ライフサイエンスコーパス: ATPase

1 d with a multi-subunit vacuolar H+-ATPase (V-ATPase).

2 f counterclockwise rotation driven by the F1-ATPase.

3 of drugs as novel inhibitors of the VCP/p97 ATPase.

4 2 is presumed to function as a DNA packaging ATPase.

5 he physiological and pathological roles of V-ATPase.

6 s in E1P and E2P conformations of Na(+)/K(+)-ATPase.

7 rand, but not on the putative 'lagging' AdnA ATPase.

8 ilament OFF state and inhibiting acto-myosin ATPase.

9 f its Mcm7 subunit and the action of the p97 ATPase.

10 iew of ATP activity in Enterococcus hirae V1-ATPase.

11 (LMCA1), an orthologue of eukaryotic Ca(2+)-ATPases.

12 fic targeting or regulation information to V-ATPases.

13 mechanism is likely conserved for other AAA+ ATPases.

14 efficient localization of Stv1-containing V-ATPases.

15 hat require activation by specialized AAA(+) ATPases.

16 sides of the apparatus, in between the VirB4 ATPases.

17 POINTS: The role of plasma membrane Ca(2+) -ATPase 1 (PMCA1) in Ca(2+) homeostasis and electrical st

18 etermine the role of plasma membrane Ca(2+) -ATPase 1 (PMCA1) in maintaining Ca(2+) homeostasis and e

19 Plasma membrane calcium ATPase 2 (PMCA2) is a calcium pump that plays important

20 cardiac sarco/endoplasmic reticulum calcium ATPase 2a (SERCA2a) in the regulation of overall calcium

21 ycling by sarco/endoplasmic reticulum Ca(2+)-ATPase 2b (SERCA2b) and ryanodine receptor 2 (RyR2).

22 no terminal (NT) domain of the yeast Golgi V-ATPase a-isoform Stv1.

23 Valosin-containing protein (VCP/p97) ATPase (a.k.a. Cdc48) is a key member of the ER-associat

24 is activation of the vacuolar H(+)-ATPase (V-ATPase), a proton pump that acidifies lysosomes.

25 The gastric proton pump H(+),K(+)-ATPase acidifies the gastric lumen, and thus its inhibit

26 gation growth and play a key role in PM H(+)-ATPase activation by inhibiting PP2C.D family protein ph

27 t HslU pseudohexamers containing mixtures of ATPase active and inactive subunits at defined positions

28 Here we report a dominant mutation in the ATPase active site of human CLPX, p.Gly298Asp, that resu

29 y the removal of the C-terminal arm from the ATPase active site.

30 e mutated Arg-84, Arg-88, and Arg-101 in the ATPase-active B, C, and D subunits of Saccharomyces cere

31 c70 complexes to bind ATP and enhances their ATPase activities in vitro.

32 Rho utilizes its RNA-dependent ATPase activities to translocate along the mRNA and even

33 osensitive to Ca(2+) in regulated actomyosin ATPase activities.

34 m channel/sarcoendoplasmic reticulum calcium-ATPase activity and cardiac tissue fibrosis.

35 , demonstrating a direct correlation between ATPase activity and Cu(I) transport.

36 a (Mtalpha) of F-ATP synthase suppresses its ATPase activity and determined the mechanism of suppress

37 th H2A nucleosome and free H2A.Z induces SWR ATPase activity and engages the histone exchange mechani

38 obtained that exhibited high actin-activated ATPase activity and in vitro actin filament motility.

39 ffect on BSEP basal and substrate-stimulated ATPase activity as well as on taurocholate transport.

40 Inhibition of Hsc70 ATPase activity blocked the slow transport of synapsin,

41 st ABC transporter inhibitors shown to block ATPase activity by binding to the transmembrane domain.

42 avacamten primarily reduces the steady-state ATPase activity by inhibiting the rate of phosphate rele

43 ides a rationale for the stimulation of MalK ATPase activity by MalE as well as by maltose.

