ライフサイエンスコーパス: lactosylceramide

1 ion, and the levels of the glycosphingolipid lactosylceramide.

2 d in neural tissue, by adding sialic acid to lactosylceramide.

3 d diseases-abnormal endocytic trafficking of lactosylceramide.

4 ommon fungal receptors, such as dectin-1 and lactosylceramide.

5 osynthesis of most complex gangliosides from lactosylceramide.

6 D3, GM4 > GM1, GD1a, GD1b, GT1b, GD2, GQ1b > lactosylceramide.

7 ng a fluorescent sphingolipid analog, BODIPY-lactosylceramide.

8 by converting GM2 to GA2 and subsequently to lactosylceramide.

9 1-3)-glucans and by a monoclonal antibody to lactosylceramide.

10 24:1; hexosylceramides-16:0, 22:0, and 24:0; lactosylceramide-16:0; and sphingomyelins 14:0, 16:0, 18

11 m human leukocytes and its identification as lactosylceramide, a major glycosphingolipid of neutrophi

12 tion of the GM3 synthase enzyme (also called lactosylceramide alpha-2,3 sialyltransferase).

13 (globotriaose and isoglobotriaose) and alpha-lactosylceramide (alpha-LacCer).

14 bcellular localization of ST3GalV (CMP-NeuAc:lactosylceramide alpha2,3 sialyltransferase/GM3 synthase

15 atly reduced levels of GM3 and GM3 synthase (lactosylceramide alpha2,3-sialyltransferase) mRNA in bot

16 utant mice that lack GM3 synthase (CMP-NeuAc:lactosylceramide alpha2,3-sialyltransferase; EC 2.4.99.-

17 was accompanied by a decrease in the mass of lactosylceramide and an increase in glucosylceramide (Gl

18 abnormal intracellular trafficking of BODIPY-lactosylceramide and an increase of sterols in the cultu

19 glycerophosphocholine, glycerophosphoserine, lactosylceramide and bilirubin were lower in the confirm

20 estoration of Golgi targeting of fluorescent lactosylceramide and endogenous GM(1) ganglioside, and a

21 orescent analogues of the glycosphingolipids lactosylceramide and globoside almost exclusively by a c

22 bstrate clone 15, we found that analogues of lactosylceramide and globoside were internalized almost

23 biosynthetic derivatives and an increase in lactosylceramide and its alternative derivatives.

24 a lesser extent, inhibited the formation of lactosylceramides and gangliosides.

25 In particular, levels of lactosylceramides and glycosphingolipids were decreased

26 Most prominently lactosylceramide, and additionally ceramide, glucosylcer

27 nd sphingomyelin but normal hexosylceramide, lactosylceramide, and different sphingosines compared wi

28 h ceramide, sphingomyelin, glucosylceramide, lactosylceramide, and ganglioside G(D3) (a composition s

29 sulfated glycosphingolipids sulfatide, sulf-lactosylceramide, and sulf-globopentaosylceramide.

30 ils, myeloblasts expressed glucosylceramide, lactosylceramide, and the neolacto-family GSLs, lactotri

31 the glycosphingolipids glucosylceramide and lactosylceramide are present at very low levels in non-i

32 ganisms, this represents the first report of lactosylceramide binding to a macromolecular carbohydrat

33 bstrates, GM3-BODIPY-FL, GM1-BODIPY-TMR, and lactosylceramide-BODIPY-650/665.

34 ructures of apo-GLTP (1.65 A resolution) and lactosylceramide-bound (1.95 A) GLTP, in which the bound

35 g it to GA2 and further hydrolysis of GA2 to lactosylceramide by HexB with the assistance of mouse GM

36 w that addition of the glycosphingolipid, C8-lactosylceramide (C8-LacCer), or free cholesterol to hum

37 We used a fluorescent analogue of lactosylceramide, called N-[5-(5,7-dimethylborondipyrrom

38 hile phosphatidylethanolamine, ceramide, and lactosylceramide cannot.

39 on by the exogenous addition of GM3, but not lactosylceramide, caused enhanced c-Src phosphorylation

40 ected against the membrane glycosphingolipid lactosylceramide (CDw17) results in a significant decrea

41 decreased levels of ceramide, sphingomyelin, lactosylceramide, ceramide trihexoside, and globoside an

42 Pro-inflammatory metabolites, including lactosylceramides, ceramides, lysophospholipids, and lys

43 However, DL-lactosylceramides containing dihydrosphingosine did not

44 tion of 12 Ga2 isoforms/analogues from their lactosylceramide counterparts, was developed and validat

45 otein-2 (MIP-2) from isolated AECs through a lactosylceramide-dependent mechanism.

46 Lactosylceramides from human leukocytes were fractionate

47 zed as galactosylceramide, glucosylceramide, lactosylceramide, galabiaosylceramide, globotriaosylcera

48 Both transferases act on lactosylceramide, Galbeta1,4Glcbeta1Cer (LacCer), to pro

49 osylceramide, the monosialoganglioside, GM3, lactosylceramide, globoside, the disialoganglioside, GD3

50 In particular, lactosylceramide, globotriaosylceramide (Gb3), and monos

51 amide, glucosylceramide, galactocerebroside, lactosylceramide, globotriaosylceramide, and the ganglio

52 y) LC/MS identified substantial increases in lactosylceramide in AB-/- mouse livers.

53 knockout mice show a massive accumulation of lactosylceramide in all tissues.

