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1 APDH and LDH) but not others (e.g. Hsp90 and cyclophilin A).
2 te of its primary cyclophilin enzyme ligand, cyclophilin A.
3 tion with the retinoblastoma protein but not cyclophilin A.
4 iciently in the presence of normal levels of cyclophilin A.
5 ncoding the prototypical cyclophilin protein cyclophilin A.
6 ied CD147 as the main signaling receptor for cyclophilin A.
7 l cis-trans isomerization catalyzed by human cyclophilin A.
8 disrupting the association of caveolin-1 and cyclophilin A.
9 sed immunophilin proteins such as FKBP12 and cyclophilin A.
10 ed for interaction with the cellular protein cyclophilin A.
11 s: annexin II, cyclophilin 40, caveolin, and cyclophilin A.
12 59, were considered as candidate targets for cyclophilin A.
13 t not by cyclosporin A, a drug that binds to cyclophilin A.
14 ells, H9 cells express greater quantities of cyclophilin A.
15 und crystal form and as a complex with human cyclophilin A.
16 apsid (residues 1-151) in complex with human cyclophilin A.
17 f high PF74 concentrations was attenuated by cyclophilin A.
18 on other isomerases such as Pin4, FKBP12, or cyclophilin A.
19 merization outpowers the holding activity of cyclophilin A.
22 sets, the top ranked gene was PPIA, encoding cyclophilin A, a druggable target using cyclosporine.
24 inhibition of HIV infection by SUN2 involves cyclophilin A, a protein that binds the HIV capsid and d
27 the finding that Gag mutants with decreased cyclophilin A affinity are dead in Jurkat cells but capa
29 oviruses encoding Gag mutants with decreased cyclophilin A affinity exhibit attenuated infectivity, a
31 EMENT We provide evidence that extracellular cyclophilin A, also known as peptidylprolyl cis-/trans-i
33 ether, these data provide evidence that both cyclophilin A and B interact with CYDV-RPV, and these in
36 interact with the peptidyl-propyl isomerases cyclophilin A and FK506-binding protein (FKBP12), respec
37 neurin inhibitors, such as the cyclosporin A-cyclophilin A and FK506-FKBP12 complexes, regulate this
38 iae, CsA and FK506 bind to the immunophilins cyclophilin A and FKBP12 and the resulting complexes inh
39 yclosporin A and tacrolimus binding proteins cyclophilin A and FKBP12 were also expressed by keratino
40 s of C2-C12 cells express similar amounts of cyclophilin A and FKBP12, immunophilins known to be intr
41 irus type 1 (HIV-1) Gag polyprotein binds to cyclophilin A and incorporates this cellular peptidyl pr
42 equired for proper interaction with the host cyclophilin A and influences its peptidyl-prolyl cis/tra
43 e cis-bound and trans-bound conformations of cyclophilin A and its substrate as the enzymatic reactio
44 ive HIV-1 capsid mutants P90A (defective for cyclophilin A and Nup358 recruitment) and N74D (defectiv
45 domain cyclophilins, including the mammalian cyclophilin A and plant Roc1 and Roc2, which are ortholo
47 cation of this putative factor-binding site, cyclophilin A and the restricting factor(s) cooperated t
49 ntified in this proof of principle work were cyclophilin A and UDP-glucose-4-epimerase, both of which
51 not CrkI, associates with the immunophilins, cyclophilin A, and 12-kDa FK506-binding protein, in rest
53 h caveolin-1, i.e. FK506-binding protein 52, cyclophilin A, and cyclophilin 40, were not necessary fo
54 ve expression of alpha-actin, alpha-tubulin, cyclophilin A, and proliferating cell nuclear antigen (P
58 he viral protein Nef and the cellular factor cyclophilin A are both required for full infectivity of
59 and its interaction with the human chaperone cyclophilin A are both targets for highly potent and pro
60 laboratory has shown that human recombinant cyclophilins A, B, and C have sequence homology with the
62 lt demonstrates that capsid dimerization and cyclophilin A binding are not thermodynamically coupled