44 The ATPase activity controls dissociation of an MVH complex

45 Cln1(-/-) mice, which mimic INCL, reduced v-ATPase activity correlates with elevated lysosomal pH.

46 tion in proteoliposomes stimulated its basal ATPase activity from 21 to 38 nmol of Pi.mg(-1).min(-1),

47 In contrast, these drugs inhibited ATPase activity in native membranes or in proteoliposome

48 Sperm stimulate V-ATPase activity in oocytes by signalling the degradation

49 Hsp90 without significantly affecting Hsp90 ATPase activity in the absence of Aha1.

50 Measurements of myofibrillar ATPase activity in the absence of Ca(2+) showed a signif

51 extensions of Drs2p can greatly increase its ATPase activity in the presence of PI4P and demonstrate

52 It has been believed that Rrp2's ATPase activity is not required for cell growth, but exp

53 RarA ATPase activity is stimulated by single-stranded DNA gap

54 Importantly, binding of Nup98 stimulates the ATPase activity of DHX9, and a transcriptional reporter

55 ically stimulate the intrinsic DNA-dependent ATPase activity of DnaA via a process termed Regulatory

56 its co-chaperone Aha1, which accelerates the ATPase activity of Hsp90.

57 demonstrate that the maximum actin-activated ATPase activity of M2beta-S1 is slowed more than 4-fold

58 The ATPase activity of MORC2 is critical for HUSH-mediated s

59 In contrast, ATPase activity of TDRD9 is dispensable for piRNA biogen

60 nAB in vitro is stringently dependent on the ATPase activity of the 'lead' AdnB motor translocating o

61 We find that ivacaftor stimulates the ATPase activity of the purified protein and can compete

62 has no significant effect on actin-activated ATPase activity or actomyosin affinity in the presence o

63 BiP's activity is regulated by its intrinsic ATPase activity that can be stimulated by two different

64 d the SecY channel complex and utilizing its ATPase activity to drive protein translocation across th

65 rge (calcium) translocation and steady-state ATPase activity under substrate conditions (various calc

66 from 21 to 38 nmol of Pi.mg(-1).min(-1), and ATPase activity was further stimulated by the NtPDR1 sub

67 Very modest decreases in G4 DNA-stimulated ATPase activity were observed for the mutant enzymes.

68 h high affinity, and this binding stimulates ATPase activity with an enzymatic efficiency similar to

69 fic molecular features, including high basal ATPase activity, a unique aggregate binding domain, and

70 ATPase activity, rather than being regulated, instead gr

71 c acid substitutions reduced actin-activated ATPase activity, slowed the in vitro sliding velocity an

72 ecific site, leading to a 2-fold increase in ATPase activity.

73 h THO and Yra1-C stimulated Sub2's intrinsic ATPase activity.

74 y less stable than wild-type IFIH1, and lack ATPase activity.

75 ndependent of KIR , NO, PGs and Na(+) /K(+) -ATPase activity.

76 and ssNucs are effective at activating Fun30 ATPase activity.

77 mc3 heads prompted by de-repression of their ATPase activity.

78 Translocation of V-type ATPase after 1 h of exposure to 30,000 muatm was also as

79 ormation about the interaction of Na(+),K(+)-ATPase alpha-isoforms with cellular matrix proteins, the

80 Mutations in the genes coding for Na(+),K(+)-ATPase alpha-subunit isoforms lead to severe human patho

81 can bind specifically to purified human Na,K-ATPase (alpha1beta1).

82 P4-ATPases, also known as phospholipid flippases, are respo

83 ndent and ATP-independent helicase, and both ATPase and ATP-dependent helicase activities are inhibit

84 also exhibited reduced expression of V-type ATPase and compromised targeting of this proton pump to

85 disengagement, which also explains residual ATPase and gating activity of dephosphorylated CFTR.

86 Na(+),K(+)-ATPase and H(+),K(+)-ATPase are electrogenic and nonelec

87 The Cdc48 ATPase and its cofactors Ufd1/Npl4 (UN) extract polyubiq

88 V-ATPase consists of soluble V1-ATPase and membrane-integral Vo proton channel sectors.

89 upts the association of axin and LKB1 with v-ATPase and ragulator.

90 rs of the sarcoendoplasmic reticulum calcium ATPase and ryanodine receptor.

