ライフサイエンスコーパス: CypA

1 CypA (Cyclophilin A) is a peptidyl-prolyl isomerase prev

2 CypA antagonists, such as cyclosporines, are potent inhi

3 CypA binds to HCV's nonstructural protein (NS)5A to prom

4 CypA can either promote or inhibit viral infection, depe

5 CypA inhibitors prevented replication of residual HCV in

6 CypA interacts with its substrate via conformational sel

7 CypA modulates HIV-1 virion core detection by this class

8 CypA was previously reported to be required for the bioc

9 cting HIV-1 at an early post-entry step by a CypA-dependent mechanism.

10 yclophilin A (CypA) chimera resulting from a CypA retrotransposition between exons 7 and 8 of the TRI

11 However, a CypA-independent HCV variant had reduced replication in

12 nemestrina and M. fascicularis identifies a CypA retrotransposition in the 3' untranslated region of

13 ng interaction between MDM2 and p53-72R in a CypA-dependent manner.

14 These studies reveal that a CypA-mediated conformational change within the PRLr/Jak2

15 el protein systems, including cyclophilin A (CypA) and the minor allele variant of human alanine:glyo

16 The peptidyl-prolyl isomerase cyclophilin A (CypA) binds a proline-rich loop on the surface of HIV-1

17 The host cell protein cyclophilin A (CypA) binds to CA of human immunodeficiency virus type 1

18 ably, in Owl monkeys (omk), a cyclophilin A (CypA) cDNA has been transposed into the TRIM5 locus, res

19 mediated by TRIMCyp, a TRIM5-cyclophilin A (CypA) chimera resulting from a CypA retrotransposition b

20 The peptidyl-prolyl isomerase cyclophilin A (CypA) embraces an exposed, proline-rich loop on HIV-1 ca

21 ve site of the dynamic enzyme cyclophilin A (CypA) has been previously linked to its catalytic functi

22 ex in which HCV NS5A and host cyclophilin A (CypA) have been shown to be present together with the vi

23 he prolyl cis-trans isomerase cyclophilin A (CypA) in its substrate-free state and during catalysis w

24 f the CA-binding host protein cyclophilin A (CypA) inhibited HIV-1 uncoating and reduced the stimulat

25 The host cell factor cyclophilin A (CypA) interacts directly with the HIV-1 capsid and regul

26 d in cell lines indicate that cyclophilin A (CypA) is a component of HIV type 1 (HIV-1) virions, and

27 Cyclophilin A (CypA) is a member of a family of cellular proteins that

28 Cyclophilin A (CypA) is an intracellular protein that is proinflammator

29 Gag protein interaction with cyclophilin A (CypA) is critical for viral fitness.

30 Cyclophilin A (CypA) is required for viral replication, and CypA inhibi

31 n mediated by owl monkey TRIM-cyclophilin A (CypA) or human TRIM5alpha.

32 Recent studies showed that cyclophilin A (CypA) promotes NF-kappaB/p65 nuclear translocation, resu

33 Host factor protein Cyclophilin A (CypA) regulates HIV-1 viral infectivity through direct i

34 yl prolyl cis/trans isomerase cyclophilin A (CypA) serves as a cellular receptor for the important im

35 Herein, we identify a novel Cyclophilin A (CypA) small molecule inhibitor (HL001) that induces non-

36 otif-containing 5 (TRIM5) and cyclophilin A (CypA) that potently blocks HIV-1 infection.

37 The binding of cyclophilin A (CypA) to the human immunodeficiency virus type 1 (HIV-1)

38 ding of the host cell protein cyclophilin A (CypA) to the viral capsid protein (CA).

39 We found that cyclophilin A (CypA) was excluded from wild-type SIV particles but was

40 Cyclophilin A (CypA) was recently reported to be overexpressed in non-s

41 eractions with both CPSF6 and cyclophilin A (CypA) were essential for the unique dose-response curve.