65 , including the N-terminal beta-hairpin, the cyclophilin A binding loop, the inter-domain linker, seg
68 but mutants that recapitulate the effect of Cyclophilin A binding on capsid conformation and dynamic
69 lpha-helices 4 and 5 of CA, analogous to the cyclophilin A-binding loop of human immunodeficiency vir
71 tants that were altered near the base of the cyclophilin A-binding loop of the N-terminal capsid doma
72 within a nuclear localization signal in the cyclophilin A-binding loop, is critical for engaging the
73 regions, including the NTD beta-hairpin, the cyclophilin A-binding loop, residues in the hexamer cent
74 -1 replication in transformed cells requires cyclophilin A but is dependent on other interactions in
75 utant) resulted in a channel unresponsive to cyclophilin A but with pore properties similar to the wi
76 , in contrast to HCV, HAV does not depend on cyclophilin A, but rather on adenosine-triphosphate-bind
82 cule-1, macrophage scavenger receptor-1, and cyclophilin A compared with controls 3 days after arteri
83 The crystal structure of human recombinant cyclophilin A complexed with a substrate of succinyl-Ala
87 ed a network of protein vibrations in enzyme cyclophilin A, coupled to its catalytic activity of pept
88 on of a non-G-protein substrate of TTS-ExoS, cyclophilin A (CpA), a peptidyl-prolyl isomerase (PPIase
91 wo immunophilin-immunosuppressant complexes, cyclophilin A-cyclosporin A (CyPA-CsA) and FKBP-FK506.
92 ith the CaN autoinhibitory peptide (CaP) and cyclophilin A/cyclosporin A (CyPA/CsA) using each peptid
95 d in a pi-stacking interaction with Arg55 of cyclophilin A (Cyp A), and the m-Tyr residue was displac
97 or the first time that the chaperone protein cyclophilin A (CyPA) acts as a Ca(2+) modulator in plate
100 eens on two model protein systems, including cyclophilin A (CypA) and the minor allele variant of hum
101 newly synthesized HIV-1 capsid with cellular cyclophilin A (CYPA) and the subsequent activation of th
105 ere, we demonstrate that substitution of the cyclophilin A (CyPA) binding region in the capsid of an
111 rly restriction mediated by TRIMCyp, a TRIM5-cyclophilin A (CypA) chimera resulting from a CypA retro
114 een CsA resistance and reduced dependency on cyclophilin A (CyPA) for replication was identified.
116 ity in the active site of the dynamic enzyme cyclophilin A (CypA) has been previously linked to its c
120 tiprotein complex in which HCV NS5A and host cyclophilin A (CypA) have been shown to be present toget
121 gp120 envelope protein and virion-associated cyclophilin A (CypA) have been shown to directly interac
122 e dynamics of the prolyl cis-trans isomerase cyclophilin A (CypA) in its substrate-free state and dur
123 ssion of small interfering RNA for targeting cyclophilin A (CypA) in p19 cells lose their potential f
126 PO3, addition of the CA-binding host protein cyclophilin A (CypA) inhibited HIV-1 uncoating and reduc
130 lyprotein-mediated incorporation of cellular cyclophilin A (CyPA) into virions is essential for the f
132 tudies conducted in cell lines indicate that cyclophilin A (CypA) is a component of HIV type 1 (HIV-1
139 interaction with the human prolyl isomerase cyclophilin A (CypA) is essential for viral RNA replicat
140 that the prolyl cis-trans isomerase (PPIase) cyclophilin A (CypA) is hijacked by Listeria at membrane
145 residues Val86-Arg97 that contain the human cyclophilin A (CypA) packaging signal have (15)N heteron
148 for the binding of cyclosporin A (CsA) to a cyclophilin A (CypA) sample in which the protein was a c
151 ng tripartite motif-containing 5 (TRIM5) and cyclophilin A (CypA) that potently blocks HIV-1 infectio
153 enhanced by binding of the host cell protein cyclophilin A (CypA) to the viral capsid protein (CA).
