ライフサイエンスコーパス: AAA

1 AAA domain containing 3A (ATAD3A) is an integral mitocho

2 AAA incidences doubled and aneurysms ruptured in XY fema

3 AAA mortality is higher among COPD patients compared wit

4 AAA prevalence and incidence of ruptures have been repor

5 AAA+ disaggregases solubilize aggregated proteins and co

6 AAA+ proteases and remodeling machines couple hydrolysis

7 AAA+ unfoldases are thought to unfold substrate through

8 AAA-specific mortality data were retrieved from the Swed

9 AAAs from XY females exhibited inflammation, and plasma

10 A AAA+ ATPase in the clamp loader clade, RarA protein is p

11 rameshifting signals: a slippery sequence (A AAA AAG), a Shine-Dalgarno (SD) sequence and a downstrea

12 n (DeltaE) at position 302/303 of TorsinA, a AAA+ ATPase that resides in the endoplasmic reticulum.

13 d and examined men, screening-detected AAAs, AAAs operated on, and surgical outcome were retrieved fr

14 p97/VCP is an essential, abundant AAA+ ATPase that is conserved throughout eukaryotes, wit

15 mino acids (BCAAs) and aromatic amino acids (AAAs) have been shown to be associated with insulin resi

16 s, fluorophores-mainly aromatic amino acids (AAAs) in proteins-might be responsible for tooth color.

17 mino acids (BCAAs) and aromatic amino acids (AAAs), have been associated with diabetes risk; however,

18 associated with diverse cellular activities (AAA(+)) ATPase Cdc48.

19 associated with various cellular activities (AAA(+)) that functions as a segregase in diverse cellula

20 associated with diverse cellular activities (AAA+) that act as substrate unfoldases.

21 To identify additional AAA risk loci using data from all available genome-wide

22 AngII infusion for 8 weeks induced advanced AAA development in AdGFP mice.

23 ic benefit to prevent AngII-induced advanced AAA in a well-established preclinical model.

24 APN levels as a strategy to prevent advanced AAA.

25 A new series of alkenyl amino alcohol (AAA) ionizable lipid nanoparticles (LNPs) capable of del

26 As an AAA-ATPase, Vps4 is important for function of multivesic

27 r (FisR) with three domains: an R domain, an AAA+ domain and a DNA-binding domain.

28 t GENERAL CONTROL NONREPRESSIBLE4 (GCN4), an AAA(+)-ATPase family protein, as one of the key proteins

29 ent ubiquitylation also involves VCP/p97, an AAA ATPase regulating the folding of various cellular su

30 Structurally, the Rep proteins share an AAA(+) domain characteristic of superfamily 3 helicases,

31 human YME1L protease is a membrane-anchored AAA+ enzyme that controls proteostasis at the inner memb

32 layered shallow corkscrew, with the AAA+ and AAA+-like domains forming one layer, and the winged-heli

33 However, the association between COPD and AAA remains inconclusive.

34 ved and essential residue in many GTPase and AAA+ ATPase enzymes that completes the active site from

35 winding mechanism whereby the N-terminal and AAA+ tiers of the MCM work in concert to translocate on

36 Main Outcomes and Measures: Mean total and AAA-related health care cost per life-year and per quali

37 Objective: To compare total and AAA-related use of health care services, costs, and cost

38 verified the close correlation of BCAAs and AAAs with insulin resistance and future development of d

39 ed-chain and aromatic amino acids (BCAAs and AAAs) are closely associated with the risk of developing

40 ino acid concentrations, including BCAAs and AAAs, in both trials.

41 lay a key role in abdominal aortic aneurysm (AAA) development.

42 e of resolvins in abdominal aortic aneurysm (AAA) has not been established.

43 Abdominal aortic aneurysm (AAA) is a common aortic disease with a progressive natur

44 RATIONALE: Abdominal aortic aneurysm (AAA) is a complex disease with both genetic and environm

45 Abdominal aortic aneurysm (AAA) is a degenerative disease characterized by aortic d

46 Abdominal aortic aneurysm (AAA) is a major cause of morbidity and mortality; howeve

47 An abdominal aortic aneurysm (AAA) is a permanent and irreversible dilation of the low

48 an metabolism and abdominal aortic aneurysm (AAA) is unknown.

49 atments to reduce abdominal aortic aneurysm (AAA) progression.

