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1 CYP4A and Nox oxidase expression was upregulated in glom
2 CYP4A(+) TAM infiltration was positively associated with
4 of NOS increased omega-hydroxylase activity, CYP4A expression, and renal efflux of 20-HETE, whereas 2
9 inhibitors of lipoxygenases (baicalein) and CYP4A (17-octadecynoic acid), but not of cyclooxygenase
11 ecific for P-450s CYP1A2, CYP2E1, CYP3A, and CYP4A and was not demonstrated to be involved in the tur
12 t members of the mammalian CYP4B, CYP4F, and CYP4A subfamilies bind their heme in an unusually tight
14 )-dependent PLD(2) through lipoxygenase- and CYP4A-derived HETEs via the Ras/ERK pathway by a mechani
15 n of lauric, myristic, and palmitic acids by CYP4A enzymes were measured and compared in rat liver mi
16 zation away from the M2 phenotype induced by CYP4A inhibition decreased VEGFR1(+) myeloid cell migrat
19 Cytochrome P450 enzymes of the 4A family (CYP4A) convert arachidonic acid to 20-hydroxyeicosatetra
20 he role of cytochrome P450 of the 4A family (CYP4A), its metabolites, and NADPH oxidases both in reac
22 that reactive oxygen species generated from CYP4A-mediated fatty acid oxidation work synergistically
23 ats were corresponding changes in functional CYP4A measured as either arachidonic acid or lauric acid
24 ROS generation, NADPH superoxide generation, CYP4A and Nox protein expression, and mRNA levels were m
27 e characterized the induction of the hepatic CYP4A genes in rats during the altered lipid metabolism
28 was accompanied by corresponding changes in CYP4A protein levels and arachidonic and lauric acid ome
29 ays for specific detection of the individual CYP4A genes in the kidneys of spontaneously hypertensive
30 expression were observed for the individual CYP4A genes, with only CYP4A3 mRNA measurable in the kid
31 hances the severity of steatosis by inducing CYP4A family proteins that generate DCAs and since they
33 ndertaken to investigate the consequences of CYP4A overexpression on blood pressure and endothelial f
35 the thyroid gland showed normal induction of CYP4A genes by DHEA in liver, suggesting that their indu
40 id state, induction of the three isozymes of CYP4A (4A1, 4A2, and 4A3) by DHEA was suppressed > 60-80
42 ARalpha-induced genes, especially members of CYP4A family, in determining the severity of steatosis i
46 riod caused as much as an 80% suppression of CYP4A mRNA levels, whereas CYP4A protein levels and func
47 s associated with sequential upregulation of CYP4A and an increase in 20-hydroxyeicosatetraenoic acid
49 are also metabolized by the cytochrome P450 CYP4A omega-oxidation enzymes to toxic dicarboxylic acid
50 are also metabolized by the cytochrome P450 CYP4A omega-oxidation system to dicarboxylic acids that
51 multifamily sequence alignment of the rabbit CYP4A members with the known structure of CYP102 indicat
53 Ts with microsomal and purified forms of rat CYP4A isoforms led to rapid NADPH-dependent metabolism t
54 of covalently bound heme in the recombinant CYP4A proteins increases with time under turnover condit
55 c) fatty acid oxidation is sensitive in some CYP4A enzymes to the presence or absence of the heme cov
62 maller region of chromosome 5 containing the CYP4A genes from a Lewis rat was introgressed onto the S
66 t the heme in cytochrome P450 enzymes of the CYP4A family is covalently attached to the protein throu
67 vailable on the active site structure of the CYP4A family of enzymes or the mechanism by which their
68 en proposed that increased expression of the CYP4A genes is an early event in the development of hype
69 g, and mass spectrometry, establish that the CYP4A class of enzymes has a covalently bound heme group
70 ced reduction in GFR, but ASODN to all three CYP4A isoforms blunted the L-NAME-induced increase in UN
71 0% suppression of CYP4A mRNA levels, whereas CYP4A protein levels and functional activity returned to
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