160 ivity to restriction factors is modulated by cyclophilin A (CypA), a host cell protein that binds the
161 tion was greatly reduced both by antibody to cyclophilin A (CyPA), a known mediator of inflammation i
164 rised of ubiquitin, ribonuclease A (RNaseA), cyclophilin A (CypA), and bovine carbonic anhydrase II (
165 ncluding ubiquitin, ribonuclease A (RNaseA), cyclophilin A (CypA), and bovine carbonic anhydrase II (
166 5 recognized a 20-kDa protein, identified as cyclophilin A (CypA), and CypA was present on the surfac
167 The cytoplasmic subtype of cyclophilin, cyclophilin A (CyPA), appears to be required for functio
168 e, using chemical inhibition or silencing of cyclophilin A (CypA), as well as CA mutant viruses, we i
169 riments showing that overexpressed wild-type cyclophilin A (CyPA), but not CyPA with a rotamase activ
170 on of the capsid with host cell factors like cyclophilin A (CypA), can influence the efficiency of re
171 rly part of the viral lifecycle by utilising cyclophilin A (CypA), cleavage and polyadenylation speci
172 ice lacking the essential cellular co-factor cyclophilin A (CypA), HCV RNA replication is markedly di
173 ding mice with ablation and/or inhibition of cyclophilin A (CypA), here we show that expression of AP
174 olecular dynamics simulations to study human cyclophilin A (CypA), in order to understand the role of
175 denylation specificity factor 6 (CPSF6), and cyclophilin A (CypA), indicating that the observed loss
177 on with the human peptidyl prolyl isomerase, cyclophilin A (CypA), that results in packaging of CypA
178 cellular peptidyl-prolyl cis-trans isomerase cyclophilin A (CyPA), the cytosolic receptor for the imm
179 y incorporates the peptidyl prolyl isomerase cyclophilin A (CyPA), the cytosolic receptor for the imm
180 tigated the effects of the host cell protein cyclophilin A (CypA), which binds to HIV-1 CA, on HIV-1
181 ort that the peptidyl-prolyl isomerase (PPI) cyclophilin A (CypA), which is implicated in the regulat
182 t residues H(219), I(223), and M(228) in the cyclophilin A (CypA)-binding loop in B57(+) individuals
183 on specific factor 6 (CPSF6), as well as the cyclophilin A (CypA)-binding loop mutation P90A, all inc
184 5A, which encompasses residues implicated in cyclophilin A (CypA)-dependent HCV RNA replication.
204 46 in TRIMCyp (or residues 66 and 143 in the cyclophilin A [CypA] domain) confer restriction specific
206 scattering measurements on a dynamic enzyme, cyclophilin A, demonstrating that these experiments are
210 ent conformational properties, rhodanese and cyclophilin A, during binding and encapsulation by GroEL
211 ss1 conditional and null mutations, and that cyclophilin A enzymatic activity is required for suppres
215 Nef are able to compensate for the need for cyclophilin A for full infectivity and that amino acids
216 type 1 (HIV-1) Gag and the cellular protein cyclophilin A form an essential complex in the virion co
217 protein processing, and the upregulation of cyclophilin A further support the notion that C. neoform
218 ontained two- to threefold reduced ratios of cyclophilin A:Gag protein as compared with untreated vir
220 roximately 61 % sequence identity with human cyclophilin A (hCyPA) and the structures are similar, co
224 hat only the trans cis form of AAPF binds to cyclophilin A implies that cyclophilin A predominantly c
226 fort, evidence of developmental functions of cyclophilin A in non-plant systems has remained obscure.
