ライフサイエンスコーパス: ATPase

1 ATPase (enzymatic hydrolysis of adenosine triphosphate t

2 ATPases associated with diverse cellular activities (AAA

3 ATPases associated with various cellular activity are a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

21 The AAA ATPase katanin severs microtubules.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

36 an additional regulatory mechanism for AAA+ ATPases.

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

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

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

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

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

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

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

44 ABC ATPases developed structural hallmarks that unambiguousl

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

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

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

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

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

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

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

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

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

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

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

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

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

58 Heterologous expression of an ATPase inhibitor completely eliminated bactericidal acti

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

60 2 domain couples substrate specificity to an ATPase step essential for DNA methylation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 The cytosolic ATPase Cdc48 drives extraction by pulling on polyubiquit

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

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

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

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

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

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

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

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

95 ALC localizes to carboxysomes and exhibits ATPase activity.

96 for polar localization of the T4P extension ATPase PilB.

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

98 RadD is a RecQ-like SF2 family ATPase.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

119 symmetrically configured with two identical ATPases.

120 Ubl domains were required for the increased ATPase activity.

121 the presence of MgATP and displays intrinsic ATPase activity.

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

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

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

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

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

127 ariable affinities but equally stimulate its ATPase activity.

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

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

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

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

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

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

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

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

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

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

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

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

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

141 -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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

156 we illustrate for bacterial DNA clamp loader ATPases.

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

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

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

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

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

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

163 and other evolutionarily related ion-motive ATPases.

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

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

166 agnesium, two traits that are unlike natural ATPases.

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

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

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

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

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

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

173 intenance of chromosome (SMC) superfamily of ATPases.

174 es conserved residues responsible for Ts OLD ATPase activity.

175 2 structures also provide no information on ATPase domain architecture and ATP hydrolysis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

192 l results regarding their intrinsic relative ATPase activities.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 It harbors a DNMT domain and SNF2 ATPase domain.

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

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

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

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

213 tant with conformational changes of the Sub2 ATPase.

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

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

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

217 The ATPase EHD2 restricts lipid diffusion and counteracts li

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

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

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

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

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

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

224 Both the ATPase activity of FtsEX and its periplasmic interaction

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

240 polypeptide translocation catalyzed by these ATPase motors.

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

242 quitin are the phenotypic hallmark of Torsin ATPase manipulation.

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

244 etection and negative regulation by a Trip13 ATPase.

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

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

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

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

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

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

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

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

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

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

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

256 post-termination ribosome recycling in UPF1 ATPase mutants.

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

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

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

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

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

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

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

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

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

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

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

268 kills cells in the absence of a functional V-ATPase.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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