Robb L, Begley C G
Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia.
Bioessays. 1997 Jul;19(7):607-13. doi: 10.1002/bies.950190711.
SCL (TAL1/TCL5) is a member of the helix-loop-helix family of transcription factors. Originally identified because of its involvement in a tumour-specific chromosomal translocation, overexpression of the SCL gene is the most common molecular abnormality found in human T cell leukaemia. Transgenic models have now formally demonstrated that overexpression of SCL within the T cell lineage is capable of causing malignant transformation. Gene targeting experiments have revealed that the SCL gene is crucial for the development of primitive haematopoiesis in the mouse and is also required for the generation of all adult haematopoietic lineages. Biochemical studies have indicated some of the proteins which interact with SCL and this has refined the hypotheses concerning the mechanisms by which SCL plays a role in leukaemogenesis and haematopoietic development.
SCL(TAL1/TCL5)是转录因子螺旋-环-螺旋家族的成员。最初因其参与肿瘤特异性染色体易位而被鉴定出来,SCL基因的过表达是人类T细胞白血病中最常见的分子异常。转基因模型现已正式证明,T细胞谱系中SCL的过表达能够导致恶性转化。基因靶向实验表明,SCL基因对小鼠原始造血的发育至关重要,也是所有成年造血谱系生成所必需的。生化研究已经指出了一些与SCL相互作用的蛋白质,这完善了关于SCL在白血病发生和造血发育中发挥作用机制的假说。