ライフサイエンスコーパス: ATPase

1 ATPase activity, rather than being regulated, instead gr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

33 mechanism is likely conserved for other AAA+ ATPases.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 ith ABCG2 was investigated by a colorimetric ATPase assay.

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

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

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

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

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

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

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

81 Cu-ATPases are membrane copper transporters present in all

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

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

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

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

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

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

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

89 f counterclockwise rotation driven by the F1-ATPase.

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

91 and ssNucs are effective at activating Fun30 ATPase activity.

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

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

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

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

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

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

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

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

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

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

102 1970s, auxin activates plasma membrane H(+)-ATPases (PM H(+)-ATPases) to facilitate cell expansion b

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 concentration by disrupting the actin-myosin ATPase pathway.

163 ilament OFF state and inhibiting acto-myosin ATPase.

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

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

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

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

168 regulation of topo II through modulation of ATPase status.

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

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

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

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

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

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

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

176 2 is presumed to function as a DNA packaging ATPase.

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

178 t unanticipated functions of the peroxisomal ATPase complex.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

196 4, Nas6, Hsm3, and Nas2 each bind a specific ATPase subunit of the base and antagonize base-CP intera

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

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

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

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

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

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

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

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

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

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

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

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

209 The ATPase activity controls dissociation of an MVH complex

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

211 The ATPase cycle of the Hsp90 molecular chaperone is essenti

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

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

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

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

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

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

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

219 BAZ1B might contact chromatin to direct the ATPase SMARCA5.

220 onstrained region of SMCHD1 encompassing the ATPase domain.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

280 he physiological and pathological roles of V-ATPase.

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

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

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

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

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

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

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

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

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

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

291 efficient localization of Stv1-containing V-ATPases.

292 fic targeting or regulation information to V-ATPases.

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

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

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

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

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

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

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

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