ライフサイエンスコーパス: ATPase

1 tant with conformational changes of the Sub2 ATPase.

2 f VopQ bound to the V(o) subcomplex of the V-ATPase.

3 has characteristics of both the BFM and F(1)-ATPase.

4 RadD is a RecQ-like SF2 family ATPase.

5 pendent lid closing, N-M domain docking, and ATPase.

6 m7 subunit and disassembled by the Cdc48/p97 ATPase.

7 mechanism other than activation of the H(+) -ATPase.

8 etection and negative regulation by a Trip13 ATPase.

9 P2-ATPases including Ca(2+)-ATPases and Na,K-ATPase.

10 agnesium, two traits that are unlike natural ATPases.

11 , sodium is essential to running costly Na-K ATPases.

12 and other evolutionarily related ion-motive ATPases.

13 we illustrate for bacterial DNA clamp loader ATPases.

14 intenance of chromosome (SMC) superfamily of ATPases.

15 an additional regulatory mechanism for AAA+ ATPases.

16 symmetrically configured with two identical ATPases.

17 oviding feedback onto the function of the P4-ATPases.

18 ered calcium pump (secretory pathway calcium ATPase 1 [SPCA1]) encoded by the ATP2C1 gene in AAV infe

19 s sarcoplasmic/endoplasmic reticulum calcium-ATPase 2a (SERCA2a) and accelerates calcium re-uptake in

20 id auxin effects, their relationship to H(+)-ATPase activation and other transporters, and dependence

21 growth theory invoking plasma membrane H(+)-ATPase activation is still useful.

22 e hypothesis that this enhancement is due to ATPase activation via re-establishing ionic homeostasis.

23 ly couples tail binding, hexamerization, and ATPase activation.

24 How the 12 ATPase active sites of ClpA, 6 in the D1 ring and 6 in t

25 l results regarding their intrinsic relative ATPase activities.

26 inhibitor dorsomorphin decreased lysosomal V-ATPase activity and also blocked any increase upon starv

27 played a significantly reduced increase in V-ATPase activity and assembly upon starvation.

28 Enzymatic ATPase activity and in vivo growth assays show that IrtA

29 ntration-dependent cooperativity for maximal ATPase activity and upon heptamerization, packing of tra

30 Msp1's ATPase activity depends on its hexameric state, and prev

31 We demonstrate that ClpB3 has ATPase activity in a wide range of pH and temperature va

32 GenX did not reduce P-gp- or BCRP-associated ATPase activity in an in vitro transport assay system.

33 mage mapping data to show that Rad26 and its ATPase activity is critical for TC-NER downstream of the

34 vivo amino acid transporter and Na(+) K(+) -ATPase activity is reduced, and ex vivo ATP levels are l

35 Interestingly, RUVBL1-RUVBL2 ATPase activity is required for NMD activation by an unk

36 mine the substrate specificity or affect the ATPase activity of CDC48.

37 its the casein-activated, but not the basal, ATPase activity of ClpB with an IC(50)~5 muM.

38 with FlrC(C) Excess cyclic-di-GMP repressed ATPase activity of FlrC(C) through destabilization of he

39 Both the ATPase activity of FtsEX and its periplasmic interaction

40 procal shift, with basal and actin-activated ATPase activity of IFI-3a showing reduced values compare

41 subdomain 1 of actin and in stimulating the ATPase activity of Myosin.

42 The basal ATPase activity of Q2O2 Rca is repressed but strongly st

43 In vitro, NUCKS1 stimulates the ATPase activity of RAD54 and the RAD51-RAD54-mediated st

44 We show that vacuolar H+-ATPase activity regulates sorting of O-glycosylated prot

45 ion at the other sites only inhibits Katanin ATPase activity stimulated by MTs.

46 YecSC had low basal ATPase activity that was moderately stimulated by apo Fl

47 ndicating that H89 and dorsomorphin modify V-ATPase activity through other cellular targets.