91 omal DNA; ParB is the stimulator of the ParA ATPase and specifically binds to the plasmid at a centro

92 om MCC by the joint action of the TRIP13 AAA-ATPase and the Mad2-binding protein p31(comet) Now we ha

93 e thus needed to functionally characterize V-ATPase and to fully evaluate the therapeutic relevance o

94 the plasma membrane anion channels and H(+)-ATPase and with the tonoplast TPK K(+) channel.

95 rgo delivery, a complex of the PEX1 and PEX6 ATPases and the PEX26 tail-anchored membrane protein rem

96 s the proton pumping vacuolar H(+)-ATPase (V-ATPase) and are extensively involved in acid-base homeos

97 ctly interacted with vacuolar H(+)-ATPase (V-ATPase), and ZnT2 deletion impaired vesicle biogenesis,

98 A- and DNA-dependent activation of MutLalpha ATPase, and MutLalpha function in in vitro mismatch repa

99 mily (FXYD1-12), which regulate Na(+) ,K(+) -ATPase, and phospholamban, sarcolipin, myoregulin and DW

100 sma membrane depends on the activities of P4-ATPases, and disruption of PS distribution can lead to v

101 ed structures of its constituent XPB and XPD ATPases, and how the core and kinase subcomplexes of TFI

102 s in male organisms, inductions of Na(+)K(+)/ATPases, and strong inhibitions of molt-related proteins

103 nd ADORA2B purinergic P1 receptors induced V-ATPase apical membrane accumulation in medullary A-ICs b

104 ions of the respective binding sites in Na,K-ATPase are crucial in determining its selectivity.

105 Na(+),K(+)-ATPase and H(+),K(+)-ATPase are electrogenic and nonelectrogenic ion pumps, r

106 Cu-ATPases are membrane copper transporters present in all

107 ATP synthases (ATPases) are enzymes that produce ATP and control the pH

108 annel and sarco/endoplasmic reticulum Ca(2+) ATPase as the principal regulators of systolic and diast

109 tal microbalance; and motor bioactivity with ATPase assay, on a set of model surfaces, i.e., nitrocel

110 ith ABCG2 was investigated by a colorimetric ATPase assay.

111 Ca(2+)-ATPase assays showed that sAnk1 ablated SLN's inhibition

112 r function requires interplay with hexameric ATPases associated with diverse cellular activities (AAA

113 geted deletion of the gene encoding the AAA+-ATPase Atad3a hyperactivated mitophagy in mouse hematopo

114 lian cells is the copper-transporting P-type ATPase ATP7A, which mediates copper transport from the c

115 with the better characterized prokaryotic Cu-ATPases, ATP7B is assumed to be a single-chain monomer.

116 For Na,K-ATPase, bilayer properties can modulate pump activity, a

117 hich was only found in bacterial proteasomal ATPases, buries the carboxyl terminus of each protomer i

118 Msp1 is a transmembrane AAA-ATPase, but its role in TA protein clearance is not know

119 s possible that the stimulation of cohesin's ATPase by Scc2 also has a post-loading function, for exa

120 t BS inhibits contractility and actin-myosin ATPase by stabilizing the OFF state of the thick filamen

121 he sarcoplasmic-endoplasmic reticulum Ca(2+)-ATPase calcium pump in mammals and is of industrial impo

122 ifferent chromatin remodelers, we found that ATPases chromodomain helicase DNA-binding protein 9 (CHD

123 evealed an overlap of the retinoschisin-Na/K-ATPase complex with proteins involved in Na/K-ATPase sig

124 , of the V1 domain of the heteromultimeric V-ATPase complex.

125 ither the assembly or the stability of the V-ATPase complex.

126 t unanticipated functions of the peroxisomal ATPase complex.

127 afficking caused by genetic defects in the V-ATPase complex.

128 V-ATPase consists of soluble V1-ATPase and membrane-integr

129 itoring diffusion of eGFP-labeled Na(+),K(+)-ATPase constructs in the plasma membrane of HEK293T cell

130 he endolysosomal lipid PI(3,5)P2 activates V-ATPases containing the vacuolar a-subunit isoform in Sac

131 In this work, the Cu-ATPase CopA from Escherichia coli was expressed and puri

132 ATP7B is a copper-transporting P1B-type ATPase (Cu-ATPase) with an essential role in human physi

133 te release, the biochemical step in myosin's ATPase cycle associated with force generation and the co

134 The ATPase cycle of the Hsp90 molecular chaperone is essenti

135 between kinesins alter kinetic rates in the ATPase cycle to produce functional changes in processivi

136 tate kinetics to model a minimal eight-state ATPase cycle.