50 ail patients with abdominal aortic aneurysm (AAA) randomized to either early endovascular aneurysm re

51 ars who underwent abdominal aortic aneurysm (AAA) repair (n = 71,422), pulmonary resection (n = 93,05

52 ars who underwent abdominal aortic aneurysm (AAA) repair (n = 71,422), pulmonary resection (n = 93,05

53 and endovascular abdominal aortic aneurysm (AAA) repair are each well described separately, but not

54 s mortality after abdominal aortic aneurysm (AAA) repair.

55 DCN is reduced in abdominal aortic aneurysm (AAA) resulting in vessel wall instability thereby predis

56 rature are due to abdominal aortic aneurysm (AAA) rupture into the left renal vein.

57 l during elective abdominal aortic aneurysm (AAA) surgery.

58 ary management of abdominal aortic aneurysm (AAA) with relation to recommended treatment guidelines f

59 ascular repair of abdominal aortic aneurysm (AAA), cost may be an important factor in choosing a proc

60 of rupture of an abdominal aortic aneurysm (AAA), mortality is very high.

61 (Ang) II-induced abdominal aortic aneurysm (AAA).

62 Abdominal aortic aneurysms (AAAs) are a deadly pathology with strong sexual dimorphi

63 Abdominal aortic aneurysms (AAAs) represent a potentially life-threatening condition

64 ent mice is intrinsic to the vasculature, as AAA was not exacerbated in WT animals that received CCN3

65 e effects of inhibiting the ESCRT-associated AAA+ ATPase VPS4 on EV release from cultured cells using

66 ons explain the observed ribosome pausing at AAA codons during translation and demonstrate how the s(

67 Mechanisms for augmented AAA severity in XY females include increased inflammatio

68 DnaA is the widely conserved bacterial AAA+ ATPase that functions as both the replication initi

69 ry AAA+, no correlation was observed between AAA titers and adalimumab trough levels (P = 0.2).Concom

70 Remarkably, the p28-bound AAA ring does not form a channel in the free RP and spon

71 uring degradation of multidomain proteins by AAA proteases may constitute a novel mechanism to produc

72 Meiotic clade AAA ATPases (ATPases associated with diverse cellular ac

73 Meiotic clade AAA ATPases function as hexamers that can cycle between

74 striking, unifying feature of meiotic clade AAA ATPases may be their MIT domain, which is a module t

75 that human CDS are devoid of >4 consecutive AAA codons, sensing of prematurely placed polyA tails by

76 Msp1 is a conserved AAA ATPase in budding yeast localized to mitochondria wh

77 ecuted by coiled-coil MDs to tightly control AAA+ chaperone activity.

78 s are recognized and unfolded by a dedicated AAA+ ATPase (Mycobacterium proteasomal AAA+ ATPase; ATPa

79 ay as a critical regulator of CCN3-dependent AAA development.

80 The prevalence of screening-detected AAA was 1.5%.

81 invited and examined men, screening-detected AAAs, AAAs operated on, and surgical outcome were retrie

82 genes, may contribute to sexually dimorphic AAA pathology.

83 an essential role for the ubiquitin-directed AAA-ATPase, p97, in the clearance of damaged lysosomes b

84 e most stable sequence-complementary duplex, AAA.DDD, so in mixtures that contain all eight sequences

85 Mortality after elective AAA repair was primarily attributable to cardiovascular

86 ed in a decrease of mortality after elective AAA repair, but results of open repair have improved as

87 tor of postoperative outcomes after elective AAA repair.

88 h we can improve outcomes following elective AAA repair, although patient referral to high-volume aor

89 Thirty-day mortality in elective AAA repair dropped significantly from 6.3% in 2000 to 20

90 44% in 3-year survival suggest that elective AAA repair is contraindicated in most severe CKD patient

91 ospital stay in patients undergoing elective AAA repair.

92 nd morbidity in patients undergoing elective AAA repair.

93 A total of 1540 patients underwent elective AAA repair during the study period.

94 Registry data for open and endovascular AAA repair (EVAR) during 2010 to 2013 were collected fro

95 ective open AAA repair (OAR) or endovascular AAA repair (EVAR) and was conducted between December 201

96 Patients scheduled for open or endovascular AAA repair were randomized to either 6 weeks of preopera

97 eparately among those receiving endovascular AAA repair (EVAR) or open AAA repair (OAR).

98 g/remodeling by this conserved and essential AAA+ protein machine and their adaption and possible bio

99 otent protective effect against experimental AAA formation.

