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HRF20/CD59补体调节蛋白的表达取决于表型,并且可被低甲基化剂5-氮杂胞苷在伯基特淋巴瘤细胞系上诱导表达。

HRF20/CD59 complement regulatory protein expression is phenotype-dependent and inducible by the hypomethylating agent 5-azacytidine on Burkitt's lymphoma cell lines.

作者信息

Kuraya M, Minarovits J, Okada H, Klein E

机构信息

Department of Tumor Biology, Karolinska Institute, Stockholm, Sweden.

出版信息

Immunol Lett. 1993 Jul;37(1):35-9. doi: 10.1016/0165-2478(93)90129-p.

Abstract

We studied the expression of the 20-kDa homologous restriction factor (CD59/HRF20), a complement regulatory protein, on two subsets of blood derived B cells and on Burkitt's lymphoma lines. Both low-density (activated) and high-density (resting) B cell populations expressed high levels of CD59. CD59 was detectable, however, only on a minority of cells or not at all on three Epstein-Barr virus (EBV)-negative BL lines (BL41, BL28 and DG75) and on clones of an EBV-positive BL line (Mutu) that phenotypically resembled resting B lymphocytes. On the other hand, CD59 was detected at high or medium levels on Mutu cells which had a lymphoblastoid cell-like phenotype. Expression of CD59 was upregulated by 5-azacytidine, a drug inhibiting cytosine methylation, on CD59-negative cell lines. Induction was accompanied by a partial hypomethylation in the 5' region of CD59 coding sequences.

摘要

我们研究了一种补体调节蛋白——20-kDa同源限制因子(CD59/HRF20)在血液来源的B细胞两个亚群以及伯基特淋巴瘤细胞系中的表达情况。低密度(活化)和高密度(静止)B细胞群体均表达高水平的CD59。然而,在三个爱泼斯坦-巴尔病毒(EBV)阴性的BL细胞系(BL41、BL28和DG75)以及一个表型类似于静止B淋巴细胞的EBV阳性BL细胞系(Mutu)的克隆中,仅在少数细胞上可检测到CD59,或者根本检测不到。另一方面,在具有淋巴母细胞样表型的Mutu细胞上,可检测到高水平或中等水平的CD59。在CD59阴性的细胞系中,5-氮杂胞苷(一种抑制胞嘧啶甲基化的药物)可上调CD59的表达。诱导过程伴随着CD59编码序列5'区域的部分去甲基化。

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