137 ves suggests that the asymmetry of the three ATPase-dependent 120 degrees power strokes imposed by th

138 /PKA pathway-dependent mechanism to induce V-ATPase-dependent H(+) secretion.

139 ytic space of gp17-adenosine triphosphatase (ATPase) determines the rate at which the 'lytic water' m

140 Surprisingly, in an ATPase devoid of a central stalk, the interfaces of this

141 We show that RPS3 inhibits ATPase, DNA binding, and helicase activities of RECQL4 t

142 We found that deletion of Lon's ATPase domain abrogated interactions with DNA.

143 te structure composed of a membrane-proximal ATPase domain and a membrane-distal substrate-recognitio

144 observe additional interactions between the ATPase domain and the adjacent DNA gyre 1.5 helical turn

145 SMARCA4 (also known as BRG1) mapping to the ATPase domain cause loss of direct binding between BAF a

146 , but that it inhibits topo II by preventing ATPase domain dimerization rather than stabilizing it.

147 and the most common alteration affecting the ATPase domain in CMT patients (p.Arg252Trp) hyperactivat

148 binding and DNA cleavage, revealing that the ATPase domain is the primary site for DNA binding, and i

149 studies revealed that Az associates with an ATPase domain of Hsc70 and thus blocks ATP binding to th

150 tic regulator SMCHD1 mapping to the extended ATPase domain of the encoded protein cause BAMS in all 1

151 lity of Lon to bind DNA is determined by its ATPase domain, that this binding is required for process

152 onstrained region of SMCHD1 encompassing the ATPase domain.

153 ular Hsp90 is attributed to their N-terminal ATPase-driven chaperone function.

154 residues of WRN involved in the binding and ATPase-driven unwinding of G4 DNA.

155 Unlike the yeast P4-ATPase Drs2, ATP8A2 is not regulated by phosphoinositide

156 ase signaling and localization, whereas Na/K-ATPase-dysregulation caused by retinoschisin deficiency

157 Existing small-molecule modulators of V-ATPase either are restricted to targeting one membranous

158 superhelix location 2 (SHL2), where the Chd1 ATPase engages nucleosomal DNA.

159 ovisional evidence for altered DNA-dependent ATPase expression in suicide only.

160 ome bromodomain-containing proteins, such as ATPase family AAA domain-containing protein 2 (ATAD2), i

161 a(2+)-ATPase (SERCA), a member of the P-type ATPases family, transports two calcium ions per hydrolyz

162 e reveals how the adenosine triphosphatases (ATPases) form a closed spiral staircase encircling an un

163 t that varying factors adversely affecting v-ATPase function dysregulate lysosomal acidification in o

164 red for nucleosome remodeling by keeping the ATPase function of BRG1 active.

165 Interestingly, oleate also inhibits v-ATPase function, yielding triacylglycerol accumulation b

166 ediated lipid uptake that directly impairs v-ATPase function.

167 iseases caused by mutations in the p-type Cu-ATPase genes ATP7A and ATP7B, respectively.

168 , we address this question for the conserved ATPase guided entry of tail-anchored protein 3 (Get3), w

169 nd synaptic vesicular proton pump protein (V-ATPase H) levels.

170 djacent region, which connects the HIRAN and ATPase/helicase domains.

171 ind that the cochaperone, activator of Hsp90 ATPase homolog 1 (Aha1), dramatically increased the prod

172 CC 7942, the gene Synpcc7942_2071 encodes an ATPase homologue of type II/type IV systems.

173 efects of the V-type proton (H(+)) ATPase (V-ATPase) impair acidification and intracellular trafficki

174 r genetic or pharmacological inhibition of v-ATPase in cardiomyocytes exposed to low palmitate concen

175 ilic quinazolines modulate the function of V-ATPase in cells.

176 ully evaluate the therapeutic relevance of V-ATPase in human diseases.

177 the role of adenosine in the regulation of V-ATPase in ICs.