48 el, where DHX34 acts to couple RUVBL1-RUVBL2 ATPase activity to the assembly of factors required to i

49 Disassembly inhibits V-ATPase activity under low-glucose conditions by releasin

50 ites face the transporter to likely modulate ATPase activity upon O antigen binding.

51 no acid transporter activity and Na(+) K(+) -ATPase activity using sarcolemmal membranes isolated fro

52 JNK2 causally enhances SERCA2-ATPase activity via increased maximal rate, without alte

53 starvation-dependent increase in lysosomal V-ATPase activity without altering basal activity.

54 isaggregase activity (but not always reduced ATPase activity), which predicts disease severity.

55 7), creating a compact conformation in which ATPase activity, actin activation and filament assembly

56 osition decrease membrane fluidity, F(0)F(1)-ATPase activity, and improve intracellular pH homeostasi

57 to a nonamer that binds DNA, stimulates TerL ATPase activity, and inhibits TerL nuclease activity.

58 Hemimethylated DNA preferentially stimulates ATPase activity, and mutating Dnmt5's ATP-binding pocket

59 starvation-dependent increase in lysosomal V-ATPase activity, indicating that H89 and dorsomorphin mo

60 ypothesis that wounding inhibits P-type H(+)-ATPase activity, leading to apoplastic alkalization.

61 Our data suggest that lower Na(+) K(+) -ATPase activity, which reduces the driving force for act

62 luding the subunit H, which is essential for ATPase activity.

63 on, and, interestingly, this binding reduces ATPase activity.

64 es conserved residues responsible for Ts OLD ATPase activity.

65 ATP-dependent FlhG dimer and stimulates FlhG ATPase activity.

66 ALC localizes to carboxysomes and exhibits ATPase activity.

67 ariable affinities but equally stimulate its ATPase activity.

68 egulate protein phosphatases to control H(+)-ATPase activity.

69 on regulation, or if it is also critical for ATPase activity.

70 ly related to Shp1-mediated control of Cdc48 ATPase activity.

71 Ubl domains were required for the increased ATPase activity.

72 the presence of MgATP and displays intrinsic ATPase activity.

73 XPB in the open conformation and reduces its ATPase activity.

74 r constitutive activation of the P-type H(+)-ATPase AHA1.

75 major loci were identified, encoding for an ATPase and a MATE protein, and contributing up to 7 and

76 te formation of asymmetric complexes with an ATPase and a non-ATPase at opposite ends.

77 The AAA(+) ATPase and bromodomain factor ATAD2/ANCCA is overexpress

78 the N-terminal cassette of BRR2 is an active ATPase and can unwind substrate RNAs.

79 , GAPDH, HSP60, HSP70, alphaTUB, UBC, RPS18, ATPase and GST, were analyzed using a panel of analytica

80 Here, we reveal that sequential ATPase and GTPase activities license release factors Rei

81 erichia coli hosts, indicating that both the ATPase and nuclease activities are required for OLD func

82 Since Yta7(ATAD2) is an AAA(+) ATPase and potential hexameric unfoldase, our results su

83 ntracellular calcium gradient by the calcium ATPase and processing within the Golgi compartment are e

84 f Na(+) and K(+) ions through the Na(+)/K(+)-ATPase and propose the significance that this work might

85 ctures reveal unique features of mammalian V-ATPase and suggest a mechanism of V1-Vo torque transmiss

86 otein (Arp) module is sandwiched between the ATPase and the rest of the complex, with the Snf2 helica

87 FAP45 to an axonemal module including dynein ATPases and adenylate kinase as well as CFAP52, whose mu

88 . coli gyrases are proficient DNA-stimulated ATPases and efficiently supercoil and decatenate DNA.

89 and dynamics of P2-ATPases including Ca(2+)-ATPases and Na,K-ATPase.

90 er-3) and Na(+)/K(+)ATPase (sodium-potassium-atpase) and phosphorylation of AT(2)R-cGMP downstream si

91 ding proteins), pH regulation (V-type proton ATPase), and inorganic carbon regulation (carbonic anhyd

92 acetylation of Pif1 stimulated its helicase, ATPase, and DNA-binding activities, whereas maintaining

93 els, nonselective (NALCN) channels, the Na K-ATPase, and hyperpolarization-activated cation channels.

