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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.
11 inds SPP with remarkable specificity as only sphinganine-1-phosphate displaced radiolabeled SPP, whil
14 specific for SPP, as only unlabeled SPP and sphinganine-1-phosphate, which lacks the trans double bo
16 c acid, caused sequential formation of [(3)H]sphinganine (220% over control) and [(3)H]ceramide (160%
19 (D-e-deh-Sph, IC50 0.25 mol %), (2S)-3-keto-sphinganine (3-keto-dh-Sph, IC50 0.34 mol %), (2S) 3-ket
23 i (AAL) toxins are members of a new class of sphinganine analog mycotoxins that occur widely in the f
27 vator of PKC, and this effect was blocked by sphinganine and PKC(19-36), inhibitors of PKC in bag cel
29 of the protein kinase C inhibitor D-erythro-sphinganine and the antitumor agent (+)-spisulosine, whe
32 bin activation was inhibited by sphingosine, sphinganine, and stearylamine in the presence but not in
35 ow direct study of cellular sphingosine- and sphinganine-based ceramide levels, we developed a mass s
36 ariations of serum SLs, with sphingosine and sphinganine being, both in univariate (P<0.05) as well a
42 ases (including C2 ceramide, sphingosine, or sphinganine) caused the accumulation of cyt c in the cyt
43 rt-chain alpha-GalCer ligand PBS-25, but its sphinganine chain is more deeply inserted into the F' po
45 It was less potently inhibited by D-erythro-sphinganine (D-e-dh-Sph, IC50 0.20 mol %), D-erythro-deh
47 ion of sphingomyelin (SM) precursors such as sphinganine, dihydroceramide, and ceramide; (b) inhibite
50 or sphingomyelin are not substrates, whereas sphinganine has a limited capacity to accept the acetate
53 eat-induced increase in incorporation of [3H]sphinganine into ceramide as well as the heat-induced in
54 amides (Cers) with consecutive elevations in sphinganine levels has been shown to cause a severe hepa
55 e liver, including elevated C16-ceramide and sphinganine levels in liver and in isolated mitochondria
56 and phosphatidylethanolamine) and cationic (sphinganine) lipids, nucleotides (ATP and CTP), N-ethylm
58 50) = 2.4 and 1.4 microm for sphingosine and sphinganine, respectively) as well as in whole plasma cl
59 es are N-acyl derivatives of sphingosine and sphinganine, respectively, which are the major sphingoid
60 and [(3)H]ceramide (160% over control), with sphinganine returning to baseline at 4 h, and ceramide c
61 its corresponding dihydro-saturated species sphinganine (Sa), are present in cell samples in low abu
63 o significantly reduced urinary excretion of sphinganine (Sa), sphingosine (So), and Sa/So ratio, but
64 of FB1, whereas the bioactive intermediates, sphinganine, sphingosine, and ceramide, were without eff
67 esemble the sphingoid bases, sphingosine and sphinganine, that are reported to play critical roles in
68 ion in response to 4-HPR treatment, although sphinganine was still generated when 4-HPR and FB(1) wer
69 e versatility of the method, spisulosine and sphinganine were synthesized in two steps from the appro
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