178 strophanthin induced inhibition of the Na-/K-ATPase in liver cells using a magnetic resonance (MR) co

179 counterclockwise rotation powered by the F1-ATPase in steps equivalent to the rotation of single c-s

180 A AAA+ ATPase in the clamp loader clade, RarA protein is part o

181 he vacuolar H(+)-adenosine triphosphatase (V-ATPase) increased the luminal concentrations of most met

182 cro domain, constitutively activate the ALC1 ATPase independent of PARylated PARP1, and alter the dyn

183 kground, we speculated that blockade of Na/K-ATPase-induced ROS amplification with a specific peptide

184 The time course of the Na-/K-ATPase inhibition in the cell culture was demonstrated b

185 The mechanism of palmitate-induced v-ATPase inhibition involved its dissociation into two par

186 A Na(+)/K(+)-ATPase inhibitor (ouabain) potentiated EA-induced cytoto

187 ADP acts as a strong ATPase inhibitor of cytosol-specific Hsp90 homologs, whe

188 her demonstrate that a previously reported V-ATPase inhibitor, 3-bromopyruvate, also targets the same

189 ly similar to more potent vacuolar-type H(+)-ATPase inhibitors, which all inhibited LGR5 internalizat

190 ATPase inhibitory factor 1 (IF1) is a nuclear-encoded, A

191 a family of dynamin-related mechano-chemical ATPases involved in cellular membrane trafficking.

192 DNA damage, an inactive conformation of the ATPase is maintained by juxtaposition of the macro domai

193 A P-type H(+)-ATPase is the primary transporter that converts ATP to e

194 at the mechanism of ATP generation by rotary ATPases is less strictly conserved than has been general

195 The vacuolar H(+) ATPase (V-ATPase) is a complex multisubunit machine that regulates

196 us of the Arabidopsis plasma membrane Ca(2+)-ATPase isoform 8 (ACA8) and that this interaction stimul

197 tinoschisin on the functionality of the Na/K-ATPase, its interaction partner at retinal plasma membra

198 nts unexpectedly revealed that, whereas Cin8 ATPase kinetics fell within measured ranges for kinesins

199 event the FSS-induced increase in Na(+)/K(+)-ATPase levels.

200 sitions in the Listeria monocytogenes Ca(2+)-ATPase (LMCA1), an orthologue of eukaryotic Ca(2+)-ATPas

201 domain against predominantly the C-terminal ATPase lobe through conserved electrostatic interactions

202 inally, retinoschisin treatment altered Na/K-ATPase localization in photoreceptors of Rs1h(-/Y) retin

203 revealed no effect of retinoschisin on Na/K-ATPase-mediated ATP hydrolysis and ion transport.

204 the RP is formed by a heterohexameric AAA(+) ATPase module, which unfolds and translocates substrates

205 SecA ATPase motor protein plays a central role in bacterial p

206 Chromatin remodelers use a helicase-like ATPase motor to reposition and reorganize nucleosomes al

207 elieves autoinhibitory interactions with the ATPase motor, which selectively activates ALC1 remodelin

208 is the proteasomal adenosine triphosphatase (ATPase) Mpa, which captures, unfolds, and translocates p

209 ties to study the consequences of Na(+),K(+)-ATPase mutations and provide information about the inter

210 sing sodium/potassium transporter Na(+)/K(+)-ATPase (NKA) into a monoolein-derived LCP.

211 CA1, the sarco(endo)plasmic reticulum Ca(2+)-ATPase of skeletal muscle, is essential for muscle relax

212 ted to targeting one membranous subunit of V-ATPase or have poorly understood mechanisms of action.

213 ion alone, or combined NO, PGs, Na(+) /K(+) -ATPase (ouabain) and KIR channel inhibition (n = 6; Prot

214 h the activity of the proteasome and the AAA ATPase p97/VCP in a similar manner to infectious viruses

215 ssential role for the ubiquitin-directed AAA-ATPase, p97, in the clearance of damaged lysosomes by au

216 concentration by disrupting the actin-myosin ATPase pathway.

217 e-dependent response of DNA as the remodeler ATPase perturbs the duplex at SHL2.

