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1 vented by supplementation with the precursor dihydrosphingosine.
2 -dependent reduction of 3-ketosphinganine to dihydrosphingosine.
3 able of phosphorylating both sphingosine and dihydrosphingosine.
4 pecifically dephosphorylate DHS-1-P to yield dihydrosphingosine.
5 al (TRP) channel by modulating the levels of dihydrosphingosine 1 phosphate (DHS1P) and sphingosine 1
6 a protein that specifically dephosphorylates dihydrosphingosine 1-phosphate (DHS-1-P), and we refer t
7 interaction between the sphingolipid agonist dihydrosphingosine 1-phosphate (dhS1P) and the transform
8 that another product of sphingosine kinase, dihydrosphingosine 1-phosphate (dhS1P), has an opposite
12 of SPP and the related phosphorylated lipids dihydrosphingosine 1-phosphate and lysophosphatidic acid
13 pecific, dose-dependent, and competed off by dihydrosphingosine 1-phosphate and lysophosphatidic acid
14 ther structurally related compounds, such as dihydrosphingosine 1-phosphate and lysophosphatidic acid
15 ae, phosphorylated long chain bases, such as dihydrosphingosine 1-phosphate and phytosphingosine 1-ph
16 SB649146 displaced the S1P1 receptor agonist dihydrosphingosine 1-phosphate from membranes expressing
18 YSR2 conferred sphingosine resistance to the dihydrosphingosine-1-P lyase-defective mutant (JS16) of
19 mentable carbon source at 25 degreesC, while dihydrosphingosine-1-phosphate (DHS-1-P) is only barely
22 ion, we propose that enhanced degradation of dihydrosphingosine-1-phosphate allows an alternative pro
23 base phosphate (LCB-P) lyase, encoded by the dihydrosphingosine-1-phosphate lyase1 (AtDPL1) gene and
27 se-1-phosphates (sphingosine-1-phosphate and dihydrosphingosine-1-phosphate) and results in the in ut
29 atment led to pronounced dihydroceramide and dihydrosphingosine accumulation, which preceded morpholo
32 long chain bases (LCBs) phytosphingosine and dihydrosphingosine also suppressed the DspA/E-induced ye
35 ansient increase in the concentration of C18-dihydrosphingosine and C18-phytosphingosine, more than a
36 re than a 100-fold transient increase in C20-dihydrosphingosine and C20-phytosphingosine, and a more
38 stitute an appreciable proportion of cardiac dihydrosphingosine and dihydroceramide, with distinct bi
39 ses occurred in more than one-third of total dihydrosphingosine and dihydroceramides in myocardium, a
40 sphingosine, and S1P but increased levels of dihydrosphingosine and dihydrosphingosine 1-phosphate (D
41 eramide formation from a free fatty acid and dihydrosphingosine and no activity with phytosphingosine
42 nt, the saturated long-chain sphingoid bases dihydrosphingosine and phytosphingosine (Phyto-Sph).
43 FA synthesis, accumulation of high levels of dihydrosphingosine and phytosphingosine, and accumulatio
44 nism by which sphingosine and its analogues, dihydrosphingosine and phytosphingosine, inhibit polymor
45 ) exhibited both an enormous accumulation of dihydrosphingosine and sphingosine and a reduction in ph
46 Vmax of 0.3 micromol/min/mg), but d-erythro-dihydrosphingosine and the three unnatural stereoisomers
48 , including sphingoid bases (sphingosine and dihydrosphingosine) and sphingoid base-1-phosphates (sph
49 malian SphK1 efficiently phosphorylated Sph, dihydrosphingosine, and 4,8-sphingadienine, but not the
50 ted the sphingoid bases phytosphingosine and dihydrosphingosine as the likely mediators of Cha1 up-re
51 ro-2-N-[12'-(1''-pyridinium)-dodecanoyl]-4,5-dihydrosphingosine bromide (C(12)-dhCCPS) to its 4,5-des
52 ollowing in vivo labeling with D-erythro-[3H]dihydrosphingosine, but it slightly affected labeling of
53 ingosine, phytosphingosine, sphingosine, and dihydrosphingosine, but not N-acetyldihydrosphingosine,
54 lecules, including 3-ketodihydrosphingosine, dihydrosphingosine, C(2)-phytoceramide (PHC), and steary
56 and clinical isolates demonstrated elevated dihydrosphingosine (DHS) and phytosphingosine (PHS) leve
57 hich encodes an exporter of long chain bases dihydrosphingosine (DHS) and phytosphingosine (PHS), and
63 C8-Cer) stereoisomers, N-octanoyl-DL-erythro-dihydrosphingosine (DL-e-DHC8-Cer), and a new ceramide d
64 , sphingoid phosphate phosphatase, lyase, or dihydrosphingosine hydroxylase were found to display the
65 duction of the levels of sphingosine but not dihydrosphingosine in response to PMA, and 4) induction
67 ecrease in the incorporation of radiolabeled dihydrosphingosine into ceramide and complex sphingolipi
68 catalysing the conversion of sphingosine or dihydrosphingosine into sphingosine-1-phosphate or dihyd
73 f ceramide resulting from the N-acylation of dihydrosphingosine or sphingosine by ceramide synthase i
75 is reversed by supplying 3-ketosphinganine, dihydrosphingosine, or phytosphingosine in the growth me
81 whether cytotoxicity was enhanced by l-threo-dihydrosphingosine (safingol); (e) whether physiological
84 he inhibitor of sphingosine kinase, DL-threo-dihydrosphingosine, significantly increased the percenta
85 es and the sphingoid bases phytosphingosine, dihydrosphingosine, sphingosine, and sphingosine 1-phosp
91 st sphingoid backbones, phytosphingosine and dihydrosphingosine, were found to be most potent in this
92 strain upon labeling with D-erythro-[4, 5-3H]dihydrosphingosine, whereas overexpression of YSR2 incre
93 ons) and much stronger than that by DL-threo-dihydrosphingosine, which had been considered to be the
94 phingoid bases, C20 phytosphingosine and C20 dihydrosphingosine, which increased 6.4- and 10.8-fold o
95 tive inhibitor of ceramide synthase 2 toward dihydrosphingosine with an apparent K(i) of 2.15 microm.