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1                                              LCAD -/- mice that reached birth appeared normal, but ha
2                                              LCAD is a homotetramer containing one FAD per 43 kDa sub
3                                              LCAD is deacetylated in wild-type mice under fasted cond
4                                              LCAD(-/-) mice demonstrated reduced pulmonary compliance
5                                              LCAD(-/-) surfactant demonstrated functional abnormaliti
6 hy, and sudden death was observed in 4 of 75 LCAD -/- mice.
7                   Approximately 10% of adult LCAD -/- males developed cardiomyopathy, and sudden deat
8 e the crucial roles of mitochondrial FAO and LCAD in vivo.
9 dentify the fatty acid oxidation pathway and LCAD in particular as factors contributing to the pathop
10                              Matings between LCAD +/- mice yielded an abnormally low number of LCAD +
11 ng from sires and dams heterozygous for both LCAD and VLCAD mutations.
12 use it is less efficiently dehydrogenated by LCAD than is its cis isomer and that the accumulation of
13                    Progeny with the combined LCAD(+/+)//VLCAD(+/-) genotype were over-represented in
14    In contrast, no live mice with a compound LCAD(-/-)//VLCAD(-/-) genotype were detected.
15  CoA synthase, ACO, CYP4A3) and other (CPT1, LCAD) genes of mitochondrial and extramitochondrial LCFA
16 cal phenotypes of mice with LCAD deficiency (LCAD(-/-)) and wild-type mice.
17 at long-chain acyl coenzyme A dehydrogenase (LCAD) is hyperacetylated at lysine 42 in the absence of
18  of human long-chain acyl-CoA dehydrogenase (LCAD) and the catalytically inactive Glu291Gln mutant, h
19  study of long-chain acyl-CoA dehydrogenase (LCAD) and very long-chain acyl-CoA dehydrogenase reveale
20           Long-chain acyl-CoA dehydrogenase (LCAD) catalyzes the initial step in mitochondrial fatty
21 nted with long-chain acyl-CoA dehydrogenase (LCAD) deficiency.
22           Long-chain acyl-CoA dehydrogenase (LCAD) is a key mitochondrial fatty acid oxidation enzyme
23           Long-chain acyl-CoA dehydrogenase (LCAD) is a mitochondrial fatty acid oxidation enzyme who
24 ciency of long-chain acyl-CoA dehydrogenase (LCAD), a key enzyme in mitochondrial fatty acid oxidatio
25 n enzyme, long-chain acyl-CoA dehydrogenase (LCAD), also developed periportal macrovesicular steatosi
26  in human long chain acyl-CoA dehydrogenase (LCAD), has been suggested to affect substrate chain leng
27 on enzyme long-chain acyl-CoA dehydrogenase (LCAD).
28 ial transporter (CPT1), B-oxidation enzymes (LCAD, HADH, ACAT1), tricarboxylic acid cycle enzyme (IDH
29  transporter (CPT1), beta-oxidation enzymes (LCAD, HADH, ACAT1), tricarboxylic acid cycle enzyme (IDH
30 background with a more severe defect in FAO (LCAD(-/-); VLCAD(+/-)) in addition to a validated mouse
31     Large aggregate surfactant isolated from LCAD(-/-) mouse lavage fluid had significantly reduced p
32 y surfactant, was significantly increased in LCAD(-/-) lavage fluid, suggesting increased epithelial
33 ed, accumulate at the air-fluid interface in LCAD(-/-) lungs.
34 ) and C(14) acylcarnitines were prominent in LCAD(-/-) mice.
35     Lung fatty acid oxidation was reduced in LCAD(-/-) mice.
36         We previously demonstrated increased LCAD lysine acetylation in SIRT3 knockout mice concomita
37 udden unexplained infant death where no lung LCAD antigen was detectable.
38 /-)) in addition to a validated mouse model (LCAD(-/-); VLCAD(+/+)) and compared them with wild-type
39               Sirt5KO liver exhibited normal LCAD activity but reduced mitochondrial acyl-CoA synthet
40              The substrate binding cavity of LCAD reveals key differences which makes it specific for
41 n vitro and in vivo; and hyperacetylation of LCAD reduces its enzymatic activity.
42      This study demonstrates localization of LCAD to human alveolar type II pneumocytes, which synthe
43                 We produced a mouse model of LCAD deficiency with severely impaired FAO.
44 +/- mice yielded an abnormally low number of LCAD +/- and -/- offspring, indicating frequent gestatio
45                    The physiological role of LCAD and the fatty acid oxidation pathway in lung was su
46 s-tetradecenoyl-CoA is a poorer substrate of LCAD than is 5-cis-tetradecenoyl-CoA, while both unsatur
47  residue at a position homologous to that of LCAD, was also synthesized and purified.
48                                 Treatment of LCAD(-/-) mice with mildronate, a drug that inhibits car
49       To study the effects of acetylation on LCAD and determine sirtuin 3 (SIRT3) target sites, we ch
50  sites, we chemically acetylated recombinant LCAD.
51 SIRT3 knockout mice concomitant with reduced LCAD activity and reduced fatty acid oxidation.
52                           Here, we show that LCAD knockout mice develop hepatic steatosis, which is a
53                These structures suggest that LCAD harbors functions beyond its historically defined r
54                   These results suggest that LCAD, ACAD10, ACAD11 constitute a distinct class of euca
55  degrees C drop in body temperature in unfed LCAD(-/-); VLCAD(+/+) mice compared with WT body tempera
56 thway in lung was subsequently studied using LCAD knock-out mice.
57 and 64% of wild-type, respectively), whereas LCAD(-/-) mice showed a more profoundly reduced activity
58 ogic and biochemical phenotypes of mice with LCAD deficiency (LCAD(-/-)) and wild-type mice.