94 Vacuoles with functional V-ATPases appear unnecessary in W303 cells for iron to ent

95 We hypothesized that ClC-5 and H(+)-ATPase are functionally coupled during H(+)-ATPase-media

96 P-type ATPases are found in all kingdoms of life and constitute

97 Inhibitors of muscle myosin ATPases are needed to treat conditions that could be imp

98 Thus, the three Cag ATPases are not functionally redundant.

99 five and up to eight distinct clades of ABC ATPases are reconstructed as being present in the last u

100 r vacuolar-type adenosine triphosphatases (V-ATPases) are ATP-driven proton pumps comprised of a cyto

101 Here, we identify the TRIP13 ATPase as a negative regulator of REV7.

102 e archazolids as well as the evaluation of V-ATPases as a novel and powerful class of anticancer targ

103 ther secretory tissues and identify vacuolar ATPases as the likely mechanisms driving acidification o

104 at amino acid starvation rapidly increases V-ATPase assembly and activity in mammalian lysosomes, but

105 This study identifies mechanisms of V-ATPase assembly and biogenesis that rely on the integrat

106 oth the catalytic nature of RAVE's role in V-ATPase assembly and the likelihood of glucose signaling

107 An exception is the assembly factor vacuolar ATPase assembly integral membrane protein (VMA21), whose

108 RAVE localization did not correlate with V-ATPase assembly levels reported previously in these muta

109 ial for viral entry and regulation of V-type ATPase assembly.

110 ve (>500 kDa) protein has an N-terminal AAA (ATPase associated with diverse cellular activities) ring

111 ium tuberculosis collaborates with the AAA+ (ATPases associated with a variety of cellular activities

112 ATPases associated with diverse cellular activities (AAA

113 orm by molecular chaperones belonging to the ATPases associated with diverse cellular activities (AAA

114 an Mg(2+)-chelatase protein belonging to the ATPases associated with various cellular activities (AAA

115 ATPases associated with various cellular activity are a

116 stem of ClpA, which is a well-studied, model ATPases associated with various cellular activity system

117 hat the valosin-containing protein (VCP), an ATPase-associated protein newly identified in the heart,

118 symmetric complexes with an ATPase and a non-ATPase at opposite ends.

119 rting activity of the plasma membrane Ca(2+)-ATPase at the postsynaptic membrane.

120 ATP13A3 encodes for an orphan P5B-ATPase (ATP13A3), a P-type transport ATPase that represe

121 and identified the V0 subunit C of vacuolar ATPase (ATP6V0C) as a Vpu-binding protein.

122 xpression of another subunit of the vacuolar ATPase, ATP6V0C", had no effect on tetherin expression.

123 tal binding domains (MBDs) of the P(1B)-type ATPase ATP7B and to determine the thermodynamic factors

124 ow that the DNA-binding site and the histone/ATPase binding site of CW are located on the opposite si

125 ity and loss of chromatin association of the ATPase Brg1.

126 The ATPase-catalysed conversion of ATP to ADP is a fundament

127 howed their involvement in the regulation of ATPase, cation transporter, kinase and UDP-glycosyltrans

128 Mutations of the ion pump alpha2-Na/K ATPase cause familial hemiplegic migraine, but the mecha

129 The cytosolic ATPase Cdc48 drives extraction by pulling on polyubiquit

130 d serves as a recruitment signal for the AAA-ATPase Cdc48/p97, which actively disassembles the comple

131 the cofactor can directly interact with the ATPase, Cdc48 and Shp1 are recruited independently to SC

132 AAA+ ATPase ClpB is a promising target for the development of

133 ate treatment (NaVO(3,) an inhibitor of many ATPases) completely halted recovery from drought-induced

134 dition to a role for the Cdc48-Npl4-Ufd1 AAA-ATPase complex, Doa1 and a mitochondrial pool of the tra

135 Intermediate vestigial ATPase complexes formed by disruption of nuclear genes f

136 ese findings establish a new role for a SNF2 ATPase: controlling an adjoined enzymatic domain's subst

137 C-terminal domain of the bacteriophage phi29 ATPase (CTD) that suggest a structural basis for these f

138 -0.59 A F(-1) and a decrease in Na(+) ,K(+) -ATPase current from 1.09 A F(-1) to 0.54 A F(-1) during

139 in I(Na,late) and a decrease in Na(+) ,K(+) -ATPase current.

