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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 missense mutations in ADP/ATP translocase 1 (ANT1), and its yeast homolog ADP/ATP carrier 2 (Aac2), c
9  including adenine nucleotide translocase 1 (ANT1), were more oxidized by HSF1 deficiency in vivo.
10 lear DNA [adenine nucleotide translocator 1 (ANT1) and nicotinamide nucleotide transhydrogenase (NNT)
11 soform of adenine nucleotide translocator 1 (ANT1) are associated with autosomal-dominant progressive
12 in-I, and adenine nucleotide translocator 1 (ANT1), have been identified as autoantigens in cardiac a
13 ial adenine nucleotide translocases 1 and 2 (ANT1/2).
14 immunodominant epitopes (namely, ANT1 21-40, ANT1 31-50, ANT1 171-190, and ANT1 181-200).
15 nt epitopes (namely, ANT1 21-40, ANT1 31-50, ANT1 171-190, and ANT1 181-200).
16 s act synergistically, as double mutant Aac2/ANT1 causes severe clogging primarily at the translocase
17 mitochondria is subject to regulation via an ANT1-sensitive pathway in muscle tissues.
18 y, ANT1 21-40, ANT1 31-50, ANT1 171-190, and ANT1 181-200).
19 ors assessed the retinal location of ANT and ANT1-beta-gal reporter protein, mitochondrial activity w
20 set of mPT, irrespective of energization and ANT1 expression, albeit the number of cells undergoing m
21  5' regions of 4q35 candidate genes FRG1 and ANT1.
22  of the human disease; by contrast, FRG2 and ANT1 transgenic mice seem normal.
23 tochondrial DNA maintenance (POLG2, PEO1 and ANT1).
24 erlying the mitochondrial myopathy caused by ANT1 mutations remain largely unknown.
25       In mice, expression of a super-clogger ANT1 variant led to neurodegeneration and an age-depende
26                     In the healthy controls, ANT1 was influenced by limited education (<8 years) and
27 rmeabilized C2C12 myotubes with knocked-down ANT1 exhibited higher calcium uptake capacity and voltag
28 ANT1 and in C2C12 myotubes with knocked-down ANT1 expression.
29 amined in vivo by deleting the gene encoding ANT1 (Slc25a4) or CypD (Ppif) in a delta-sarcoglycan (Sg
30                     Mutant plants lacking ER-ANT1 exhibit a dwarf phenotype and their seeds contain r
31 ervation demonstrates that the absence of ER-ANT1 activity mainly affects photorespiration (maybe sol
32                                     Since ER-ANT1 homologs are restricted to higher plants, it is tem
33                      The observation that ER-ANT1 activity is associated with cellular ROS levels rev
34 plasmic Reticulum Adenylate Transporter1 (ER-ANT1) resides in the endoplasmic reticulum (ER) membrane
35 swelling in control and partially-expressing ANT1 fibroblasts, but not in cells lacking ANT1, despite
36 her wild-type or transgenic mice deleted for ANT1.
37 ductions in steady-state mRNA expression for ANT1 and betaF1 relative to normal (n = 8) occur in CHF,
38  above observations, we proposed a model for ANT1 regulation of cell proliferation and leaf growth, v
39 bes causes functional changes different from ANT1 mutants.
40     Here, we successfully express functional ANT1 in differentiated mouse myotubes, which naturally c
41   The adenine nucleotide transporter 1 gene (ANT1) encodes an inner mitochondrial membrane protein th
42    The core promoters of the mouse and human ANT1 and ANT2 genes are very similar.
43                          The mouse and human ANT1 and ANT2 genes showed substantial homology starting
44 ream OXBOX and REBOX elements found in human ANT1 genes, thought to be important for muscle-specific
45 -relevant mammalian cells, that mutant human ANT1 causes dominant mitochondrial defects characterized
46  skeletal muscle and heart, similar to human ANT1.
47                                           In ANT1-deficient skeletal muscle, mitochondrial gene expre
48 energy depletion and nucleotide imbalance in ANT1 mutant muscle cells.
49           Disease-causing human mutations in ANT1 abrogate binding to TIM44 and TIM23 and inhibit mit
50 vely, our data highlight that, by inhibiting ANT1 and mitochondrial dysfunction, SHP2 orchestrates an
51 enine nucleotide translocator (ANT) isoforms ANT1 and ANT2 that are present in the plasma membrane of
52 ly-dependent tyrosine phosphorylation of L1, ANT1, ANT2, and MMP14.
53                               Mice that lack ANT1 show blunted mitophagy and consequent profound accu
54 g ANT1 fibroblasts, but not in cells lacking ANT1, despite greater losses of mitochondrial membrane p
55     Although the molecular mechanism linking ANT1-Cys(57) nitroalkylation and uncoupling is not yet k
56 ults indicate that plasma membrane-localized ANT1 and ANT2 regulate L1-mediated neurite outgrowth in
57  maize embryonic leaves suggested that maize ANT1 (ZmANT1) regulates vascular development.
58 hypothesis that nitroalkenes directly modify ANT1 and that nitroalkene-mediated cardioprotection requ
59            The modified properties of mutant ANT1 can be responsible for disease pathogenesis in adPE
60 es multiple immunodominant epitopes (namely, ANT1 21-40, ANT1 31-50, ANT1 171-190, and ANT1 181-200).