218 sults here demonstrate that the T4P assembly ATPase PilB functions as an intermediary in the EPS regu

219 1970s, auxin activates plasma membrane H(+)-ATPases (PM H(+)-ATPases) to facilitate cell expansion b

220 Plasma membrane Ca(2+)-ATPase (PMCA) protein expression was confirmed in vitro

221 t into an overall architecture of a human Cu-ATPase, positions of the main domains, and a dimer inter

222 action of CCT chaperonin with that of TRIP13 ATPase promotes the complete disassembly of MCC, necessa

223 independently of the action of the DEAD-box ATPase Prp5.

224 hat inhibits the membranous sodium-potassium ATPase pump across cell types and can cause rapid death

225 of a lysosomal complex containing at least v-ATPase, ragulator, axin, liver kinase B1 (LKB1) and AMPK

226 We find that She1 affects the ATPase rate, microtubule-binding affinity, and stepping

227 PAX4 or its target gene encoding the p97/VCP ATPase reduced myofibril disassembly and degradation on

228 w that p37/UBXN2B, a cofactor of the p97 AAA ATPase, regulates spindle orientation in mammalian cells

229 ubiquitylation also involves VCP/p97, an AAA ATPase regulating the folding of various cellular substr

230 To investigate the mechanism of V-ATPase regulation by reversible disassembly, we recently

231 ock Proteins 70 and 40 is at the core of the ATPase regulation of the chaperone machinery that mainta

232 l degradation of HIF1alpha, disrupting the V-ATPase results in intracellular iron depletion, thereby

233 lectroneutral C932R mutant of the Na(+),K(+)-ATPase retained a wild-type-like enzyme turnover rate fo

234 cle to select a specific conformation of the ATPase ring for RP engagement and is released in a shoeh

235 main that binds UN and two stacked hexameric ATPase rings (D1 and D2) surrounding a central pore.

236 peptide (cTP), and N-terminal domains to the ATPase, Rubisco recognition and C-terminal domains.

237 The sarcoplasmic reticulum Ca(2+)-ATPase SERCA promotes muscle relaxation by pumping calci

238 THADA binds the sarco/ER Ca(2+) ATPase (SERCA) and acts on it as an uncoupler.

239 the sarco/endoplasmic reticulum (SR) Ca(2+) ATPase (SERCA) and is abnormally elevated in the muscle

240 and the sarco/endoplasmic reticulum Ca(2+) -ATPase (SERCA) as the principal regulators of systolic a

241 sarcoendoplasmic reticulum calcium trasport ATPase (SERCA) pump activity with thapsigargin prolonged

242 The sarco/endoplasmic reticulum Ca ATPase (SERCA) pump then refills SR Ca stores.

243 Sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA), a member of the P-type ATPases family, t

244 the sarco/endoplasmic reticulum (ER) Ca(2+)-ATPase (SERCA), disrupts Ca(2+) homeostasis, and causes

245 increased sarco/endoplasmic reticulum Ca(2+) ATPase (SERCA)-mediated reuptake rather than changes in

246 nd sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase (SERCA).

247 late the sarco/endoplasmic reticulum Ca(2+) -ATPase (SERCA).

248 purified sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA1a).

249 a regulatory effect of retinoschisin on Na/K-ATPase signaling and localization, whereas Na/K-ATPase-d

250 TPase complex with proteins involved in Na/K-ATPase signaling, such as caveolin, phospholipase C, Src

251 in combination with NO, PGs and Na(+) /K(+) -ATPase significantly reduced the vasodilatatory response

252 islandicusPilT N-terminal-domain-containing ATPase (SisPINA), encoded by the gene adjacent to the re

253 Point mutations at the ATPase site bias Get3 toward closed conformations, uncou

254 , and NBD2 contains the catalytically active ATPase site in CFTR.

255 f communication between the TA-binding site, ATPase site, and effector interaction surfaces of Get3.

256 create Rad50 dimers with only one functional ATPase site, we find that both ATPase sites are required

257 ne functional ATPase site, we find that both ATPase sites are required for the stimulation by DNA.

258 BAZ1B might contact chromatin to direct the ATPase SMARCA5.

259 gi/secretory pathway Ca(2+)/Mn(2+)-transport ATPase (SPCA1a) is implicated in breast cancer and Haile

260 regulation of topo II through modulation of ATPase status.

