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1                                              ANT1 also contains redox-sensitive cysteines that may be
2                                              ANT1-deficient animals are insulin-hypersensitive, gluco
3                                              ANT1-null fibroblasts were also resistant to H2O2-induce
4  is interleaved between two extant groups, 0.ANT1 and 0.ANT2, and is distant from strains associated
5 n adenine nucleotide translocator isoform 1 (ANT1) was inactivated.
6 ctive, and adenine nucleotide translocase 1 (ANT1) is a key mediator of mitochondrial uncoupling.
7 sphorylate adenine nucleotide translocase 1 (ANT1), a central molecule controlling mitochondrial perm
8  including adenine nucleotide translocase 1 (ANT1), were more oxidized by HSF1 deficiency in vivo.
9 lear DNA [adenine nucleotide translocator 1 (ANT1) and nicotinamide nucleotide transhydrogenase (NNT)
10 soform of adenine nucleotide translocator 1 (ANT1) are associated with autosomal-dominant progressive
11 in-I, and adenine nucleotide translocator 1 (ANT1), have been identified as autoantigens in cardiac a
12 immunodominant epitopes (namely, ANT1 21-40, ANT1 31-50, ANT1 171-190, and ANT1 181-200).
13 nt epitopes (namely, ANT1 21-40, ANT1 31-50, ANT1 171-190, and ANT1 181-200).
14 mitochondria is subject to regulation via an ANT1-sensitive pathway in muscle tissues.
15 y, ANT1 21-40, ANT1 31-50, ANT1 171-190, and ANT1 181-200).
16 ors assessed the retinal location of ANT and ANT1-beta-gal reporter protein, mitochondrial activity w
17 set of mPT, irrespective of energization and ANT1 expression, albeit the number of cells undergoing m
18  5' regions of 4q35 candidate genes FRG1 and ANT1.
19  of the human disease; by contrast, FRG2 and ANT1 transgenic mice seem normal.
20 tochondrial DNA maintenance (POLG2, PEO1 and ANT1).
21 erlying the mitochondrial myopathy caused by ANT1 mutations remain largely unknown.
22                     In the healthy controls, ANT1 was influenced by limited education (<8 years) and
23 rmeabilized C2C12 myotubes with knocked-down ANT1 exhibited higher calcium uptake capacity and voltag
24 ANT1 and in C2C12 myotubes with knocked-down ANT1 expression.
25                     Mutant plants lacking ER-ANT1 exhibit a dwarf phenotype and their seeds contain r
26 ervation demonstrates that the absence of ER-ANT1 activity mainly affects photorespiration (maybe sol
27                                     Since ER-ANT1 homologs are restricted to higher plants, it is tem
28                      The observation that ER-ANT1 activity is associated with cellular ROS levels rev
29 plasmic Reticulum Adenylate Transporter1 (ER-ANT1) resides in the endoplasmic reticulum (ER) membrane
30 swelling in control and partially-expressing ANT1 fibroblasts, but not in cells lacking ANT1, despite
31 her wild-type or transgenic mice deleted for ANT1.
32 ductions in steady-state mRNA expression for ANT1 and betaF1 relative to normal (n = 8) occur in CHF,
33 bes causes functional changes different from ANT1 mutants.
34     Here, we successfully express functional ANT1 in differentiated mouse myotubes, which naturally c
35   The adenine nucleotide transporter 1 gene (ANT1) encodes an inner mitochondrial membrane protein th
36    The core promoters of the mouse and human ANT1 and ANT2 genes are very similar.
37                          The mouse and human ANT1 and ANT2 genes showed substantial homology starting
38 ream OXBOX and REBOX elements found in human ANT1 genes, thought to be important for muscle-specific
39 -relevant mammalian cells, that mutant human ANT1 causes dominant mitochondrial defects characterized
40  skeletal muscle and heart, similar to human ANT1.
41                                           In ANT1-deficient skeletal muscle, mitochondrial gene expre
42 energy depletion and nucleotide imbalance in ANT1 mutant muscle cells.
43 vely, our data highlight that, by inhibiting ANT1 and mitochondrial dysfunction, SHP2 orchestrates an
44 enine nucleotide translocator (ANT) isoforms ANT1 and ANT2 that are present in the plasma membrane of
45 ly-dependent tyrosine phosphorylation of L1, ANT1, ANT2, and MMP14.