230 nnel had been opened by PKA phosphorylation, cyclophilin A increased the open probability of wild-typ
231 3-Rpd3 histone deacetylase complex, and that cyclophilin A increases and Ess1 decreases disruption of
232 us to identify a third cyclophilin protein, cyclophilin A, interacting directly or in complex with p
235 The observation that disruption of the Gag-cyclophilin A interaction rescues A224E mutant replicati
237 ye et al. (2013) demonstrate that HIV capsid-cyclophilin A interactions affect viral cDNA sensing by
239 unodeficiency virus (SIV) do not incorporate cyclophilin A into virions or need it for full infectivi
244 ntiated genetically from its ability to bind cyclophilin A is further demonstrated by the rescue of a
245 the more expanded and unstructured denatured cyclophilin A is not encapsulated but is expelled into s
246 f cyclophilin A with hensin, suggesting that cyclophilin A is the PPIase that mediates the polymeriza
249 cyclosporin A (CsA), an inhibitory ligand of cyclophilin A, is a widely used immunosuppressive drug,
250 dentity with the central conserved region of cyclophilin A, is evolutionarily conserved by Southern b
252 sponsible for the alteration of phenotype in cyclophilin A knockdown (CypA-KD) P19 cells, we observed
253 Roc2, which are orthologs of the yeast Cpr1p cyclophilin, a known inhibitor of TBSV replication in ye
254 ellular ligands for cyclosporine include the cyclophilins, a large family of phylogenetically conserv
257 with increased activity of the BBB-degrading cyclophilin A-matrix metalloproteinase-9 pathway(19) in
258 particularly activation of a proinflammatory cyclophilin A-mediated pathway in brain vascular pericyt
259 r findings support a model in which Ess1 and cyclophilin A modulate the activity of the Sin3-Rpd3 com
263 Mutations in a tomato (Solanum lycopersicum) cyclophilin A ortholog, DIAGEOTROPICA (DGT), have been s
264 rated by the rescue of a mutation precluding cyclophilin A packaging by a mutation conferring cyclosp
268 inhibits virion infectivity, indicating that cyclophilin A plays an essential role in the HIV-1 life
269 phosphorylation during transcription of the cyclophilin A (PPIA), glyceraldehyde-3-phosphate dehydro
270 wn, including kallikrein-7 (KLK7; 2.2-fold), cyclophilin A (PPIA; 0.9-fold), and cofilin-1 (CFL1, 1.3
272 of AAPF binds to cyclophilin A implies that cyclophilin A predominantly catalyzes the trans to cis i
273 n binding interaction of Cyclosporine A with cyclophilin A protein in a yeast cell lysate is successf
275 hat the Gly89-Pro90 dipeptide is the primary cyclophilin A recognition motif, with Pro85, Val86, His8
280 infectivity imposes narrow constraints upon cyclophilin A stoichiometry in virions and that infectiv
282 variants, rhesus TRIM5alpha (RhT5) and TRIM-cyclophilin A (TCyp), are attractive candidates owing to
283 orthologs, rhesus TRIM5alpha (RhT5) and TRIM-cyclophilin A (TCyp), both of which are potent restricto
284 o binds the human peptidyl prolyl isomerase, cyclophilin A, thereby packaging the enzyme into the vir
285 A content resulting in decreased binding of cyclophilin A to Gag could account, in part, for the obs
287 was promoted by binding of the host protein cyclophilin A to the HIV-1 capsid, and PF74 and cyclospo
288 as well as literature values for uncomplexed cyclophilin A, to theoretical predictions using a combin
289 The expression levels of alpha-actin and cyclophilin A varied little during the course of develop
290 UP153 depletion, as was wild-type HIV-1 when cyclophilin A was depleted simultaneously or when infect
291 teins was confirmed by Western blotting, and cyclophilin A was localized to the tumor cells by immuno
294 lar to that of the peptidyl-prolyl isomerase cyclophilin A, we probed purified virions with antibodie
295 aturation, virus infectivity, and binding to cyclophilin A, whereas the subtype B portion of RT was l
296 nal domains on TRIM5alpha (SPRY) or TRIMCyp (cyclophilin A), which interact weakly with capsids.
297 ntiviral effect is mediated by inhibition of cyclophilin A, which is an essential host factor in the
298 at Pro-222 decreases virion incorporation of cyclophilin A, while mutation at Pro-231 abolishes infec
299 sing disparity is the weaker interactions of cyclophilin A with a transiently formed GroEL-GroES comp
300 onstant expression levels of alpha-actin and cyclophilin A with development, suggest that these are u
301 fied the direct CsA-sensitive interaction of cyclophilin A with hensin, suggesting that cyclophilin A
302 We have obtained HDX data for the complex of cyclophilin A with the immunosuppressant cyclosporin A.