在人类T细胞白血病中，tal-1基因的编码序列因染色体易位而被破坏。
Coding sequences of the tal-1 gene are disrupted by chromosome translocation in human T cell leukemia.
作者信息
Chen Q, Yang C Y, Tsan J T, Xia Y, Ragab A H, Peiper S C, Carroll A, Baer R
机构信息
Department of Microbiology, University of Texas Southwestern Medical Center, Dallas 75235.
出版信息
J Exp Med. 1990 Nov 1;172(5):1403-8. doi: 10.1084/jem.172.5.1403.
Abstract
The tal-1 proto-oncogene encodes a helix-loop-helix DNA-binding protein that has been implicated in the formation of T cell acute lymphoblastic leukemia (T-ALL). Patients with T-ALL harbor structural rearrangements of tal-1 that result from either local DNA deletion or t(1;14)(p34;q11) chromosome translocation. By analyzing t(1;14)(p34;q11) chromosomes from a series of patients, we have now identified a discrete region of tal-1 wherein most of the translocation breakpoints occur. Moreover, mapping of tal-1 genomic DNA revealed that coding exons are situated on both sides of the t(1;14)(p34;q11) major breakpoint region. Hence, the translocated allele of tal-1 is truncated in a manner that reduces its amino acid coding potential.
摘要
tal-1原癌基因编码一种螺旋-环-螺旋DNA结合蛋白，该蛋白与T细胞急性淋巴细胞白血病（T-ALL）的形成有关。T-ALL患者存在tal-1的结构重排，这是由局部DNA缺失或t(1;14)(p34;q11)染色体易位导致的。通过分析一系列患者的t(1;14)(p34;q11)染色体，我们现已确定tal-1的一个离散区域，其中大多数易位断点发生在此处。此外，tal-1基因组DNA的定位显示，编码外显子位于t(1;14)(p34;q11)主要断点区域的两侧。因此，tal-1的易位等位基因以一种降低其氨基酸编码潜力的方式被截断。
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