100 n-containing proteins, such as ATPase family AAA domain-containing protein 2 (ATAD2), isoform A, have

101 ATPase family AAA-domain containing protein 3A (ATAD3A) is a nuclear-e

102 serve as a target for therapeutic agents for AAA in males.

103 hospitals meeting the Leapfrog criteria for AAA repair (OR, 0.64; 95% CI, 0.38-1.09; P = .09).

104 hing hospitals and nonteaching hospitals for AAA repair ($29,946 vs $27,993; P = 0.18) and pulmonary

105 ore expensive than nonteaching hospitals for AAA repair ($45,570 vs $31,426; P < 0.001), $9,812 more

106 ore expensive than nonteaching hospitals for AAA repair ($45,570 vs $31,426; P < 0.001), $9,812 more

107 The 4 new risk loci for AAA seem to be specific for AAA compared with other card

108 costs and 31.3% and 34.3%, respectively, for AAA-related costs.

109 ew risk loci for AAA seem to be specific for AAA compared with other cardiovascular diseases and rela

110 All patients treated for AAA in Finland, a country with a population of 5.5 milli

111 Ring-forming AAA+ chaperones exert ATP-fueled substrate unfolding by

112 r repair were offset by increased costs from AAA-related secondary procedures and imaging studies.

113 to annually prevent 90 premature deaths from AAA and to gain 577 quality-adjusted life-years.

114 Cross-linked reads originating from AAA-decoding tRNA(Lys)(UUU) were 10-fold enriched over i

115 stimulation-deficient G mutant, V209 VG --> AAA.

116 r to the plasma-derived molecule, rIIa(SLQ-->AAA) with mutations S478A/L480A/Q481A was deficient in c

117 served with an increase in AAA content in HA-AAAs.

118 ly, significantly decreased absorbance of HA-AAAs between 250 and 300 nm in ultraviolet spectra, decl

119 e intensity, and decolored performance of HA-AAAs were observed after bleaching treatment.

120 A and that hydrogen peroxide might whiten HA-AAAs by oxidizing the benzene ring in AAAs.

121 ase of the RP is formed by a heterohexameric AAA(+) ATPase module, which unfolds and translocates sub

122 p97 is a hexameric AAA+ adenosine triphosphatase (ATPase) that is an attrac

123 transcriptional activators forms a hexameric AAA+ ATPase that acts through conformational changes bro

124 is a dynamic ring translocase and hexameric AAA+ protein found in yeast, which couples ATP hydrolysi

125 The hexameric AAA ATPase Vps4 drives membrane fission by remodeling an

126 How AAA+ chaperones conformationally remodel specific target

127 Human AAA(+) protein p97 consists of an N-domain and two tande

128 Finally, human AAA samples had stronger staining with the antibodies ag

129 sis and proliferation were observed in human AAA (HAAA) sections compared to normal aortae (HA).

130 acent nonaneurysmal aortic sections of human AAA samples.

131 t specific degron sequence within a native i-AAA protease substrate.

132 The i-AAA protease is a component of the mitochondrial quality

133 Here, we reconstruct the yeast i-AAA protease, Yme1p, to examine the in vitro degradation

134 role of systemically-administered CAR-DCN in AAA progression and rupture was assessed in a murine mod

135 n Finland, likely because of the decrease in AAA prevalence.

136 eper color were observed with an increase in AAA content in HA-AAAs.

137 ch is a product of tryptophan metabolism, in AAA formation.

138 s associated with a significant reduction in AAA-specific mortality (mean, 4.0% per year of screening

139 emonstrate that CCN3 is a nodal regulator in AAA biology and identify CCN3 as a potential therapeutic

140 usion in apoE(-/-) mice for 4 wk resulted in AAA formation in 36% (4/11) of surviving animals.

141 images showed higher uptake of the tracer in AAA than nondilated aortae.

142 ten HA-AAAs by oxidizing the benzene ring in AAAs.

143 C4-Fc overexpression significantly increased AAA severity.

144 angiotensin II (AngII) for 28 days to induce AAA formation.

145 ed with angiotensin II for 28 days to induce AAAs.

146 multiple mechanisms inhibiting AngII-induced AAA and increasing plasma APN levels as a strategy to pr

147 ributed to the development of Ang II-induced AAA and associated pathogenic events in mice, likely by

148 AAA models, including angiotensin II-induced AAA and elastase perfusion-stimulated AAA.

149 omosome complement on angiotensin II-induced AAA formation and rupture in phenotypically female mice.

150 ed both elastase- and angiotensin II-induced AAA formation in mice.