42 Also, virion incorporation of cyclophilin A (CypA), a cellular peptidyl-prolyl isomerase that binds s

43 The host protein cyclophilin A (CypA), a cis-trans prolyl isomerase, in some way seems t

44 Cyclophilin A (CypA), a cytoplasmic, human immunodeficiency virus type

45 tin, ribonuclease A (RNaseA), cyclophilin A (CypA), and bovine carbonic anhydrase II (BCAII).

46 tin, ribonuclease A (RNaseA), cyclophilin A (CypA), and bovine carbonic anhydrase II (BCAII).

47 20-kDa protein, identified as cyclophilin A (CypA), and CypA was present on the surface of Hc yeasts.

48 al inhibition or silencing of cyclophilin A (CypA), as well as CA mutant viruses, we implicated CypA

49 d with host cell factors like cyclophilin A (CypA), can influence the efficiency of reverse transcrip

50 viral lifecycle by utilising cyclophilin A (CypA), cleavage and polyadenylation specificity factor-6

51 essential cellular co-factor cyclophilin A (CypA), HCV RNA replication is markedly diminished, provi

52 ablation and/or inhibition of cyclophilin A (CypA), here we show that expression of APOE4 and lack of

53 cs simulations to study human cyclophilin A (CypA), in order to understand the role of enzyme motions

54 ects of the host cell protein cyclophilin A (CypA), which binds to HIV-1 CA, on HIV-1 infection of no

55 ptidyl-prolyl isomerase (PPI) cyclophilin A (CypA), which is implicated in the regulation of protein

56 9), I(223), and M(228) in the cyclophilin A (CypA)-binding loop in B57(+) individuals with progressiv

57 tor 6 (CPSF6), as well as the cyclophilin A (CypA)-binding loop mutation P90A, all increase sensitivi

58 passes residues implicated in cyclophilin A (CypA)-dependent HCV RNA replication.

59 by targeting a host protein, cyclophilin A (CypA).

60 interaction with target cell cyclophilin A (CypA).

61 ion with the cellular protein cyclophilin A (CypA).

62 fficient for CD147 binding to cyclophilin A (CypA).

63 1 (HIV-1) CA binding protein cyclophilin A (CypA).

64 to the HIV-1 binding protein Cyclophilin A (CypA).

65 es host cell factors, such as cyclophilin A (CypA).

66 ype controls through secreted cyclophilin A (CypA).

67 Cyclophilin A (CypA, encoded by Ppia) is highly expressed in vascular s

68 or residues 66 and 143 in the cyclophilin A [CypA] domain) confer restriction specificity.

69 CsA abolished CypA-Vpr binding but had no effect on induction of G2 ar

70 In addition, CypA and its enzyme family have been found to play criti

71 he known binding interaction between CsA and CypA was detected using both the MALDI- and LC-MS-based

72 ein, identified as cyclophilin A (CypA), and CypA was present on the surface of Hc yeasts.

73 ample containing NS5B(Delta21), NS5A-D2, and CypA specifically inhibits the interaction between CypA

74 We show that both NS5B(Delta21) and CypA share a common binding site on NS5A that contains r

75 ch concluded that beta-hairpin formation and CypA-binding are energetically independent events.

76 A comparative analysis of Fv1Cyp and CypA binding to a preformed HIV-1 CA lattice reveals how

77 molecular interplay between NS5B, NS5A, and CypA, three essentials proteins for HCV replication.

78 bunit 6 (CPSF6) and cyclophilins (Nup358 and CypA), respectively, cannot replicate in primary human m

79 bound to the viral replication proteins, and CypA and Roc1 also bound to the viral RNA.

