescue cytokinesis failure when the GTPase-activating protein (GAP) CYK-4 is disrupted, Rac
290 fect highly conserved amino acids within the GTPase domain of the protein that are critical for GTP a
292 ave the way to further studies into how this GTPase regulates bacterial physiology, including persist
293 the preprotein-binding regions on the Toc159 GTPase domain (Toc159G) of pea (Pisum sativum) using cle
295 e recycling small guanosine triphosphatases (GTPases) Rab4 or Rab11 was sufficient to maintain GJs up
297 ignal via the Rag guanosine triphosphatases (GTPases) to promote the localization of mTORC1 to the ly
298 Rho family small guanosine triphosphatases (GTPases), which are regulated by the opposing actions of
300 s granule responses and co-localisation with GTPase Activating Protein (SH3 domain) Binding Proteins
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