Shilatifard A, Lane W S, Jackson K W, Conaway R C, Conaway J W
Program in Molecular and Cell Biology, Oklahoma Medical Research Foundation, Oklahoma City, 73104, USA.
Science. 1996 Mar 29;271(5257):1873-6. doi: 10.1126/science.271.5257.1873.
The human ELL gene on chromosome 19 undergoes frequent translocations with the trithorax-like MLL gene on chromosome 11 in acute myeloid leukemias. Here, ELL was shown to encode a previously uncharacterized elongation factor that can increase the catalytic rate of RNA polymerase II transcription by suppressing transient pausing by polymerase at multiple sites along the DNA. Functionally, ELL resembles Elongin (SIII), a transcription elongation factor regulated by the product of the von Hippel-Lindau (VHL) tumor suppressor gene. The discovery of a second elongation factor implicated in oncogenesis provides further support for a close connection between the regulation of transcription elongation and cell growth.
在急性髓性白血病中,位于19号染色体上的人类ELL基因经常与位于11号染色体上的类三体胸苷酸合成酶MLL基因发生易位。在此,ELL被证明编码一种以前未被鉴定的延伸因子,该因子可通过抑制RNA聚合酶在DNA上多个位点的短暂停顿来提高RNA聚合酶II转录的催化速率。在功能上,ELL类似于延伸蛋白(SIII),后者是一种受冯·希佩尔-林道(VHL)肿瘤抑制基因产物调控的转录延伸因子。发现另一种与肿瘤发生有关的延伸因子,为转录延伸调控与细胞生长之间的紧密联系提供了进一步的支持。