151 the formation and rupture of Ang II-induced AAA in mice by reinforcing the aortic wall.

152 In murine models of induced AAA, germline deletion of Ccn3 resulted in severe phenot

153 r lower incidences of angiotensin II-induced AAAs than males.

154 pical length and position of this infrarenal AAA model was statistically similar to the length and ta

155 On day 28 of Ang II infusion, AAAs were analyzed by ultrasound and ex vivo by Vernier

156 Intact AAA repairs numbered 4956.

157 51 153 patients, 86% were treated for intact AAA (iAAA) and 14% for ruptured AAA.

158 Intact AAAs were repaired at diameters smaller than recommended

159 loped and are now widely used to investigate AAA pathogenesis.

160 e found that only the modified U1 snRNA (IVS-AAA) that completely matched both the intronic and exoni

161 Midasin, an essential approximately 540-kDa AAA+ (ATPases associated with diverse cellular activitie

162 We also compare NSF with other known AAA+ family members.

163 bserved no new associations between the lead AAA single nucleotide polymorphisms and coronary artery

164 e delivered near the aorta and locally limit AAA expansion.

165 e report that the nuclear envelope-localized AAA+ (ATPase associated with various cellular activities

166 is FtsH1, a homolog of a bacterial membrane AAA+ metalloprotease.

167 substrate-bound inner mitochondrial membrane AAA+ quality control protease in yeast, YME1.

168 previously discovered that the mitochondrial AAA+ unfoldase ClpX promotes heme biosynthesis by activa

169 A commonly used infrarenal mouse AAA model was used to determine the target location of t

170 Regulatory ATPase variant A (RavA) is a MoxR AAA+ protein that functions together with a partner prot

171 olvins (RvD2 or RvD1) would attenuate murine AAA formation through alterations in macrophage polariza

172 ulation of 9.5 million, the Swedish national AAA-screening program was predicted to annually prevent

173 es and 107 766 controls, we identified 4 new AAA risk loci: 1q32.3 (SMYD2), 13q12.11 (LINC00540), 20q

174 es and 107 766 controls, we identified 4 new AAA risk loci: 1q32.3 (SMYD2), 13q12.11 (LINC00540), 20q

175 nic electron microscopy, we analyzed the non-AAA structure of the p28-bound human RP at 4.5 A resolut

176 r among hospitals performing at least 25% of AAA repairs using open techniques (OR, 0.68; 95% CI, 0.5

177 oftware system to facilitate the analysis of AAA using a finite element analysis based approach.

178 Data on all patients who had died of AAA during the same time period were obtained from Stati

179 an efficient tool for accurate estimation of AAA rupture risk is still not available.

180 archers to perform comparative evaluation of AAA using a standardised approach.

181 in a small proportion of the heritability of AAA.

182 ensin II markedly increased the incidence of AAA in Apoe(-/-) mice, but not in Apoe(-/-)/IDO(-/-) mic

183 ficant variation exists in the management of AAA, most notably for iAAA diameter at repair, use of EV

184 the risk of AAA, morbidity and mortality of AAA patients underwent endovascular aortic repair.

185 An association between the presence of AAA+ and a worse uveitis outcome was observed only in pa

186 Although the prevalence of AAA was similar between vehicle and CAR-DCN groups, the

187 ut there was a slightly higher proportion of AAA-related late deaths in patients treated with EVAR.

188 tients undergoing planned elective repair of AAA who were candidates for open and endovascular repair

189 een elective open and endovascular repair of AAA.

190 s the formation of a heterohexameric ring of AAA-ATPases, which is guided by at least four RP assembl

191 In conclusion, COPD may increase the risk of AAA, morbidity and mortality of AAA patients underwent e

192 vehicle and CAR-DCN groups, the severity of AAA in the CAR-DCN group was significantly reduced.

193 n, and because of the conserved structure of AAA+ initiator proteins these findings raise the possibi

194 cted the elective and emergency treatment of AAA and their results in Finland.

195 The treatment of AAA has also undergone a change in recent decades with a

196 ology and contribute to sexual dimorphism of AAAs.

197 r, our study shed light on the importance of AAAs and might provide new ideas for investigations of b

198 that only HA, synthesized in the presence of AAAs, exhibited remarkable fluorescence and color proper

199 We investigated their combined effect on AAA formation.

200 analysis was used to estimate the effect on AAA-specific mortality among all men >/=65 years of age

201 cluded all patients undergoing elective open AAA repair (OAR) or endovascular AAA repair (EVAR) and w

202 ations in patients undergoing elective, open AAA repair.

