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Cancer Res. 1999 Jul 1;59(13):3053-8.
4
The extracellular-signal-regulated protein kinases (Erks) are required for UV-induced AP-1 activation in JB6 cells.细胞外信号调节蛋白激酶(Erks)是JB6细胞中紫外线诱导的AP-1激活所必需的。
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Translocation of protein kinase Cepsilon and protein kinase Cdelta to membrane is required for ultraviolet B-induced activation of mitogen-activated protein kinases and apoptosis.蛋白激酶Cε和蛋白激酶Cδ转位至细胞膜是紫外线B诱导丝裂原活化蛋白激酶激活及凋亡所必需的。
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7
N-Oleoylethanolamine inhibits glucosylation of natural ceramides in CHP-100 neuroepithelioma cells: possible implications for apoptosis.N-油酰乙醇胺抑制CHP-100神经上皮瘤细胞中天然神经酰胺的糖基化:对细胞凋亡的潜在影响。
Biochem Biophys Res Commun. 1999 Feb 16;255(2):456-9. doi: 10.1006/bbrc.1999.0230.
8
Accumulation of various N-acylethanolamines including N-arachidonoylethanolamine (anandamide) in cadmium chloride-administered rat testis.在给予氯化镉的大鼠睾丸中,包括N-花生四烯酰乙醇胺(花生四烯酸乙醇胺)在内的各种N-酰基乙醇胺的积累。
Arch Biochem Biophys. 1998 Jun 15;354(2):303-10. doi: 10.1006/abbi.1998.0688.
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Alternative pathways of anandamide biosynthesis in rat testes.大鼠睾丸中花生四烯酸乙醇胺生物合成的替代途径。
Chem Phys Lipids. 1998 Mar;92(1):27-35. doi: 10.1016/s0009-3084(97)00109-6.
10
'Endocannabinoids' and other fatty acid derivatives with cannabimimetic properties: biochemistry and possible physiopathological relevance.“内源性大麻素”及其他具有大麻素模拟特性的脂肪酸衍生物:生物化学及可能的生理病理相关性
Biochim Biophys Acta. 1998 Jun 15;1392(2-3):153-75. doi: 10.1016/s0005-2760(98)00042-3.

应激诱导小鼠表皮JB6 P+细胞中N-酰基乙醇胺的生成。

Stress-induced generation of N-acylethanolamines in mouse epidermal JB6 P+ cells.

作者信息

Berdyshev E V, Schmid P C, Dong Z, Schmid H H

机构信息

The Hormel Institute, University of Minnesota, 801 16th Avenue NE, Austin, MN 55912, USA.

出版信息

Biochem J. 2000 Mar 1;346 Pt 2(Pt 2):369-74.

PMID:10677355
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1220862/
Abstract

It has long been known that N-acylethanolamine phospholipids [N-acylphosphatidylethanolamine (N-acyl PE)] and N-acylethanolamines (NAEs) accumulate in mammalian tissues undergoing degenerative membrane changes associated with necrosis. Here we studied the effects of stress factors (UVB irradiation and serum deprivation) on the endogenous levels of N-acyl PE and NAE in mouse epidermal JB6 P(+) cells. We found that 16:0, 18:0, 18:1,n-9 and 18:1,n-7 are the predominant amide-linked fatty acids in both N-acyl PE and NAE in these cells. UVB irradiation and serum deprivation resulted in significantly increased levels of N-acyl PE and NAE, especially 18:1, n-9 N-acyl PE and NAE. UVB challenge increased the cellular content of anandamide (20:4,n-6 NAE), but this increase was the lowest of all NAEs measured. Serum deprivation resulted in a decreased cellular anandamide level, as well as a decrease in 20:4,n-6 N-acyl PE. Interestingly, the replacement of serum-free medium with medium containing 5% (v/v) fetal calf serum after 36 h of serum deprivation restored N-acyl PE and NAE levels almost completely within 4-8 h. These data suggest the involvement of N-acyl PE and NAE in cellular responses to stress.

摘要

长期以来,人们一直知道N-酰基乙醇胺磷脂[N-酰基磷脂酰乙醇胺(N-酰基PE)]和N-酰基乙醇胺(NAEs)在经历与坏死相关的退行性膜变化的哺乳动物组织中积累。在此,我们研究了应激因素(UVB照射和血清剥夺)对小鼠表皮JB6 P(+)细胞中N-酰基PE和NAE内源性水平的影响。我们发现,16:0、18:0、18:1,n-9和18:1,n-7是这些细胞中N-酰基PE和NAE中主要的酰胺连接脂肪酸。UVB照射和血清剥夺导致N-酰基PE和NAE水平显著升高,尤其是18:1,n-9 N-酰基PE和NAE。UVB刺激增加了花生四烯乙醇胺(20:4,n-6 NAE)的细胞含量,但这种增加在所有测量的NAEs中是最低的。血清剥夺导致细胞花生四烯乙醇胺水平降低,以及20:4,n-6 N-酰基PE减少。有趣的是,在血清剥夺36小时后,用含有5%(v/v)胎牛血清的培养基替换无血清培养基,在4-8小时内几乎完全恢复了N-酰基PE和NAE水平。这些数据表明N-酰基PE和NAE参与了细胞对应激的反应。