140 say, only HSP70 was required, along with its ATPase cycle and relevant cochaperones, for Ubr1-mediate

141 HX MS reveals that the ATPase cycle is rate-limited by ADP release from nucleot

142 ced by expression of known dominant-negative ATPase-defective forms of VPS4A.

143 fore generated a mouse model that harbors an ATPase-deficient allele and demonstrates that mutant CHD

144 ABC ATPases developed structural hallmarks that unambiguousl

145 , we tested how the yeast plasma membrane P4-ATPase, Dnf2, responds to changes in membrane compositio

146 proteasomes are symmetric, with a regulatory ATPase docked at each end of the cylindrical 20S.

147 isoforms of the DOMINO nucleosome remodeling ATPase, DOM-A and DOM-B, directly specify two distinct m

148 Hsp90 has an N-terminal ATPase domain (N), a middle domain (M) that interacts wi

149 OLD family nucleases contain an N-terminal ATPase domain and a C-terminal Toprim domain.

150 2 structures also provide no information on ATPase domain architecture and ATP hydrolysis.

151 etween HELLS and CtIP and establish that the ATPase domain of HELLS is required to promote DSB repair

152 Although the ATPase domain of Isw1 docks at the SHL2 position when IS

153 ORC5, the protein would lack 80% of the AAA+ ATPase domain, including the Walker A motif.

154 hat face each other in the core of the NLRP3 ATPase domain.

155 It harbors a DNMT domain and SNF2 ATPase domain.

156 t simultaneous conformational changes in all ATPase domains at each catalytic step generate movement

157 he structure places the nucleic acid-binding ATPase domains of the helicase directly in front of the

158 A are bound within the C-tier of MCM2-7 AAA+ ATPase domains.

159 er structures in different states suggest an ATPase-driven, ratchet-like translocation of the tubulin

160 The ATPase EHD2 restricts lipid diffusion and counteracts li

161 ATPase (enzymatic hydrolysis of adenosine triphosphate t

162 rily conserved microtubule (MT)-severing AAA-ATPase enzyme Katanin is emerging as a critical regulato

163 h the ER Ca(2+) uptake pump, sarco/ER Ca(2+) ATPase, ER Ca(2+) release channels, inositol 1,4,5-trisp

164 s EsxC, EsxA and EsxB, or the membrane-bound ATPase EssC, compared to the wild-type (WT).

165 regulated primarily by ion channels, pumps (ATPases), exchangers and Ca(2+)-binding proteins.

166 report its divergent optimization toward the ATPase family AAA domain containing 2 (ATAD2) and cat ey

167 Many members of the AAA+ ATPase family function as hexamers that unfold their pro

168 In many species, the MinD-type ATPase FlhG (also YlxH/FleN) is central to the numerical

169 ation domain inserted into an N-terminal ABC ATPase fold and a C-terminal Toprim domain.

170 ts form a luminal glycan coat critical for V-ATPase folding, localization, and stability.

171 ABC ATPases form one of the largest clades of P-loop NTPase

172 eport two cryo-EM structures of the intact V-ATPase from bovine brain with all the subunits including

173 While disruption of either V-PPase or V-ATPase had no obvious effect on plant embryo development

174 Vacuolar type ATPase (V-ATPase) has recently emerged as a promising novel antica

175 and DNA promote the engagement of cohesin's ATPase head domains and ATP binding.

176 he two HEAT-repeat subunits bound to the SMC ATPase head domains.

177 led by acetylation and engagement of the Smc ATPase head domains.