61          The myocarditis-inducing ability of ANT1 21-40 was associated with the generation of T cells
62                      In yeast, expression of ANT1 carrying mutations corresponding to the human adPEO
63 teostasis, and cell viability independent of ANT1's nucleotide transport activity.
64 hemia-reperfusion injury, siRNA knockdown of ANT1 inhibited the cardioprotective effect of LNO(2).
65 lasts exhibiting partial or complete lack of ANT1 and in C2C12 myotubes with knocked-down ANT1 expres
66 ubes, which naturally contain high levels of ANT1, without causing cell death.
67 for direct modification (nitroalkylation) of ANT1 on cysteine 57.
68  plants indicated that the overexpression of ANT1 caused the upregulation of genes that encode protei
69  ant1 was confirmed by the overexpression of ANT1 in transgenic tomato and in tobacco under the contr
70                              The presence of ANT1 in a subset of inner retinal cells accompanied by s
71       Our study revealed biological roles of ANT1 in several developmental processes beyond its known
72               However, functional studies of ANT1 mutations in mammalian cells are lacking, because t
73 ice that expressed a P62A mutated version of ANT1.
74 des induce comparable T-cell responses, only ANT1 21-40 was found to be a major myocarditogenic epito
75 skeletal muscle the 4q35 genes FRG1, FRG2 or ANT1.
76 coupling was not driven by increased UCP3 or ANT1 expression.
77 e-dependent dominant myopathy that phenocopy ANT1-induced human disease, suggesting clogging as a mec
78 troalkene-mediated cardioprotection requires ANT1.
79                                         An S-ANT1 of <10 animals was abnormal.
80  adjusting procedure, the simplified ANT1 (S-ANT1 ) was obtained.
81    By sample random split validation, both S-ANT1 and its three-level score showed prognostic value r
82           Thus, a three-level score (0 for S-ANT1 >/=15, 1 for 10 </= S-ANT1 < 15, 2 for S-ANT1 <10)
83 NT1 >/=15, 1 for 10 </= S-ANT1 < 15, 2 for S-ANT1 <10) was obtained.
84 4 versus 16 +/- 0.7, P < 0.001) and higher S-ANT1 than those with HE >/=grade 2 (4 +/- 0.9).
85                       This group had lower S-ANT1 than unimpaired patients (12 +/- 0.4 versus 16 +/-
86 el score (0 for S-ANT1 >/=15, 1 for 10 </= S-ANT1 < 15, 2 for S-ANT1 <10) was obtained.
87                                        The S-ANT1 is an easily obtainable measure useful for the asse
88                          In grade 1 HE the S-ANT1 was lower than in MHE.
89 ducation adjusting procedure, the simplified ANT1 (S-ANT1 ) was obtained.
90 he adenine nucleotide translocator (SLC25A4, ANT1) gene, with the severity of cardiomyopathy mediated
91 replication, such as TK2, DGUOK, TP, SUCLA2, ANT1, and possibly the newly identified MPV17.
92                 Moreover, our data suggested ANT1 as the most likely site of mediating increased mito
93       We examined if the animal naming test (ANT1 ) (maximum number of animals listed in 1 minute) is
94                             We conclude that ANT1 confers sensitivity of the pore to the electrochemi
95                       Results confirmed that ANT1 is the predominant binding partner for the BART.ARL
96                  Herein, we demonstrate that ANT1 can induce autoimmune myocarditis in A/J mice by ge
97     This study provides direct evidence that ANT1 and CypD are required MPTP components governing in
98 use they have been hindered by the fact that ANT1 expression leads to apoptotic cell death in commonl
99                                 We show that ANT1 encompasses multiple immunodominant epitopes (namel
100  detectable morphologic changes suggest that ANT1 is not essential for ATP transport in the retina.
101 ng is not yet known, these data suggest that ANT1-mediated uncoupling may be a mechanism for nitroalk
102 d by supernormal ERG responses suggests that ANT1 may be localized to hyperpolarizing bipolar cells.
103                                          The ANT1-deficient muscle mitochondria produce excess reacti
104 n deletion and two frameshift mutants of the ANT1 ortholog in the C4 millet Setaria viridis by the CR
105 cutive patients with cirrhosis underwent the ANT1 .
106                          Oxidative damage to ANT1 protein, a structural component of the mitochondria
107           These abnormalities are not due to ANT1 loss of function, because knocking down Ant1 in myo
108 receptor and adenine nucleotide translocase (ANT1) were downregulated at 128 dGA and 142 dGA, respect
109 form of the adenine nucleotide translocator (ANT1) exhibit many of the hallmarks of human oxidative p
110                         To better understand ANT1 functions, we determined the binding motif of ZmANT
111                                       VDAC1, ANT1, and HKII were present in the PKCepsilon complex at
112 iration appears to be the mechanism by which ANT1-deficient mice prevent diabetes, demonstrating that
113 hondrial function by direct association with ANT1 and the mitochondrial ATP synthasome, and leads to
114                             Mutations within ANT1 produce a syndrome of chronic progressive external

 
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