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1                                              ACBP binds very-long-chain acyl-CoA esters, which is req
2                                              ACBP displays an atypical compliance along two nearly or
3                                              ACBP does not cross the blood-brain barrier.
4                                              ACBP increases the activity of ceramide synthase 2 (CerS
5                                              ACBP inhibition also prevented the senescence of tubular
6                                              ACBP interacts with the alpha1-subunit of the GABA(A) re
7                                              ACBP is a topologically simple and highly conserved four
8                                              ACBP lacks a signal sequence for secretion through the e
9                                              ACBP neutralization by means of a monoclonal antibody (m
10                                              ACBP overexpression in COS-7 or rat hepatoma cells enhan
11                                              ACBP was localized to Muller glial cells by hybridizatio
12                                              ACBP-astrocytes were observed in apposition with proopio
13                                              ACBP/DBI has been identified as the endogenous PBR ligan
14 itutive Gabrg2(F77I) mutation that abolishes ACBP/DBI binding to the GABA(A) receptor.
15 ual triple fluorescent-labeled (HNF-4 alpha, ACBP, and luciferase) rat hepatoma cells showed a high c
16 alpha in vitro and in intact cells, although ACBP expression level directly correlated with HNF-4 alp
17  denaturant concentrations, unfolded CI2 and ACBP are more compact and display larger fluctuations th
18 ection increased ACBP mRNA transcription and ACBP protein expression.
19 n cardiomyocytes, doxorubicin caused an anti-ACBP-reversible dysregulation of mRNAs coding for cardio
20        Senescence was also prevented by anti-ACBP mAb treatment in additional mouse models of acceler
21 nic kidney injury induced by cisplatin, anti-ACBP mAb administration counteracted both histopathologi
22             Moreover, administration of anti-ACBP mAb prevented natural and doxorubicin-accelerated c
23  had been exposed to doxorubicin and/or anti-ACBP in vivo.
24   In contrast, cotransfection with antisense ACBP expression vector inhibited transactivation.
25  fluorescence dynamics demonstrated that apo-ACBP was an ellipsoidal protein (axes of 15 and 9 A) who
26 d an intermolecular distance of 53 A between ACBP and HNF-4 alpha in rat hepatoma cell nuclei.
27 lciparum ACBP-acyl-CoA complex and of bovine ACBP in two crystal forms.
28 ng specificity different from that of bovine ACBP.
29                          Overall, the bovine ACBP crystal structures are similar to the NMR structure
30 f very-long acyl chain ceramide synthesis by ACBP, which we anticipate is of crucial importance in un
31 fected COS-7 cells significantly colocalized ACBP and HNF-4 alpha within the nucleus and in the perin
32  (v) Immunogold electron microscopy detected ACBP within 43 A of HNF-4 alpha.
33 n, however, is not affected by the disrupted ACBP gene.
34 olerance, yet the contribution of endogenous ACBP in energy homeostasis is unknown.
35 lution crystal structures of a P. falciparum ACBP-acyl-CoA complex and of bovine ACBP in two crystal
36 chemical properties of Plasmodium falciparum ACBP are described together with the 2.0 A resolution cr
37 hat, even in the earliest stages of folding, ACBP dynamics are governed by native-like contacts on a
38 tivates CerS3 activity, whereas cytosol from ACBP knock-out mice does not.
39 mation was altered by oleoyl-CoA in the holo-ACBP as shown by a 2-A decrease of ACBP hydrodynamic dia
40                         In the hypothalamus, ACBP is enriched in arcuate nucleus (ARC) astrocytes, ep
41                                          (i) ACBP interaction with HNF-4 alpha elicited significant c
42 apting and thriving in the bone and identify ACBP as a key regulator of this process.
43                                         (ii) ACBP and HNF-4 alpha were coimmunoprecipitated by antibo
44 yl-CoA-induced conformational alterations in ACBP may be significant to its putative functions in lip
45    HOKS in the preferred direction increased ACBP mRNA transcription and ACBP protein expression.
46 -binding protein/diazepam binding inhibitor (ACBP/DBI) motif.