203 iving endovascular AAA repair (EVAR) or open AAA repair (OAR).

204 tion mechanism is likely conserved for other AAA+ ATPases.

205 stationary phase distinguish ClpG from other AAA+ disaggregases.

206 seven distinct conformations of the Rpn1-p28-AAA subcomplex within the p28-bound RP at subnanometer r

207 show that p37/UBXN2B, a cofactor of the p97 AAA ATPase, regulates spindle orientation in mammalian c

208 AA+ HslU; the ClpP protease with its partner AAA+ ClpX; and Anbu, a recently characterized ancestral

209 In all patients with permanent AAA+, trough adalimumab levels became undetectable (P <

210 was observed only in patients with permanent AAA+, which correlated with undetectable adalimumab trou

211 r abundance, and poly-lysine encoded by poly(AAA) induced RQC in a ZNF598-dependent manner.

212 all organisms, initiator proteins possessing AAA+ (ATPases associated with various cellular activitie

213 th muscle cell (VSMC) apoptosis precipitates AAA formation, whereas VSMC proliferation repairs the ve

214 tical-based therapeutics designed to prevent AAA expansion are currently being evaluated with these a

215 el therapeutic targets are needed to prevent AAA.

216 gradation in vivo, and LonA is the principal AAA+ (ATPases associated with diverse cellular activitie

217 aortic gene expression profiles and promoted AAA severity.

218 cated AAA+ ATPase (Mycobacterium proteasomal AAA+ ATPase; ATPase forming ring-shaped complexes).

219 Care of r-AAA in the US should be centralized to centers equipped

220 Overall, r-AAA mortality at the MC was 20% lower than CH (27% vs 46

221 was to assess the impact of regionalizing r-AAA care to centers equipped for both open surgical repa

222 retrospective review of all patients with r-AAA undergoing open or endovascular repair in a 12-hospi

223 Four hundred fifty-one patients with r-AAA were treated from 2002 to 2015.

224 d CCN3-deficient BM and WT BM did not reduce AAA severity in CCN3-deficient mice.

225 bl1) and Reptin (Ruvbl2) are closely related AAA ATPases.

226 AA, matrix metallopeptidase 2, and resultant AAA formation by angiotensin II infusion.

227 r protein CCN3 is strongly reduced in rodent AAA models, including angiotensin II-induced AAA and ela

228 Ruptured AAA incidence for men >65 years has declined by nearly 3

229 half of the 4949 patients who had a ruptured AAA died outside the hospital.

230 d for intact AAA (iAAA) and 14% for ruptured AAA.

231 The annual incidence of ruptured AAA was 16.4 per 100 000 population over 50 years and de

232 echanistically, this is dependent on SAF-A's AAA(+) ATPase domain, which mediates cycles of protein o

233 Crystal structures of FleQ's AAA+ ATPase domain in its apo-state or bound to ADP or A

234 The viral protein binds to the loader's AAA+ ATPase domain, allowing binding of the host replica

235 to synthesize all possible 3-mer sequences: AAA, AAD, ADA, DAA, ADD, DAD, DDA, and DDD.

236 and trafficking) domain followed by a single AAA ATPase cassette.

237 population-based reimbursement model (small AAA repair, 16%; octogenarians, 18%; P<0.01).

238 the United States), the proportions of small AAA (33%) and octogenarians undergoing iAAA repair (25%)

239 Treatment of existing small AAAs with RvD2 demonstrated a 25% reduction in aneurysm

240 riment, RvD2 was provided to mice with small AAAs 3 d after elastase treatment (n = 8 per group).

241 lexes that require activation by specialized AAA(+) ATPases.

242 may serve as novel targets for sex-specific AAA therapeutics.

243 nduced AAA and elastase perfusion-stimulated AAA.

244 The N-terminal AAA(+) domain of ChlD is essential for complex formation

245 The results showed that AAAs contributed to the fluorescence and color propertie

246 The AAA postoperative morbidity was found to be positively a

247 The AAA+ (ATPases associated with a variety of cellular acti

248 The AAA+ ATPase TRIP13 regulates both MAD2 and meiotic HORMA

249 The AAA+ Cdc48 ATPase (alias p97 or VCP) is a key player in

250 The AAA+ chaperone ClpC with the peptidase ClpP forms a bact

251 The AAA+ Lon protease is conserved from bacteria to humans,

252 The AAA+ motor-driven acceleration of Rpn11 is therefore imp

253 rough the activity of the proteasome and the AAA ATPase p97/VCP in a similar manner to infectious vir

254 we showed that reductions in alanine and the AAA tyrosine were significantly related to improved insu

255 ylation, we demonstrated that Rbd2 binds the AAA-ATPase Cdc48 through a C-terminal SHP box.

