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1                                              CYP4A and Nox oxidase expression was upregulated in glom
2                                              CYP4A(+) TAM infiltration was positively associated with
3 through lipoxygenase and cytochrome P450 4A (CYP4A) pathways.
4 of NOS increased omega-hydroxylase activity, CYP4A expression, and renal efflux of 20-HETE, whereas 2
5  activity is sensitive in some, but not all, CYP4A enzymes to the extent of covalent heme binding.
6 and ubiquitin conjugates, but does not alter CYP4A or most other microsomal proteins.
7                                     Although CYP4A expression was not derepressed in liver or kidneys
8                                     Although CYP4A-derived 20-HETE is known to have prohypertensive a
9  inhibitors of lipoxygenases (baicalein) and CYP4A (17-octadecynoic acid), but not of cyclooxygenase
10            Cytochromes P450 of the CYP2C and CYP4A gene subfamilies metabolize arachidonic acid to 5,
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
13 xylase activity (1.4-2.0-fold increases) and CYP4A protein levels.
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
17 gration and fibroblast activation induced by CYP4A.
18                         Generation of ROS by CYP4A monooxygenases, 20-HETE, and Nox oxidases is invol
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
21 asal UNaV suggesting a differential role for CYP4A isoforms in the regulation of renal function.
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
25 t PPARalpha is strictly required for hepatic CYP4A induction by starvation and diabetes.
26                                  The hepatic CYP4A enzymes are important fatty acid and prostaglandin
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
32      Clofibrate-induced expression of kidney CYP4A mRNAs was also blocked in the PPAR alpha gene knoc
33 ndertaken to investigate the consequences of CYP4A overexpression on blood pressure and endothelial f
34 ynthesis and downregulated the expression of CYP4A isoforms in renal microsomes.
35 the thyroid gland showed normal induction of CYP4A genes by DHEA in liver, suggesting that their indu
36            The pharmacological inhibition of CYP4A reduced lung pre-metastatic niche formation (evide
37 enol) formamidine (HET0016), an inhibitor of CYP4A, and were mimicked by 20-HETE.
38 tment with HET0016, a selective inhibitor of CYP4A-catalyzed reactions.
39 was offset by treatment with an inhibitor of CYP4A.
40 id state, induction of the three isozymes of CYP4A (4A1, 4A2, and 4A3) by DHEA was suppressed > 60-80
41           After 4 weeks of age, the level of CYP4A mRNA, enzyme activity, and protein were similar in
42 ARalpha-induced genes, especially members of CYP4A family, in determining the severity of steatosis i
43                Conversely, overexpression of CYP4A or exogenous addition of 20-hydroxyeicosatetraenoi
44      These results suggest that a product of CYP4A product, possibly 20-HETE, plays a critical role i
45 s ARE-containing genes, and up-regulation of CYP4A genes.
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
48 reactive protein but not of CYP1A, CYP3A, or CYP4A.
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
52 dogenous substrates so far described for rat CYP4A isoforms.
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
56                                  In summary, CYP4A in TAMs is crucial for lung pre-metastatic niche f
57             We conclude from these data that CYP4A isoforms contribute to different extents to basal
58 l ring-hydroxylase activity, indicating that CYP4A, 1A, and 2E1 do not support this reaction.
59                                          The CYP4A enzymes catalyze the formation of 20-hydroxyeicosa
60                                          The CYP4A fatty acid omega-hydroxylases are involved in impo
61 s reversible by a low-sodium diet and by the CYP4A inhibitor HET0016.
62 maller region of chromosome 5 containing the CYP4A genes from a Lewis rat was introgressed onto the S
63      Transfer of chromosome 5 containing the CYP4A genes responsible for the formation of 20-HETE fro
64             The prosthetic heme group in the CYP4A family of cytochrome P450 enzymes is covalently at
65                             Induction of the CYP4A enzymes by peroxisome proliferators is mediated th
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
72  and metastatic burden in the lungs, whereas CYP4A inhibition attenuated these effects.

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