47                           Thus, native liver ACBP binds >14-carbon fatty acyl-CoAs with nanomolar aff
48 troscopy directly established that rat liver ACBP bound 18-carbon cis- and trans-parinaroyl-CoA, Kd =
49                             Mechanistically, ACBP-mediated FAO increased ATP and NADPH production, re
50                                    Moreover, ACBP required the presence of the peripheral benzodiazep
51 P was engineered to contain the native mouse ACBP amino acid sequence expressed as a fusion protein a
52 test this hypothesis, mouse recombinant (mr) ACBP was engineered to contain the native mouse ACBP ami
53 ated that the expression of a Brassica napus ACBP (BnACBP) complementary DNA in the developing seeds
54 n tag resulted in mrACBP identical to native ACBP as shown by mass (10000.5 Da) and amino acid sequen
55 ection of a monoclonal antibody neutralizing ACBP/DBI (alpha-DBI) protects the murine liver against i
56                   The mechanical behavior of ACBP is discussed in terms of topology and helix propens
57 We have previously described the behavior of ACBP under tension, revealing a highly extended transiti
58 on was confirmed by coimmunoprecipitation of ACBP and the alpha1-subunit of the GABA(A) receptor usin
59  the holo-ACBP as shown by a 2-A decrease of ACBP hydrodynamic diameter and increased Trp segmental m
60           Surprisingly, the deformability of ACBP is greater than that observed for the highly pliant
61  in favor of a broad age-promoting effect of ACBP across different organ systems.
62         To address this issue, the effect of ACBP on liver LCFA-CoA pool size, acyl chain composition
63 onstraints for the acid-unfolded ensemble of ACBP.
64 gic transmission, HOKS-induced expression of ACBP could provide a molecular basis for adaptation to H
65 , smaller truncated proteolytic fragments of ACBP do, increasing the excitability of central cortical
66 A establishes with the four alpha-helices of ACBP and showed that the unfolding pathway is marginally
67  alpha-DBI were mimicked by the induction of ACBP/DBI-specific autoantibodies, an inducible Acbp/Dbi
68 chain fatty acyl-CoAs, direct interaction of ACBP with >14-carbon fatty acyl-CoAs has not been establ
69 experiments to study the folding kinetics of ACBP on the microsecond time scale.
70                                 Knockdown of ACBP or ELOVL1 inhibited oleate-induced beta-cell prolif
71                      Conversely, knockout of ACBP in highly bone metastatic cancer cells abrogated me
72 een the level of luciferase and the level of ACBP expression.
73 transgenic mice expressing a higher level of ACBP.
74  induces the rapid release and processing of ACBP to the active peptides.
75 s as a conserved element in the promoters of ACBP genes in invertebrates and vertebrates.
76 on free energy for the unfolding reaction of ACBP without affecting the position of the transition st
77  rapamycin also resulted in rapid release of ACBP indicating that this protein uses components of the
78 mice, an effect prevented by viral rescue of ACBP in ARC astrocytes.
79      Overall, these data support the role of ACBP in acyl trafficking in developing seeds and validat
80                      We discuss the roles of ACBP/DBI in central and tissue-specific functions in mam
81 better understand the physiological roles of ACBP/DBI in vivo.
82               The functional significance of ACBP interaction with HNF-4 alpha was evidenced by mamma
83 irst demonstrate that the denatured state of ACBP at near-zero denaturant is unusually compact and en
84 e structures in this acid-denatured state of ACBP, we rationalize the effects of single-point mutatio
85                               Suppression of ACBP levels by small interfering RNA inhibited the t-Bid
86 s are significantly reduced in the testes of ACBP(-/-) mice, concomitant with a significant reduction
87 y curved membranes to facilitate transfer of ACBP-bound ligands.
88 previously; however, the bovine and parasite ACBP structures are less similar.
89                                 The parasite ACBP is shown to have a different ligand-binding pocket,
90 dentified between the mammalian and parasite ACBPs.
91  yeast suggest that acyl-CoA binding protein ACBP may modulate long-chain fatty acyl-CoA (LCFA-CoA) d
92 id-denatured state of the 86-residue protein ACBP.
93 c disruption of an acyl-CoA binding protein (ACBP) alters mitochondrial accumulation of LCACoAs.
94  binding proteins, acyl CoA binding protein (ACBP) and sterol carrier protein-2 (SCP-2), by 45 and 80
95 ntify acyl-coenzyme A (CoA) binding protein (ACBP) as a bone metastasis driver.