261 ese inhibitors can abrogate the Aha1-induced ATPase stimulation of Hsp90 without significantly affect

262 he mRNA-binding protein Yra1 by the DEAD-box ATPase Sub2 as assisted by the hetero-pentameric THO com

263 Moreover, v-ATPase subunit a1 of the V0 sector (V0a1) requires palmi

264 4, Nas6, Hsm3, and Nas2 each bind a specific ATPase subunit of the base and antagonize base-CP intera

265 Here we reveal that BRG1, the essential ATPase subunit of the SWI/SNF chromatin-remodelling comp

266 mutations involving PSMD12, encoding the non-ATPase subunit PSMD12 (aka RPN5) of the 19S regulator of

267 ng site but rather the interface between the ATPase subunits and the transmembrane subunits of the LP

268 We show that accessory (non-ATPase) subunits of ISWI remodellers can distinguish bet

269 l and functional characterization of a novel ATPase, Sulfolobus islandicusPilT N-terminal-domain-cont

270 his arginine is conserved with the HerA/FtsK ATPase superfamily; (iv) a molecular docking model of th

271 D-1, a translational repressor that blocks V-ATPase synthesis.

272 ParA is an ATPase that binds to chromosomal DNA; ParB is the stimul

273 aining protein 2 (EHD2) is a dynamin-related ATPase that confines caveolae to the cell surface by res

274 such viruses: the adenosine triphosphatase (ATPase) that powers DNA translocation and an endonucleas

275 Hence, in the H(+),K(+)-ATPase, the ability of the M8 arginine to donate an inte

276 However, in a complete V1-ATPase, the mechanical property of the central stalk is

277 our prior work that showed autoinhibited V1-ATPase to be arrested in state 2, we propose a model in

278 /lysosome and interacts with the lysosomal v-ATPase to negatively regulate mTORC1 activation.

279 iated expansion growth by activating PM H(+)-ATPases to facilitate apoplast acidification and mechani

280 Folding and transporting of P4-ATPases to their cellular destination requires the beta

281 ivates plasma membrane H(+)-ATPases (PM H(+)-ATPases) to facilitate cell expansion by both loosening

282 he C-Mad2-binding protein p31(comet) and the ATPase TRIP13 promote MCC disassembly and checkpoint sil

283 The AAA+ ATPase TRIP13 regulates both MAD2 and meiotic HORMADs by

284 re enabled us to evaluate whether Na(+)/K(+)-ATPase uses the same sites to alternatively transport Na

285 Cs) express the proton pumping vacuolar H(+)-ATPase (V-ATPase) and are extensively involved in acid-b

286 Defects of the V-type proton (H(+)) ATPase (V-ATPase) impair acidification and intracellular

287 The vacuolar H(+) ATPase (V-ATPase) is a complex multisubunit machine that

288 storation is activation of the vacuolar H(+)-ATPase (V-ATPase), a proton pump that acidifies lysosome

289 ZnT2 directly interacted with vacuolar H(+)-ATPase (V-ATPase), and ZnT2 deletion impaired vesicle bi

290 associated with a multi-subunit vacuolar H+-ATPase (V-ATPase).

291 n Schizosaccharomyces pombe, deletion of the ATPase vps4 leads to severe defects in nuclear morpholog

292 ects of inhibiting the ESCRT-associated AAA+ ATPase VPS4 on EV release from cultured cells using two

293 disassembly of ESCRT-III polymers by the AAA ATPase Vps4.

294 ctin concentration required for half-maximal ATPase was reduced dramatically (30-fold).

295 highly conserved, alkaline-regulated, sodium ATPase was tolerant of genetic or chemical perturbations

296 s to prevent unintended reassembly of holo V-ATPase when activity is not needed.

297 nding requires the beta2-subunit of the Na/K-ATPase, whereas the alpha-subunit is exchangeable.

298 e formation of a heterohexameric ring of AAA-ATPases, which is guided by at least four RP assembly ch

299 is a copper-transporting P1B-type ATPase (Cu-ATPase) with an essential role in human physiology.

300 nnels, NO and PG synthesis, and Na(+) /K(+) -ATPase would not alter the ability of ATP to blunt alpha