范科尼贫血细胞中，ADP-核糖基转移酶活性的基础水平和诱变剂诱导水平均未改变。

The basal and the mutagen-induced levels of ADP-ribosyl transferase activity are not modified in Fanconi's anemia cells.

作者信息

Scovassi A I, Stefanini M, Izzo R, Lagomarsini P, Bertazzoni U, Moustacchi E

机构信息

Istituto di Genetica Biochimica Evoluzionistica del CNR, Pavia, Italy.

出版信息

Mutat Res. 1989 Jan-Feb;225(1-2):65-9. doi: 10.1016/0165-7992(89)90035-3.

DOI:10.1016/0165-7992(89)90035-3

PMID:2492368

Abstract

The activity of ADP-ribosyl transferase, an enzyme thought to be involved in several basic functions of the chromatin and in DNA repair, has been investigated in normal and Fanconi's anemia (FA) cells. Fibroblasts and lymphoblasts treated with alkylating (dimethyl sulfate) or cross-linking (mitomycin C, psoralen plus UVA) agents were compared to untreated cells. The basal level of the enzymatic activity was found to be the same in normal and FA cells and the enzymatic response to treatments with DNA-damaging agents was similar in both cell types. Consequently it is unlikely that the molecular defect in FA cells is due to a decreased activity in ADP-ribosyl transferase.

摘要

人们认为，ADP核糖基转移酶参与染色质的多种基本功能以及DNA修复过程。我们已对正常细胞和范科尼贫血（FA）细胞中的该酶活性展开了研究。将经烷化剂（硫酸二甲酯）或交联剂（丝裂霉素C、补骨脂素加紫外线A）处理的成纤维细胞和淋巴细胞与未处理的细胞进行了比较。结果发现，正常细胞和FA细胞中酶活性的基础水平相同，且两种细胞类型对DNA损伤剂处理的酶促反应相似。因此，FA细胞中的分子缺陷不太可能是由于ADP核糖基转移酶活性降低所致。