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1 fluids as a result of P450 7A1 oxidation of 7-dehydrocholesterol.
2 rs of ecdysone biosynthesis, cholesterol and 7-dehydrocholesterol.
3 d in skin through ultraviolet irradiation of 7-dehydrocholesterol.
4 (2020) reveal that type I IFN signaling and 7-dehydrocholesterol (7-DHC) accumulation form a positiv
5 ciency or treatment with the natural product 7-dehydrocholesterol (7-DHC) could specifically promote
8 ) is biochemically characterized by elevated 7-dehydrocholesterol (7-DHC) levels in neonates, raising
12 ased activation of SREBP2 and a reduction in 7-dehydrocholesterol (7-DHC) reductase (DHCR7) expressio
15 n with standard, the identity of this ion is 7-dehydrocholesterol (7-DHC), an immediate dehydrogenate
16 radical chain oxidation of highly oxidizable 7-dehydrocholesterol (7-DHC), initiated by 2,2'-azobis(4
17 The mechanism of free radical oxygenation of 7-dehydrocholesterol (7-DHC), one of the biologically im
18 g ferroptosis through dictating the level of 7-dehydrocholesterol (7-DHC)-an intermediate metabolite
24 d adrenals produced robust transformation of 7-dehydrocholesterol (7-DHC; precursor to cholesterol an
26 hether novel pathways of vitamin D3 (D3) and 7-dehydrocholesterol (7DHC) metabolism initiated by CYP1
30 urprisingly ergosterol, a fungal sterol, and 7-dehydrocholesterol, a sterol present in elevated level
31 cholesterol synthesis, increasing levels of 7-dehydrocholesterol-a potent endogenous ferroptosis inh
32 synthesis pathway to generate intermediates-7-dehydrocholesterol and 7-dehydrodesmosterol-with prote
33 duced 94 mug/g vitamin D(3) from crystalline 7-dehydrocholesterol and 74 mug/g vitamin D(2) from crys
34 roduction.(12-16) Two other pathways produce 7-dehydrocholesterol and bile acid intermediates, neithe
36 e potently reversed by crude lipid extracts, 7-dehydrocholesterol, and a recently identified DAF-12 s
37 In addition, we describe the metabolism of 7-dehydrocholesterol by CYP11A1 to a single product iden
39 piperazin-4-yl]ethyl]-benzoic acid) inhibits 7-dehydrocholesterol delta 7-reductase activity, reduces
40 ed birth disorder caused by markedly reduced 7-dehydrocholesterol delta 7-reductase activity, the fin
41 reductase, lathosterol 5-dehydrogenase, and 7-dehydrocholesterol delta 7-reductase are down-regulate
42 tic pathway, lathosterol 5-dehydrogenase and 7-dehydrocholesterol delta 7-reductase, were measured.
44 , lovastatin, and BM 15.766, an inhibitor of 7-dehydrocholesterol delta7-reductase, and were compared
47 e catalyzes the conversion of lathosterol to 7-dehydrocholesterol in the next to last step of cholest
48 old increase of the 27-hydroxy metabolite of 7-dehydrocholesterol in the plasma of children with Smit
49 The content of the vitamin D(3) precursor 7-dehydrocholesterol in the skin of obese and nonobese s
50 Solar ultraviolet B photons are absorbed by 7-dehydrocholesterol in the skin, leading to its transfo
51 in the pathway, lead to the accumulation of 7-dehydrocholesterol in tissues and fluids of SLOS patie
52 ncentrations reduced 25%, and the precursor, 7-dehydrocholesterol, increased to represent 71% of the
55 holesterol (k(p)= 11 +/- 2 M(-1) s(-1)), and 7-dehydrocholesterol (k(p)= 2260 +/- 40 M(-1) s(-1)).
57 ces plasma cholesterol levels, and increases 7-dehydrocholesterol levels to reproduce the biochemical
60 he consequences of the extreme reactivity of 7-dehydrocholesterol on human health is the focus of a c
63 shed by a strong and selective inhibition of 7-dehydrocholesterol reductase (7-DHCR, EC 1.3.1.21), an
64 rol reductase (C14SR, also known as TM7SF2), 7-dehydrocholesterol reductase (DHCR7) and 24-dehydrocho
65 Here, we identify proferroptotic activity of 7-dehydrocholesterol reductase (DHCR7) and an unexpected
66 utations in both copies in the gene encoding 7-dehydrocholesterol reductase (DHCR7) cause Smith-Lemli
69 sterol reductases in cholesterol production, 7-dehydrocholesterol reductase (DHCR7), 14-dehydrocholes
70 pitz syndrome (SLOS) is caused by defects in 7-dehydrocholesterol reductase (DHCR7), an enzyme cataly
72 fferent autosomal recessive mutations of the 7-dehydrocholesterol reductase gene leading to deficient
74 1790349, located in DHCR7, the gene encoding 7-dehydrocholesterol reductase that synthesizes choleste
77 crophage cells with a raft-promoting sterol (7-dehydrocholesterol) rescued this phagocytic deficiency
80 reductase that synthesizes cholesterol from 7-dehydrocholesterol; rs6599638 in the region harboring
82 76% and was associated with a marked rise of 7-dehydrocholesterol that could be almost entirely preve
83 esterol have been established, we found that 7-dehydrocholesterol (the immediate precursor of cholest
84 free radical propagation rate constants, and 7-dehydrocholesterol, the immediate biosynthetic precurs
85 nd relative plasma cholesterol, but not with 7-dehydrocholesterol, the immediate precursor, confirmin
86 aenoate (20:5), docosahexaenoate (22:6), and 7-dehydrocholesterol to be 115 +/- 7, 145 +/- 8, 172 +/-
87 y rat liver microsomes, of the conversion of 7-dehydrocholesterol to cholesta-5,8-dien-3 beta-ol is a
88 an enzyme responsible for the conversion of 7-dehydrocholesterol to cholesterol in the last step of
90 tase gene leading to deficient conversion of 7-dehydrocholesterol to cholesterol, the RSH (so-called
92 UVB, 280-310 nm) results in isomerization of 7-dehydrocholesterol to previtamin D that spontaneously
93 that is initiated by the photoconversion of 7-dehydrocholesterol to previtamin D(3) An action spectr
94 olet B light we found that the conversion of 7-dehydrocholesterol to previtamin D3 was reduced in chi
95 7A1 converted lathosterol (Delta(5)-dihydro-7-dehydrocholesterol) to a mixture of the 7-keto and 7al
98 containing 7-8 double bonds (lathosterol and 7-dehydrocholesterol) were better raft stabilizers than
99 s of cholesterol/desmosterol and cholesterol/7-dehydrocholesterol (which represent 24- and 7-reductas