46 g ANT1 fibroblasts, but not in cells lacking ANT1, despite greater losses of mitochondrial membrane p
47     Although the molecular mechanism linking ANT1-Cys(57) nitroalkylation and uncoupling is not yet k
48 ults indicate that plasma membrane-localized ANT1 and ANT2 regulate L1-mediated neurite outgrowth in
49 hypothesis that nitroalkenes directly modify ANT1 and that nitroalkene-mediated cardioprotection requ
50            The modified properties of mutant ANT1 can be responsible for disease pathogenesis in adPE
51 es multiple immunodominant epitopes (namely, ANT1 21-40, ANT1 31-50, ANT1 171-190, and ANT1 181-200).
52          The myocarditis-inducing ability of ANT1 21-40 was associated with the generation of T cells
53                      In yeast, expression of ANT1 carrying mutations corresponding to the human adPEO
54 hemia-reperfusion injury, siRNA knockdown of ANT1 inhibited the cardioprotective effect of LNO(2).
55 lasts exhibiting partial or complete lack of ANT1 and in C2C12 myotubes with knocked-down ANT1 expres
56 ubes, which naturally contain high levels of ANT1, without causing cell death.
57 for direct modification (nitroalkylation) of ANT1 on cysteine 57.
58  plants indicated that the overexpression of ANT1 caused the upregulation of genes that encode protei
59  ant1 was confirmed by the overexpression of ANT1 in transgenic tomato and in tobacco under the contr
60                              The presence of ANT1 in a subset of inner retinal cells accompanied by s
61               However, functional studies of ANT1 mutations in mammalian cells are lacking, because t
62 des induce comparable T-cell responses, only ANT1 21-40 was found to be a major myocarditogenic epito
63 skeletal muscle the 4q35 genes FRG1, FRG2 or ANT1.
64 coupling was not driven by increased UCP3 or ANT1 expression.
65 troalkene-mediated cardioprotection requires ANT1.
66                                         An S-ANT1 of <10 animals was abnormal.
67  adjusting procedure, the simplified ANT1 (S-ANT1 ) was obtained.
68    By sample random split validation, both S-ANT1 and its three-level score showed prognostic value r
69           Thus, a three-level score (0 for S-ANT1 >/=15, 1 for 10 </= S-ANT1 < 15, 2 for S-ANT1 <10)
70 NT1 >/=15, 1 for 10 </= S-ANT1 < 15, 2 for S-ANT1 <10) was obtained.
71 4 versus 16 +/- 0.7, P < 0.001) and higher S-ANT1 than those with HE >/=grade 2 (4 +/- 0.9).
72                       This group had lower S-ANT1 than unimpaired patients (12 +/- 0.4 versus 16 +/-
73 el score (0 for S-ANT1 >/=15, 1 for 10 </= S-ANT1 < 15, 2 for S-ANT1 <10) was obtained.
74                                        The S-ANT1 is an easily obtainable measure useful for the asse
75                          In grade 1 HE the S-ANT1 was lower than in MHE.
76 ducation adjusting procedure, the simplified ANT1 (S-ANT1 ) was obtained.
77 replication, such as TK2, DGUOK, TP, SUCLA2, ANT1, and possibly the newly identified MPV17.
78       We examined if the animal naming test (ANT1 ) (maximum number of animals listed in 1 minute) is
79                             We conclude that ANT1 confers sensitivity of the pore to the electrochemi
80                       Results confirmed that ANT1 is the predominant binding partner for the BART.ARL
81                  Herein, we demonstrate that ANT1 can induce autoimmune myocarditis in A/J mice by ge
82 use they have been hindered by the fact that ANT1 expression leads to apoptotic cell death in commonl
83                                 We show that ANT1 encompasses multiple immunodominant epitopes (namel
84  detectable morphologic changes suggest that ANT1 is not essential for ATP transport in the retina.
85 ng is not yet known, these data suggest that ANT1-mediated uncoupling may be a mechanism for nitroalk
86 d by supernormal ERG responses suggests that ANT1 may be localized to hyperpolarizing bipolar cells.
87                                          The ANT1-deficient muscle mitochondria produce excess reacti
88 cutive patients with cirrhosis underwent the ANT1 .
89                          Oxidative damage to ANT1 protein, a structural component of the mitochondria
90           These abnormalities are not due to ANT1 loss of function, because knocking down Ant1 in myo
91 form of the adenine nucleotide translocator (ANT1) exhibit many of the hallmarks of human oxidative p
92                                       VDAC1, ANT1, and HKII were present in the PKCepsilon complex at
93 iration appears to be the mechanism by which ANT1-deficient mice prevent diabetes, demonstrating that
94                             Mutations within ANT1 produce a syndrome of chronic progressive external

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