80 CypA) is required for viral replication, and CypA inhibitors are in development.

81 The interaction between Vpr and CypA is intriguing, and further studies should examine i

82 pecifically inhibits the interaction between CypA and NS5A-D2 without altering the one between NS5A-D

83 ermolecular hydrophobic interactions between CypA and the substrate, an intricate enzyme-substrate in

84 id substitutions can release HIV-1 from both CypA dependence in human cells and TRIM-Cyp restriction

85 Simultaneous knock-down of both CypA and TRIM5 caused minimal additional increase in tit

86 s of active site residues of substrate-bound CypA is inherent in the substrate-free enzyme.

87 This activity required capsid binding by CypA and correlated with CypA linkage to the TRIM5a caps

88 HIV-1 CA is similarly greeted by CypA soon after entry into rhesus macaque or African gre

89 for TNPO3 in HIV-1 infection is modulated by CypA-CA interactions.

90 human TRIM5alpha orthologue is precluded by CypA.

91 dependent of the well-characterized HIV-1 CA-CypA interaction.

92 striction activity, particularly when the CA-CypA interaction is disrupted.

93 vity was not altered by disruption of the CA-CypA interaction or by elimination of CypA protein.

94 wer drug concentrations upon blocking the CA-CypA interaction suggests a protective role for CypA aga

95 depending on the capsid and the target cell, CypA-CA binding either stabilized or destabilized the ca

96 urring HIV-1 variant exists that circumvents CypA dependence in human cells.

97 Collectively, CypA dually exerts pro-osteogenic and anti-osteoclastic

98 g ability of a retrotransposed CyclophilinA (CypA), resulting in novel antiviral specificity against

99 mains 2 and 3 of NS5A (NS5A-D2 and NS5A-D3), CypA, and NS5B(Delta21).

100 ROS-dependent CypA secretion by ECs is an important signaling mechanis

101 olates from the Main group naturally develop CypA-independent strategies to replicate in human cells.

102 In Jurkat T lymphocytes, disrupting CypA-CA interaction either by cyclosporine (Cs) treatmen

103 a cyclosporine A (CsA) analog that disrupts CypA-capsid interaction.

104 The structure exhibits a distinct CypA-binding pattern in which CypA selectively bridges t

105 tidyl-prolyl isomerase A (PPIA) that encodes CypA on HCV infection and replication of human hepatocyt

106 The re-expression of an exogenous CypA escape protein, which contains escape mutations at

107 As expected, CypA depletion had no additional effect on the behavior

108 VSMC-derived intracellular and extracellular CypA are required for ROS generation and matrix metallop

109 tion of the second CA Cys (C218A) allows for CypA-induced conformational changes but alters the kinet

110 ne motif in the helix 4-5 loop important for CypA binding; instead, the helix 4-5 loop in these SIVs

111 ng capsid substitutions obviate the need for CypA.

112 Antagonism of the extracellular receptor for CypA (CD147) also reduced acetaminophen-induced liver in

113 A interaction suggests a protective role for CypA against high concentrations of PF74.

114 ata define a previously undescribed role for CypA in AAA formation and suggest CypA as a new target f

115 To address this issue, we sought viruses for CypA independence using Debio-025, a cyclosporine A (CsA

116 le in HIV-1 CA assemblies in the escape from CypA dependence, by magic-angle spinning (MAS) NMR and m

117 a determining factor in HIV-1's escape from CypA dependence.

118 However, F/TE from CypA-silenced yeasts still inhibited binding of wild-typ

119 d the dynamics profiles of the A92E and G94D CypA escape mutants closely resemble that of wild-type C

120 R spectra of wild-type and the A92E and G94D CypA escape mutants, we demonstrate that assembled CA is

121 Silencing of Hc CypA by RNA interference reduced yeast binding to DC by

122 His-CypA was first captured on a Ni2+-nitrilotriacetic acid

123 inant human hexahistidine cyclophilin A (His-CypA) is described.

124 te constants for the interaction between His-CypA and CsA.

125 rved due to dissociation of weakly bound His-CypA from the Ni2+-NTA moiety was eliminated, resulting

126 CsA (K(dCsA)) binding to the immobilized His-CypA was 23+/-6 nM, with on and off rates of 0.53+/-0.1

127 ctroscopy between HCV NS5B(Delta21) and host CypA.