54 DO-P4 depleted cellular glucosylceramide and lactosylceramide in cultured ECV304 cells at nanomolar c

55 The levels of glucosylceramide and lactosylceramide increased in parallel with Gb3 levels i

56 creased sphingomyelines, hexosylceramide and lactosylceramide indicated impaired sphingolipid metabol

57 Lactosylceramide (LacCer 44:5) and glucosylceramide (Glc

58 Since lactosylceramide (LacCer) accumulates in large quantitie

59 n the endocytosis of BODIPYtrade mark-tagged lactosylceramide (LacCer) analogs via caveolae.

60 Lactosylceramide (LacCer) and globotriaosylceramide (Tri

61 lation increased the intracellular levels of lactosylceramide (LacCer) and induced GFAP expression an

62 atment increased the intracellular levels of lactosylceramide (LacCer) and induced iNOS gene expressi

63 aposin C led to moderate increases in GC and lactosylceramide (LacCer) and their deacylated analogues

64 ere incubated with a fluorescent analogue of lactosylceramide (LacCer) at 16 degrees C to label early

65 Previously, our laboratory has shown that lactosylceramide (LacCer) can serve as a mitogenic agent

66 In addition, fluorescent lactosylceramide (LacCer) colocalized with DsRed-cav-1 i

67 Lactosylceramide (LacCer) is a key intermediate in glyco

68 Lactosylceramide (LacCer) is a pivotal intermediate in t

69 we found that glucosylceramide (GlcCer) and lactosylceramide (LacCer) levels are significantly highe

70 Previously, our laboratory reported that lactosylceramide (LacCer) stimulated human aortic smooth

71 Here we report that lactosylceramide (LacCer) synthesized by beta-1,4-galact

72 s a sialic acid to the terminal galactose of lactosylceramide (LacCer) to produce the monosialylated

73 Minor storage of lactosylceramide (LacCer) was observed when compared wit

74 A fluorescent analog of lactosylceramide (LacCer) was used to study plasma membr

75 We have previously reported that lactosylceramide (LacCer), a ubiquitous GSL, stimulates

76 fluorescent glycosphingolipid analog, BODIPY-lactosylceramide (LacCer), and compared this to fluoresc

77 Glucosylceramide (GlcCer), lactosylceramide (LacCer), and globotriaosylceramide (Gb

78 tein gp120 (rgp120) with natural isolates of lactosylceramide (LacCer), glucosylceramide (GlcCer), an

79 Addition of its product, lactosylceramide (LacCer), reversed apoptosis due to UGC

80 of mhtt inhibited internalization of BODIPY-lactosylceramide (LacCer), which is internalized by a ca

81 by the co-analysis of its structural isomer, lactosylceramide (LacCer), which is not an alpha-GAL A s

82 nied with a 32-fold increase in the level of lactosylceramide (LacCer).

83 We identified an association of lactosylceramides (LacCer) with AD-related single-nucleo

84 iGb(3) synthase acts on lactosylceramide, LacCer (Galbeta1,4Glcbeta1Cer) to form

85 pids such as phosphatidylethanolamines (PE), lactosylceramides (LCER) and phosphatidylinositols (PI)

86 ficantly decreased renal neuraminidase 1 and lactosylceramide levels.

87 cholesterol levels and a 3-fold increase in lactosylceramide levels.

88 declining activity of the regulatory enzyme lactosylceramide N-acetylglucosaminyltransferase (GlcNAc

89 The enzymes studied were lactosylceramide: N-acetylglucosaminyl transferase (GlcN

90 oated plates through interaction of GM3 with lactosylceramide or Gg3, whereby not only adhesion but a

91 containing glycolipid (galactosylceramide or lactosylceramide) or from monosialoganglioside dispersio

92 abetes, whereas scores of glycosylceramides, lactosylceramides, or other unsaturated sphingomyelins (

93 nt presence of ganglioside GM3 and adhere to lactosylceramide- or Gg3-coated plates through interacti

94 alactosidase functions in the degradation of lactosylceramide preferentially in the liver.

95 of the anti-CDw17 antibody with solubilized lactosylceramide reverses this effect.

96 Lactosylceramide specifically induced c-fos mRNA express

97 We found that lactosylceramide stimulated (7-fold) the loading of GTP

98 -galactosidase activities than HBEC, whereas lactosylceramide synthase (GalT2) activity was higher in

99 gmented, ceramide glucosyltransferase (CGT), lactosylceramide synthase (GalT2), Gb3 synthase (GalT6),

100 n inhibitor of glucosylceramide synthase and lactosylceramide synthase (LCS: beta-1,4-GalT-V), showed

101 amide synthase activities but did not affect lactosylceramide synthase activities or mRNA content.

102 n, Ca(2+) deposits, and glucosylceramide and lactosylceramide synthase activity.

103 e (D2); (C). reduced expression 3 gene; (D). lactosylceramide synthase; and (E). septin 4, respective

104 s hexosylceramides (HexCers) and galabiosyl-/lactosylceramides that appear to be correlated with the

105 nd that application of the glycosphingolipid lactosylceramide to CLN3-deficient cells rescues protein

106 eliglustat, partially corrected the impaired lactosylceramide trafficking defect and immediately sugg

107 The binding of radiolabeled PGG-glucan to lactosylceramide was not inhibited by glycogen, dextran,

108 nding of radiolabeled PGG-glucan to purified lactosylceramide was saturable, specific, and time- and

109 (D1a), was the most active molecule, whereas lactosylceramide was the least active one, indicating re