178 The vacuolar-type H(+)-ATPases (V-ATPase) hydrolyze ATP to pump protons across the plasma

179 ith cytosolic ubiquitin ligase UBE3C and p97 ATPase in degrading their membrane substrates.

180 MinD is a cell division ATPase in Escherichia coli that oscillates from pole to

181 d retrotranslocase cooperates with the Cdc48 ATPase in membrane protein extraction.

182 the structure, function, and dynamics of P2-ATPases including Ca(2+)-ATPases and Na,K-ATPase.

183 ts D-loop formation by Rad51 and Rad54 in an ATPase-independent manner.

184 Heterologous expression of an ATPase inhibitor completely eliminated bactericidal acti

185 de4-(trifluoromethoxy)phenylhydrazone or the ATPase inhibitor N,N'-dicyclohexylcarbodiimide.

186 y is eliminated by introducing lidocaine, an ATPase inhibitor.

187 macrolides, which present the most potent V-ATPase inhibitors known to date.

188 The Na(+)/K(+)-ATPase is a chemical molecular machine responsible for t

189 Here, we show that mice in which alpha2-Na/K ATPase is conditionally deleted in astrocytes display ep

190 Vacuolar H+-ATP complex (V-ATPase) is a multisubunit protein complex required for a

191 The vacuolar H(+)-ATPase (V-ATPase) is an ATP-dependent proton pump that is essentia

192 d nonstructural protein 2C, which is an AAA+ ATPase, is a promising target for drug development.

193 d that assembly of RCV, comprising F(1)/F(o)-ATPase, is rapid with little excess subunit synthesis, b

194 In AIG, the gastric proton pump, H(+)/K(+) ATPase, is the major autoantigen recognized by autoreact

195 The AAA ATPase katanin severs microtubules.

196 in, a cardiac glycoside, in humanized Na+,K+-ATPase-knockin mice reduced I/R injury.

197 imaging reveals that conditional alpha2-Na/K ATPase knockout triggers spontaneous cortical spreading

198 Msp1 is a conserved eukaryotic AAA+ ATPase localized to the outer mitochondrial membrane, wh

199 aining protein 2 (EHD2) is a dynamin-related ATPase located at the neck of caveolae, but its physiolo

200 d metabolomic analyses show that alpha2-Na/K ATPase loss alters metabolic gene expression with conseq

201 As a ring-shaped adenosine triphosphatase (ATPase) machine, cohesin organizes the eukaryotic genome

202 quitin are the phenotypic hallmark of Torsin ATPase manipulation.

203 -ATPase are functionally coupled during H(+)-ATPase-mediated endosomal acidification, crucial for ClC

204 t shunt conductance facilitated further H(+)-ATPase-mediated endosomal acidification.

205 e an invaluable tool for future studies on V-ATPase-mediated membrane fusion and autophagy.

206 Moreover, glycolysis is essential for V-ATPase-mediated proton pumping.

207 while binding directly to subunit c of the V-ATPase membrane-embedded subcomplex V(o).

208 long been recognized that smooth muscle Na/K ATPase modulates vascular tone and blood pressure (BP),

209 encing who harbor pathogenic variants in the ATPase module of MORC2.

210 n before PCNA opening, with the clamp loader ATPase modules forming an overtwisted spiral that is inc

211 anges that are linked to the active site via ATPase motif VI.

212 and SMARCA2's central domains, including its ATPase motif, are required for this interaction.

213 polypeptide translocation catalyzed by these ATPase motors.

214 els of intracellular Ca(2+) uptake and Na, K-ATPase mRNA were determined in the cultured epithelial c

215 The mitochondrial AAA ATPase Msp1 is well known for extraction of mislocalized

216 post-termination ribosome recycling in UPF1 ATPase mutants.

217 ine, but the mechanisms by which alpha2-Na/K ATPase mutations lead to the migraine phenotype remain i

218 The Ca(2+) ATPase NCA-2 was found to be involved in the initial int

219 es could only be closed by the action of the ATPase, NSF.

220 ned and installed onto DNA by a clamp loader ATPase of the AAA+ family.