128 ) has been known for nearly two decades, how CypA interacts with the viral capsid and modulates HIV-1

129 These results provide new insights into how CypA stabilizes the HIV-1 capsid and is recruited to fac

130 orescence polarization-based assay for human CypA that can be adapted to high-throughput screening fo

131 bitor modeled after AoT5Cyp, by fusing human CypA to human TRIM5 (hT5Cyp).

132 el vif-sensitive antiviral activity of human CypA that may limit zoonotic transmission of SIV and the

133 eled cyclosporin A analog and purified human CypA to quantitatively measure the binding capacity of u

134 as well as CA mutant viruses, we implicated CypA in the SUN2-imposed block to HIV infection.

135 of the SP1 tail, the functionally important CypA loop, and the loop preceding helix 8 are modulated

136 show that many alternative conformations in CypA are populated only at 240 K and above, yet others r

137 Vpr expression in CypA-/- cells leads to induction of G2 arrest in a manne

138 ed by these substitutions was far greater in CypA-rich MT-2 and H9 cells than in Jurkat cells and per

139 pecific PCR revealed DNA hypermethylation in CypA-KD P19 cells, as the normally unmethylated paternal

140 x9 and Runx2 were all significantly lower in CypA knockdown chondrogenic cells than in wild-type cell

141 ne methylation leads to silencing of Peg3 in CypA-KD P19 cells.

142 ication flow through the distinct regions in CypA and, therefore, as targets for future mutational st

143 anner that is indistinguishable from that in CypA+ cells.

144 es than in other cell types, we investigated CypA and CsA activities in HIV-1-infected primary human

145 ion of phenotype in cyclophilin A knockdown (CypA-KD) P19 cells, we observed a silent paternally expr

146 Our data demonstrated that mice lacking CypA (Ppia(-/-)) were resistant to acetaminophen toxicit

147 e a TRIMCyp chimera containing a full-length CypA.

148 ar cells (PBM), both of which contained less CypA.

149 Thus, among multiple potential ligands, CypA is the primary mediator of immunosuppression by cyc

150 motif, rendering HIV-1 replicative in a low CypA environment.

151 e (WT) ability is bimodal (both high and low CypA content limits HIV-1 replication), that the conform

152 is required during uncoating for maintaining CypA-CA interaction, which promotes optimal stability of

153 Newborn CypA-deficient pups double stained with alcian blue and

154 icted phenotype also restored the ability of CypA-restricted HIV-1 mutants to infect growth-arrested

155 s observed between the levels or activity of CypA and the extent of PRL-induced signaling and gene ex

156 r the isomerase or the chaperone activity of CypA to replicate in hepatocytes and that CypA is the pr

157 r the hydrophobic pocket binding activity of CypA.

158 ransformed cells and show that the amount of CypA incorporated into virions is variable and that CsA

159 zed construct of CA, we show that binding of CypA induces a large-scale conformational change in CA t

160 In contrast, reduction of the binding of CypA to HIV-1 capsids in Jurkat T lymphocytes resulted i

161 Reducing the binding of CypA to the A92E mutant capsid, either by Cs treatment o

162 es as a ligand for DC VLA-5, that binding of CypA to VLA-5 is at a site different from FN, and that t

163 rCypA did not further inhibit the binding of CypA-silenced yeasts to DC.

164 nally important alternative conformations of CypA, confirming earlier synchrotron-based results.

165 e evidence for the important contribution of CypA as a pertinent component acting through NF-kappaB-S

166 ission of SIV and the first demonstration of CypA encapsidation into a virus other than human immunod

167 , and F/TE from wild-type yeasts depleted of CypA also inhibited yeast binding to DC.

168 Cores isolated from WT virus depleted of CypA had an unstable-core phenotype, confirming a role o

169 or by RNA interference-mediated depletion of CypA expression in target cells.