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

257 that DNA-locked Ku rings are released by the AAA-ATPase p97.

258 nd a regulatory particle (RP) containing the AAA-ATPase module.

259 t targeted deletion of the gene encoding the AAA+-ATPase Atad3a hyperactivated mitophagy in mouse hem

260 vely removes the hydrophobic domain from the AAA+ domain of TorsinA, which retains catalytic activity

261 mechanical substrate translocation into the AAA+ motor.

262 Except semi-automatic segmentation of the AAA and intraluminal thrombus (ILT) from medical images,

263 for the construction of atomic models of the AAA(+) ATPase module as it progresses through the functi

264 p97/VCP, a member of the AAA+ (ATPases associated with diverse cellular activitie

265 ATPases are the only representatives of the AAA+ ATPase family that reside in the lumen of the endop

266 a bacterial enhancer-binding protein of the AAA+ ATPase superfamily, is inhibited by an unprecedente

267 s involved in nucleotide binding, and of the AAA+ domain of DnaC.

268 de translocases are conserved members of the AAA+ family (adenosine triphosphatases associated with d

269 It is a member of the AAA+ family (ATPases associated with diverse cellular ac

270 Here, we investigated the mechanism of the AAA+ protein Rubisco activase (Rca) in metabolic repair

271 eals previously unidentified features of the AAA-ATPase heterohexamer.

272 the cytosol in a manner that depends on the AAA-ATPase p97/VCP [3].

273 also relieves autoinhibition and primes the AAA ATPase cassettes for substrate binding.

274 Exclusion requires the AAA+-ATPase Pch2 and is directly coupled to synaptonemal

275 o this event, two of the three subunits, the AAA(+) proteins ChlI and ChlD, form a ChlID-MgATP comple

276 depend on partner proteins, which target the AAA+ disaggregases to protein aggregates while concurren

277 ansplantation experiments suggested that the AAA phenotype of CCN3-deficient mice is intrinsic to the

278 Saunders et al. show that the AAA+ ATPase torsinA and its partner LAP1 are required fo

279 ction of initiator proteins belonging to the AAA+ superfamily of ATPases.

280 a double-layered shallow corkscrew, with the AAA+ and AAA+-like domains forming one layer, and the wi

281 leQ, the second messenger interacts with the AAA+ ATPase domain at a site distinct from the ATP bindi

282 olog HslV, which functions together with the AAA+ HslU; the ClpP protease with its partner AAA+ ClpX;

283 asis of phylogenetic classification of their AAA ATPase cassette, include four relatively well charac

284 Mortality due to AAA rupture was significantly reduced in CAR-DCN-treated

285 Costs related to AAA, including the initial repair, constituted nearly 40

286 ver, in patients who demonstrated transitory AAA+, no correlation was observed between AAA titers and

287 ly applicable to other protein-translocating AAA ATPases.

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

289 d from MCC by the joint action of the TRIP13 AAA-ATPase and the Mad2-binding protein p31(comet) Now w

290 A pure triploid (AAA group) of Musa acuminata subgroup Cavendish ( degree

291 ing to determine the mechanochemistry of two AAA+ proteases, Escherichia coli ClpXP and ClpAP, as the

292 -compartmentalized peptidase, and one or two AAA+ HslU ring hexamers that hydrolyze ATP to power the

293 VAT), the archaeal homolog of the ubiquitous AAA+ protein Cdc48/p97, functions in concert with the 20

294 Patients who underwent AAA repair from 2006 to 2007 were retrospectively identi

295 isingly, without the involvement of the Vps4 AAA-ATPase.

296 eters were quantified by ultrasound, whereas AAA diameters were quantified at study end point.

297 protein that we termed VWA interacting with AAA+ ATPase (ViaA) containing a von Willebrand Factor A

298 er a mean of 4.5 years, 29% of patients with AAA had been operated on, with a 30-day mortality rate o

299 in the United Kingdom aged >/=60 years with AAA >5.5 cm in diameter were randomized 1:1 using comput

300 bolus at postnatal day 1, markedly worsened AAA outcomes in XY in comparison with XX adult females.