96 study, we identify acyl-CoA-binding protein (ACBP) as playing a critical role in the activation of ca
97 ndle protein acyl co-enzyme binding protein (ACBP) as seen from both perturbations in nuclear magneti
98 (CI2) and unfolded acyl-CoA binding protein (ACBP) even under conditions where folded and unfolded su
99                    Acyl-CoA-binding protein (ACBP) functions both intracellularly as part of fatty ac
100 ) cytosolic acyl-coenzyme A-binding protein (ACBP) has a substantial influence over fatty acid (FA) c
101           Although acyl-CoA-binding protein (ACBP) has been detected in the nucleus, the physiologica
102 ough the cytosolic acyl-CoA binding protein (ACBP) has high affinity for medium chain fatty acyl-CoAs
103 e four-alpha-helix acyl-CoA binding protein (ACBP) in the low-force regime using optical tweezers and
104                    Acyl-CoA binding protein (ACBP) maintains a pool of fatty acyl-CoA molecules in th
105                    Acyl-CoA-binding protein (ACBP) mRNA was one of four mRNAs selected by this screen
106                    Acyl-CoA binding protein (ACBP) plays a role in determining the level of FAR eleme
107 e show that acyl-coenzyme A-binding protein (ACBP) potently facilitates very-long acyl chain ceramide
108           Although acyl-CoA binding protein (ACBP) stimulates utilization of long-chain fatty acyl-Co
109 on study of acyl-coenzyme A binding protein (ACBP), a two-state folder (folding time ~10 ms) exhibiti
110                    Acyl-CoA binding protein (ACBP), a ubiquitously expressed and highly conserved pro
111       Acyl-coenzyme A (CoA)-binding protein (ACBP), also known as diazepam-binding inhibitor (DBI), i
112                    Acyl-CoA binding protein (ACBP)-derived endozepines are secreted peptides that mod
113 ase 1 (ELOVL1) and acyl-CoA-binding protein (ACBP).
114 sis, and was named acyl-CoA binding protein (ACBP).
115 pe of acyl-coenzyme A (CoA)-binding protein (ACBP).
116 sue hormone acyl coenzyme A-binding protein (ACBP, encoded by the gene diazepam-binding inhibitor, DB
117       Acyl coenzyme A (CoA)-binding protein (ACBP; AcbA in Dictyostelium discoideum), an unconvention
118 n experimentally well-characterized protein, ACBP, to explore the extent to which state-of-the-art si
119 bidopsis thaliana acyl-CoA-binding proteins (ACBPs) are important in seed development but did not aff
120 ing affinity exhibited by murine recombinant ACBP: saturated > monounsaturated > polyunsaturated C14-
121                     Muller cells may secrete ACBP in the inner plexiform layer, thereby decreasing th
122                         Following secretion, ACBP is proteolytically cleaved to the active neuropepti
123                                   Similarly, ACBP overexpression in ARC astrocytes reduced feeding an
124       These interactions were specific since ACBP did not interact with Sp1 or glucocorticoid recepto
125                                  In summary, ACBP physically interacted with HNF-4 alpha in vitro and
126  "pull-down" assay in which histidine-tagged ACBP was used to pull down the GABA(A)alpha1.
127  when manipulated from the N- and C-termini, ACBP unfolds by populating a transition state that resem
128 e first time in a physiological context that ACBP expression may play a role in LCFA-CoA metabolism.
129                         We demonstrated that ACBP deletion in GFAP+ astrocytes, but not in Nkx2.1-lin
130                                We found that ACBP expression correlated with metabolic signaling, bon
131      Time-resolved fluorometry revealed that ACBP-bound parinaroyl-CoAs had high rotational freedom w
132                    Importantly, we show that ACBP interacts with CerS2 and CerS3.
133                           Here, we show that ACBP plasma concentrations are elevated in (close-to-)ce
134           Five lines of evidence showed that ACBP bound HNF-4 alpha in vitro and in the nucleus of in
135            A Markov state model (MSM) of the ACBP folding reaction, constructed from over 30 ms of mo
136                            Disruption of the ACBP gene causes a >5-fold activation of OLE1 transcript
137 dentification of a G4 in the promoter of the ACBP gene in silkworm and human cancer cells.
138 ogether, our findings suggest that G4 of the ACBP genes is involved in regulation of lipid metabolism
139            These effects were not due to the ACBP transgene altering the protein levels of liver micr
140                                  Since then, ACBP/DBI has been studied in parallel without a clear an
141          As shown herein for the first time, ACBP in the nucleus physically and functionally interact
142 ic cancer cells, overexpression of wild-type ACBP, but not the acyl-CoA-binding deficient mutant, sti
143                       These findings uncover ACBP as an ARC gliopeptide playing a key role in energy
144 brane-bound enzymes, it is not known whether ACBP directly interacts with membranes.
145 eripheral benzodiazepine receptor (for which ACBP is a ligand) to be retained at the mitochondria, to
146                                        While ACBP transgenic mice did not exhibit altered body or liv

 
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