170 Conversely, the stimulatory effect of CypA on HIV-1 infectivity was completely independent of

171 he present data suggested that the effect of CypA on HIV-1 replicative (WT) ability is bimodal (both

172 Importantly, the inhibitory effect of CypA was restricted to virus-producing cells and was TRI

173 Here the effects of CypA and TRIM5alpha on HIV-1 restriction were examined d

174 HC) analyses further verified the effects of CypA deficiency on chondrogenic differentiation.

175 However, the effects of CypA on osteoclast activity and bone maintenance are ent

176 the CA-CypA interaction or by elimination of CypA protein.

177 es of SIVagm Vif to inhibit encapsidation of CypA and to increase viral infectivity were shared by rh

178 e we compare the conformational ensembles of CypA by multitemperature synchrotron crystallography and

179 Exclusion of CypA from SIVagm particles was not associated with intra

180 e of motions with the use of mutant forms of CypA.

181 demonstration of the epigenetic function of CypA in protecting the paternal allele of Peg3 from DNA

182 for viral fitness, and that the function of CypA is to maintain the conformation.

183 1 transduction of these cells independent of CypA.

184 Infection of CypA knockout Jurkat cells or treatment of Jurkat cells

185 tion network, connectivity, and influence of CypA residues upon substrate binding, mutation, and duri

186 emonstrates that pharmacologic inhibition of CypA offers a potential therapeutic strategy via specifi

187 Knockdown of CypA correlated in vivo with slower growth, less fluorod

188 Knockdown of CypA in ECs abolished the increase in vascular smooth mu

189 NA interference (RNAi)-mediated knockdown of CypA was established in two non-small-cell lung cancer c

190 We reduced levels of CypA in these cells using small hairpin RNAs (shRNAs).

191 In osteoclasts, loss of CypA activates BtK (Bruton's tyrosine kinase) and subseq

192 Thus, modulation of CypA may be useful in future efforts targeting osteoporo

193 A catalytically inactive mutant of CypA was also able to inhibit TBSV replication in vitro

194 Overexpression of CypA and its mutant in yeast or plant leaves led to inhi

195 ues that reside in the hydrophobic pocket of CypA where proline-containing peptide substrates and cyc

196 The presence of CypA in vif-defective SIVagm was correlated with reduced

197 Surprisingly, the presence of CypA or its binding to Vpr is dispensable for the abilit

198 n of the speedup in rates in the presence of CypA, which is in notable agreement with experimental es

199 RNA interference-mediated reduction of CypA expression enhanced the permissiveness of HeLa cell

200 These results establish the relevance of CypA to tumor growth in vivo, specifically to proliferat

201 yp, which arose from a retrotransposition of CypA into the TRIM5 alpha gene.

202 To determine the role of CypA in oncogenesis, stable RNA interference (RNAi)-medi

203 nstable-core phenotype, confirming a role of CypA in promoting optimal core stability.

204 In this report, we unveil the role of CypA in signal-induced chondrogenic differentiation and

205 Elucidation of the precise role of CypA in these pathways may lead to new targeted therapie

206 e cells) and aortas had greater secretion of CypA both at baseline and in response to Ang II stimulat

207 Overexpression and gene silencing of CypA verified osteogenic and anti-osteoclastic effects.

208 the retroviral capsid-binding specificity of CypA.

209 We determined the cryoEM structure of CypA in complex with the assembled HIV-1 capsid at 8-A r

210 Although the crystal structure of CypA in complex with the N-terminal domain of the HIV-1

211 Treatment of CypA-KD P19 cells with the DNA demethylating agent 5-aza

212 ication, these mutants no longer depended on CypA, suggesting that naturally occurring capsid substit

213 ts in nondividing cells that is dependent on CypA-CA interactions.

214 odulate the dependence of HIV-1 infection on CypA.

