Diatloff-Zito C, Duchaud E, Viegas-Pequignot E, Fraser D, Moustacchi E
Institut Curie-Biologie, CNRS URA 1292, Paris, France.
Mutat Res. 1994 May 1;307(1):33-42. doi: 10.1016/0027-5107(94)90275-5.
Fanconi anemia (FA) cells, complementation group D, which had been transfected with mouse genomic DNA were partially corrected for their mitomycin C (MMC) hypersensitivity. A genomic DNA fragment which complements the resistance of FA(D) cells to MMC close to normal level has been cloned; it has no correcting activity in FA group A cells. It contains two highly conserved regions between the mouse and human genome, which flank mouse repeated DNA. This DNA fragment detects a 3.6-4-kb mRNA transcript in human cells. Moreover this fragment maps to chromosome 11q23, a region of particular interest since several genes involved in the control of major cellular functions are located in this area. This DNA fragment may belong to a gene directly or indirectly involved in FA(D) function.
用小鼠基因组DNA转染的范可尼贫血（FA）D互补组细胞，其对丝裂霉素C（MMC）的超敏反应得到了部分纠正。一个能使FA（D）细胞对MMC的抗性恢复至接近正常水平的基因组DNA片段已被克隆；它对FA A组细胞没有纠正活性。它在小鼠和人类基因组之间包含两个高度保守的区域，这两个区域位于小鼠重复DNA两侧。该DNA片段在人类细胞中检测到一个3.6 - 4kb的mRNA转录本。此外，该片段定位于11号染色体q23区，这是一个特别受关注的区域，因为几个参与主要细胞功能控制的基因位于该区域。这个DNA片段可能属于一个直接或间接参与FA（D）功能的基因。
