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本文引用的文献

1
CCR7 coordinates the primary immune response by establishing functional microenvironments in secondary lymphoid organs.CCR7 通过在次级淋巴器官中建立功能性微环境来协调初级免疫反应。
Cell. 1999 Oct 1;99(1):23-33. doi: 10.1016/s0092-8674(00)80059-8.
2
The transcriptional program in the response of human fibroblasts to serum.人类成纤维细胞对血清反应中的转录程序。
Science. 1999 Jan 1;283(5398):83-7. doi: 10.1126/science.283.5398.83.
3
MAL, a novel integral membrane protein of human T lymphocytes, associates with glycosylphosphatidylinositol-anchored proteins and Src-like tyrosine kinases.MAL是人类T淋巴细胞的一种新型整合膜蛋白,与糖基磷脂酰肌醇锚定蛋白和Src样酪氨酸激酶相关。
Eur J Immunol. 1998 Nov;28(11):3675-84. doi: 10.1002/(SICI)1521-4141(199811)28:11<3675::AID-IMMU3675>3.0.CO;2-5.
4
Expression of the MAL gene in the thyroid: the MAL proteolipid, a component of glycolipid-enriched membranes, is apically distributed in thyroid follicles.MAL基因在甲状腺中的表达:MAL蛋白脂质是富含糖脂的膜的一个组成部分,在甲状腺滤泡中呈顶端分布。
Endocrinology. 1998 Apr;139(4):2077-84. doi: 10.1210/endo.139.4.5875.
5
Deletions of p15 and/or p16 genes as a poor-prognosis factor in adult T-cell leukemia.
J Clin Oncol. 1997 May;15(5):1778-85. doi: 10.1200/JCO.1997.15.5.1778.
6
Molecular cloning of a novel human CC chemokine EBI1-ligand chemokine that is a specific functional ligand for EBI1, CCR7.一种新型人类CC趋化因子EBI1配体趋化因子的分子克隆,该趋化因子是EBI1、CCR7的特异性功能配体。
J Biol Chem. 1997 May 23;272(21):13803-9. doi: 10.1074/jbc.272.21.13803.
7
Endocytosis of GPI-anchored proteins in human lymphocytes: role of glycolipid-based domains, actin cytoskeleton, and protein kinases.人淋巴细胞中糖基磷脂酰肌醇锚定蛋白的内吞作用:基于糖脂的结构域、肌动蛋白细胞骨架和蛋白激酶的作用
J Cell Biol. 1996 May;133(4):791-9. doi: 10.1083/jcb.133.4.791.
8
Structural analysis of NADH: ubiquinone oxidoreductase from bovine heart mitochondria.牛心线粒体中NADH:泛醌氧化还原酶的结构分析
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9
Cloning and characterization of MVP17: a developmentally regulated myelin protein in oligodendrocytes.
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10
VIP17/MAL, a proteolipid in apical transport vesicles.VIP17/MAL,一种存在于顶端运输小泡中的蛋白脂质。
FEBS Lett. 1995 Dec 27;377(3):465-9. doi: 10.1016/0014-5793(95)01396-2.

与成人T细胞白血病(ATL)进展相关基因的鉴定。

Identification of genes associated with the progression of adult T cell leukemia (ATL).

作者信息

Kohno T, Moriuchi R, Katamine S, Yamada Y, Tomonaga M, Matsuyama T

机构信息

Department of Molecular Microbiology and Immunology, Nagasaki University Graduate School of Medicine, Nagasaki 852-8523, Japan.

出版信息

Jpn J Cancer Res. 2000 Nov;91(11):1103-10. doi: 10.1111/j.1349-7006.2000.tb00892.x.

DOI:10.1111/j.1349-7006.2000.tb00892.x
PMID:11092974
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5926287/
Abstract

Patients with adult T-cell leukemia/lymphoma (ATL) exhibit a variety of clinical features, and this disease is therefore clinically subclassified into acute, lymphomatous, chronic, and smoldering types. Acute ATL is a typical leukemic form of ATL with rapid progression, and chronic ATL is a less aggressive clinical form allowing long-term survival even without chemotherapy. In the present study, we used fresh peripheral blood mononuclear cells (PBMC) from both types of ATL patients to identify molecules that may contribute to the difference between acute and chronic ATL. Isolated mRNAs expressed differentially between the two types of ATL include a T-cell differentiation antigen (MAL), a lymphoid-specific member of the G-protein-coupled receptor family (EBI-1 / CCR7), a novel human homologue to a subunit (MNLL) of the bovine ubiquinone oxidoreductase complex, and a human fibrinogen-like protein (hpT49). We found that the former three are upregulated in acute ATL and the last is down-regulated in both chronic and acute ATL. We speculate that dysregulation of the genes may account for the malignant features of ATL cells, in terms of growth, energy metabolism, and motility.

摘要

成人T细胞白血病/淋巴瘤(ATL)患者表现出多种临床特征,因此该疾病在临床上被分为急性、淋巴瘤样、慢性和隐匿型。急性ATL是ATL的典型白血病形式,进展迅速,而慢性ATL是一种侵袭性较小的临床形式,即使不进行化疗也能长期存活。在本研究中,我们使用了这两种类型ATL患者的新鲜外周血单个核细胞(PBMC)来鉴定可能导致急性和慢性ATL差异的分子。在两种类型的ATL之间差异表达的分离mRNA包括一种T细胞分化抗原(MAL)、G蛋白偶联受体家族的淋巴特异性成员(EBI-1 / CCR7)、牛泛醌氧化还原酶复合物一个亚基(MNLL)的新型人类同源物以及一种人纤维蛋白原样蛋白(hpT49)。我们发现前三种在急性ATL中上调,最后一种在慢性和急性ATL中均下调。我们推测,这些基因的失调可能在生长、能量代谢和运动性方面解释了ATL细胞的恶性特征。