215 titutions into viruses that normally rely on CypA for replication, these mutants no longer depended o

216 duced dependence of the compensated virus on CypA that is normally essential for optimal infectivity.

217 Thus, EBOV does not depend on (CypA) for replication, in contrast to many other viruses

218 In osteoblasts, CypA is necessary for BMP-2 (Bone Morphogenetic Protein-

219 Loss of PRLr-CypA binding, following treatment with the PPI inhibitor

220 riants in PPIA that destabilize its product, CypA, and prevent HCV infection and replication.

221 BB breakdown by activating a proinflammatory CypA-nuclear factor-kappaB-matrix-metalloproteinase-9 pa

222 pistatic to both TRIM5alpha and the putative CypA-regulated restriction factor.

223 We found that recombinant CypA, Roc1, and Roc2 strongly inhibited TBSV replication

224 Cys-198 of CA since mutation to Ala renders CypA unable to induce this change and alters the kinetic

225 Here, we simulate CypA using multiple-microsecond-long atomistic molecular

226 e CypA-binding pattern is achieved by single-CypA molecules simultaneously interacting with two CA su

227 d role for CypA in AAA formation and suggest CypA as a new target for treating cardiovascular disease

228 In summary, CypA is a DAMP that mediates acetaminophen poisoning.

229 some SIV lineages to evolve means other than CypA binding to stabilize the capsid.

230 -sensitive host cell cyclophilins other than CypA contribute to the activity of IFN-alpha-induced blo

231 might be resistant to HCV infection and that CypA is a good therapeutic target.

232 of CypA to replicate in hepatocytes and that CypA is the principal mediator of the Cyp inhibitor anti

233 cells further supported the conclusion that CypA is needed for chondrogenic differentiation.

234 of tombusvirus replication, confirming that CypA is a restriction factor for TBSV.

235 These data demonstrate that CypA serves as a ligand for DC VLA-5, that binding of Cy

236 We hypothesized that CypA is released from necrotic liver cells and acts as a

237 These results indicate that CypA-restricted mutants are specifically impaired at a s

238 or destabilized the capsid, indicating that CypA modulates HIV-1 capsid disassembly.

239 lls than in wild-type cells, indicating that CypA plays a functional role in chondrogenic differentia

240 observations argue against the proposal that CypA binding is coupled with beta-hairpin formation and

241 Additional in vitro studies revealed that CypA, Roc1, and Roc2 cyclophilins bound to the viral rep

242 Using shRNAs, we showed that CypA was required for replication of HCV in Huh-7.5 cell

243 Our data suggest that CypA is a key target for treating APOE4-mediated neurova

244 These results suggest that CypA loop dynamics is a determining factor in HIV-1's es

245 th previous reports, these data suggest that CypA protects HIV-1 from an unknown antiviral activity i

246 dditional increase in titer, suggesting that CypA inhibits HIV-1 replication in these cells because i

247 The CypA loop in assembled wild-type CA from two strains exh

248 ication of HIV-1(P222A) in PBM, although the CypA content in HIV-1(H219Q/P222A) was comparable with t

249 is located between the beta-hairpin and the CypA-binding loop.

250 The variants appeared to destabilize the CypA protein; the single amino acid changes led to rapid

251 ation, demonstrating the specificity for the CypA requirement.

252 that is partially overcome by changes in the CypA-binding loop and identify a mechanism for an HIV-1

253 ntified two mutations, A92E and G94D, in the CypA-binding loop of CA that confer the ability of HIV-1

254 The complexes included the CypA-cyclosporin A complex and the BCAII-4-carboxybenzen

255 stitutions, no significant distortion of the CypA binding loop of Gag occurred.