221 BRG1, when placed into the orthologous Sth1 ATPase of the yeast RSC remodeler, separate into two cat

222 The ATPase of this machinery, PscN (SctN), is thought to be

223 A4 (BRG1), one of the two mutually exclusive ATPases of the SWI/SNF chromatin remodeling complex.

224 pposite ends of 20S are coupled: binding one ATPase opens a gate locally, and also opens the opposite

225 eta had little effect on the actin-activated ATPase or motile activities of Myo1c.

226 cribed as inhibitor leads for the human AAA+ ATPase p97, an antitumor target.

227 kdown of the E3 ubiquitin ligase MARCH4, the ATPase p97/VCP, the deubiquitinating enzyme USP8, the cu

228 inhibition of a conserved Dictyostelium AAA ATPase, p97, a homolog of the human transitional endopla

229 The AAA+ ATPase, p97, also referred to as VCP, plays an essential

230 We show that the conserved AAA-ATPase PCH-2/TRIP13, which remodels the checkpoint effec

231 aling is attenuated by a homolog of the AAA+ ATPase Pch2/TRIP13, which binds and disassembles the act

232 Blocking V-ATPase pharmacologically in beta-cells increased mTORC1

233 for polar localization of the T4P extension ATPase PilB.

234 ither of the mutually exclusive BRG1 and BRM ATPases, promoted NIPBL recruitment at active enhancers.

235 pendent on the conserved inner-membrane AAA+ ATPase/protease, FtsH.

236 C1 activity, suggesting involvement of the V-ATPase proton pump in the phenotype.

237 microscopy shows a greater accumulation of V-ATPase proton pumps at the apical surface of A-ICs in KO

238 G-patch region of Spp2 binds to the DEAH-box ATPase Prp2, and both proteins together are essential fo

239 spliceosome formation requires the DEAD-box ATPase PRP5(2-7).

240 -binding module of SAGA and the spliceosomal ATPase Prp5p mediate a balance between transcription ini

241 he sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase pump inhibitors, and only the release of the Thg-

242 a critical subunit of the vacuolar ATPase (V-ATPase) pump.

243 SERCAs (sarco-endoplasmic reticulum Ca(2+)-ATPases) pump Ca(2+) into internal stores that play a ma

244 h FliY concentrations, YecSC reached maximal ATPase rates independent of the presence or nature of th

245 d bactericidal activity, while loss of the F-ATPase reduced the electrophysiological response to amin

246 Vma2Delta cells have dysfunctional V-ATPases, rendering their vacuoles nonacidic.

247 pS's inhibition of substrate binding and its ATPase repression are separable activities.

248 ticus T3SS effector VopQ targets host-cell V-ATPase, resulting in blockage of autophagic flux and neu

249 yosin contractility (specifically, of myosin ATPase, Rho kinase, or myosin light-chain kinase activit

250 nce caused by dysfunction of sarco/ER Ca(2+) ATPase, ryanodine receptor, and inositol 1,4,5-trisphosp

251 The ATPase SecA is an essential component of the bacterial S

252 Sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) activity was reduced and western blot ana

253 to the increased sarcoplasmic reticulum Ca2+-ATPase (SERCA) Ca2+ reuptake, modulated by increased pho

254 of the sarco(endo)plasmic reticulum calcium ATPase (SERCA) in cardiac myocytes is modulated by an in

255 The sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) is a P-type ATPase that transports Ca(2+)

256 ty of the sarco-endoplasmic reticulum Ca(2+)-ATPase (SERCA) pump during Ca(2+) refilling of the ER.

257 sregulation of sarcoplasmic reticulum Ca(2+) ATPase (SERCA) pump is one of the key determinants of th

258 zed by the sarcoendoplasmic reticulum Ca(2+)-ATPase (SERCA), which plays a lead role in muscle contra

259 p sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA).

260 e 2a sarco/endoplasmic reticulum (ER) Ca(2+)-ATPase (SERCA2a) plays a key role in intracellular Ca(2+

261 ctivities) ring, which, like dynein, has six ATPase sites.

