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1 evation of C16-ceramide, and/or elevation of sphinganine.
2 lol, and the sphingoid bases sphingosine and sphinganine.
3 species is conserved up to the formation of sphinganine.
4 t was inhibited by preincubating clusters in sphinganine.
5 increase cellular levels of sphingosine and sphinganine.
6 the 2-amino-1,3-diol polar head of D-erythro-sphinganine.
7 ectively reduced to either erythro- or threo-sphinganines.
13 inds SPP with remarkable specificity as only sphinganine-1-phosphate displaced radiolabeled SPP, whil
15 ntrations of key phosphosphingolipids (e.g., sphinganine-1-phosphate) were associated with increased
16 d-like metabolites such as 9S- and 13S-HODE, sphinganine-1-phosphate, the branched-chain amino acid 3
19 specific for SPP, as only unlabeled SPP and sphinganine-1-phosphate, which lacks the trans double bo
22 c acid, caused sequential formation of [(3)H]sphinganine (220% over control) and [(3)H]ceramide (160%
25 (D-e-deh-Sph, IC50 0.25 mol %), (2S)-3-keto-sphinganine (3-keto-dh-Sph, IC50 0.34 mol %), (2S) 3-ket
29 i (AAL) toxins are members of a new class of sphinganine analog mycotoxins that occur widely in the f
34 vator of PKC, and this effect was blocked by sphinganine and PKC(19-36), inhibitors of PKC in bag cel
37 of the protein kinase C inhibitor D-erythro-sphinganine and the antitumor agent (+)-spisulosine, whe
38 pentacosane, monogalactosyldiacylglycerols, sphinganine, and 12-hydroxyjasmonic acid), which are rec
41 bin activation was inhibited by sphingosine, sphinganine, and stearylamine in the presence but not in
44 ow direct study of cellular sphingosine- and sphinganine-based ceramide levels, we developed a mass s
45 ariations of serum SLs, with sphingosine and sphinganine being, both in univariate (P<0.05) as well a
51 ases (including C2 ceramide, sphingosine, or sphinganine) caused the accumulation of cyt c in the cyt
53 rt-chain alpha-GalCer ligand PBS-25, but its sphinganine chain is more deeply inserted into the F' po
55 It was less potently inhibited by D-erythro-sphinganine (D-e-dh-Sph, IC50 0.20 mol %), D-erythro-deh
57 ion of sphingomyelin (SM) precursors such as sphinganine, dihydroceramide, and ceramide; (b) inhibite
60 or sphingomyelin are not substrates, whereas sphinganine has a limited capacity to accept the acetate
63 eat-induced increase in incorporation of [3H]sphinganine into ceramide as well as the heat-induced in
65 amides (Cers) with consecutive elevations in sphinganine levels has been shown to cause a severe hepa
66 e liver, including elevated C16-ceramide and sphinganine levels in liver and in isolated mitochondria
67 and phosphatidylethanolamine) and cationic (sphinganine) lipids, nucleotides (ATP and CTP), N-ethylm
69 50) = 2.4 and 1.4 microm for sphingosine and sphinganine, respectively) as well as in whole plasma cl
70 es are N-acyl derivatives of sphingosine and sphinganine, respectively, which are the major sphingoid
71 and [(3)H]ceramide (160% over control), with sphinganine returning to baseline at 4 h, and ceramide c
72 its corresponding dihydro-saturated species sphinganine (Sa), are present in cell samples in low abu
74 o significantly reduced urinary excretion of sphinganine (Sa), sphingosine (So), and Sa/So ratio, but
75 ted with improvements in plasma sphingosine, sphinganine sphingomyelin, and dihydrosphingomyelin lipi
76 of FB1, whereas the bioactive intermediates, sphinganine, sphingosine, and ceramide, were without eff
79 esemble the sphingoid bases, sphingosine and sphinganine, that are reported to play critical roles in
80 g1p) capable of catalyzing the conversion of sphinganine to ceramide, in contrast TgCerS2 was catalyt
81 ion in response to 4-HPR treatment, although sphinganine was still generated when 4-HPR and FB(1) wer
82 e versatility of the method, spisulosine and sphinganine were synthesized in two steps from the appro
83 ed with a decrease in plasma sphingosine and sphinganine, which was accompanied by a decrease in sphi