256 1 replication), that the conformation of the CypA binding region of Gag is important for viral fitnes

257 that H219Q affected the conformation of the CypA-binding motif, rendering HIV-1 replicative in a low

258 pharmacological or genetic disruption of the CypA-CA interaction or by RNA interference-mediated depl

259 Disruption of the CypA-CA interaction, either by mutation of the CA residu

260 A second-site suppressor of the CypA-restricted phenotype also restored the ability of C

261 Only the CypA knockdown drastically decreased HCV replication.

262 ts indicate that CA determinants outside the CypA-binding loop can modulate the dependence of HIV-1 i

263 Remarkably, the CypA loop dynamics of wild-type CA HXB2 assembly is sign

264 ecreted APOE3, but not APOE4, suppressed the CypA-nuclear factor-kappaB-matrix-metalloproteinase-9 pa

265 and solid-state NMR further reveal that the CypA-binding pattern is achieved by single-CypA molecule

266 ine-35 of Vpr as well as incubation with the CypA inhibitor cyclosporine A (CsA).

267 ruses encode capsid substitutions within the CypA-binding site (V86P/H87Q/I91V/M96I).

268 nstructs, we illustrate the ability of these CypA loop changes to partially restore replication of th

269 Remarkably, these CypA mutants fail to restore HCV replication, suggesting

270 Thus, CypA is required for HIV-1 restriction by Old World monk

271 ppressive analogs bind with high affinity to CypA and inhibit HIV-1 replication.

272 reduced binding of CD147-derived peptides to CypA and also diminished transport of CD147 to the plasm

273 HIV-1 infectivity increased in response to CypA knock-down to the same extent that it increased in

274 isolates and determines their sensitivity to CypA inhibitors.

275 ive at inhibiting leukocyte migration toward CypA in vitro as well as in the recruitment of leukocyte

276 TRIM-CypA is an owl monkey-specific variant of the retrovirus

277 teasome inhibition prevented owl monkey TRIM-CypA restriction of HIV-1 reverse transcription, even th

278 Moreover, tagged TRIM-CypA proteins can be fully active as restriction factors

279 (OMK) cell assay that is based on timed TRIM-CypA-mediated restriction of HIV-1 replication.

280 losporine (CsA) washout assay, in which TRIM-CypA-mediated restriction of viral replication is used t

281 However, while TRIM-CypA restriction is partly dependent on a RING domain, r

282 tivation and HIV-1 restriction by the Trim12-CypA fusions were inhibited by disruption of TAK1.

283 The three Trim12-CypA fusions all activated AP-1 and restricted HIV-1 tra

284 icted HIV-1 transduction, whereas the Trim30-CypA fusions did neither.

285 nimals coexpressing the TRIM5(TFP) and TRIM5(CypA) alleles took significantly longer to become infect

286 ocus, resulting in the expression of a TRIM5-CypA fusion protein (TRIMCyp) that restricts retroviral

287 In Fv1Cyp, two CypA moieties are located at opposing ends, creating a m

288 B2 assembly is significantly attenuated upon CypA binding, and the dynamics profiles of the A92E and

289 In humans, urinary CypA concentration was significantly increased in patien

290 , H219Q and H219P substitutions in the viral CypA binding loop confer the greatest replication advant

291 resent study, we examine the role of the Vpr-CypA interaction on Vpr-induced G2 arrest.

292 ost inflammatory response was increased when CypA was injected with necrotic liver.

293 of HIV type 1 (HIV-1) virions, and that when CypA incorporation into virions is inhibited by treatmen

294 its a distinct CypA-binding pattern in which CypA selectively bridges the two CA hexamers along the d

295 that the HCV NS5B polymerase associates with CypA via its enzymatic pocket.

296 We find that Vpr coimmunoprecipitates with CypA and that this interaction is disrupted by substitut

297 luorescence polarization in combination with CypA is highly advantageous for the accurate assessment

298 hat of wild-type CA assembly in complex with CypA.

299 d capsid binding by CypA and correlated with CypA linkage to the TRIM5a capsid-specificity determinan

300 esults, we propose that the interaction with CypA is independent of the ability of Vpr to induce cell

301 EC conditioned media, and preincubation with CypA augmented Ang II-induced vascular smooth muscle cel