262 (sodium-hydrogen exchanger-3) and Na(+)/K(+)ATPase (sodium-potassium-atpase) and phosphorylation of

263 sDNA junctions and possesses ssDNA-dependent ATPase, ssDNA binding, ssDNA endonuclease, 5' to 3' ssDN

264 2 domain couples substrate specificity to an ATPase step essential for DNA methylation.

265 Saccharomyces cerevisiae RSC comprising its ATPase (Sth1), the essential actin-related proteins (ARP

266 TP-binding pocket disproportionately reduces ATPase stimulation by hemimethylated versus unmethylated

267 of alpha3 (ERAD); larger differences in Na,K-ATPase subunit distributions among subcellular fractions

268 Inactivation of SMARCA4/BRG1, the core ATPase subunit of mammalian SWI/SNF complexes, occurs at

269 avage or shedding of vacuolar-type ATPase (V-ATPase) subunits Ac45 and prorenin receptor, respectivel

270 on promote conformational changes within the ATPase that are transmitted to the Smc coiled-coil domai

271 RAD51 is an ATPase that forms a nucleoprotein filament on single-str

272 replication as a ring-shaped heterohexameric ATPase that is believed to be essential to recruit and l

273 gin recognition complex (ORC), a DNA-binding ATPase that loads the Mcm2-7 replicative helicase onto r

274 MORC2 encodes an ATPase that plays a role in chromatin remodeling, DNA re

275 nse mutations in VPS4A, a gene coding for an ATPase that regulates the ESCRT-III machinery in a varie

276 han P5B-ATPase (ATP13A3), a P-type transport ATPase that represents a candidate polyamine transporter

277 reticulum Ca(2+)-ATPase (SERCA) is a P-type ATPase that transports Ca(2+) from the cytosol into the

278 echanism regulated by astrocytic alpha2-Na/K ATPase that triggers episodic motor paralysis in mice.

279 terial plasmids is driven by plasmid-encoded ATPases that are represented by the P1 plasmid ParA prot

280 katanin, spastin, fidgetin - are related AAA-ATPases that cut microtubules into shorter filaments.

281 It contains the DotL ATPase, the DotM and DotN proteins, the chaperone module

282 , through the action of the Hsc70 "uncoating ATPase." The J- and PTEN-like domain-containing proteins

283 We isolated homogeneous rat brain V-ATPase through its interaction with SidK, a Legionella p

284 leads to cooperative binding of proteasomal ATPases to 20S and promotes formation of proteasomes sym

285 In turn, the AAA+ ATPase torsinA is thought to regulate force transmission

286 of C- and N-terminal tagging of the luminal ATPase torsinA on its ability to associate with nuclear

287 raJ receptor, and VirB11-like and VirB4-like ATPases, TraG and TraB, respectively.

288 ocessing factors including the RNA-dependent ATPase UAP56/DDX39B and histone modifiers such as the SI

289 -terminal stalk, a dynein-like core with six ATPase units, and a multidomain E3 module.

290 Vacuolar type ATPase (V-ATPase) has recently emerged as a promising no

291 The vacuolar H(+)-ATPase (V-ATPase) is an ATP-dependent proton pump that i

292 ATP6v1g1, a critical subunit of the vacuolar ATPase (V-ATPase) pump.

293 paired cleavage or shedding of vacuolar-type ATPase (V-ATPase) subunits Ac45 and prorenin receptor, r

294 The vacuolar-type H(+)-ATPases (V-ATPase) hydrolyze ATP to pump protons across

295 impedes acidification via defective vacuolar ATPase (vATPase) V0a1 subunit delivery to lysosomes.

296 the human transitional endoplasmic reticulum ATPase (VCP/p97) protein.

297 reas activation of the plasma membrane H(+) -ATPase was not.

298 , which encodes a Cu(2+)-transporting P-type ATPase, were investigated following the introduction of

299 Activity of Na(+) K(+) -ATPase, which is responsible for establishing the sodium

300 It is catalysed by the RecA family of ATPases, which form a helical filament with single-stran