B 细胞中 E3 泛素连接酶 ARF-BP1 缺失导致的体内平衡缺陷可通过 MYC 的增强表达得到恢复。
Homeostatic defects in B cells deficient in the E3 ubiquitin ligase ARF-BP1 are restored by enhanced expression of MYC.
机构信息
Virology and Cellular Immunology Section, Laboratory of Immunogenetics, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, United States.
出版信息
Leuk Res. 2013 Dec;37(12):1680-9. doi: 10.1016/j.leukres.2013.09.009. Epub 2013 Sep 20.
Abstract
The E3 ligase ARF-BP1 governs the balance of life and death decisions by directing the degradation of p53 and enhancing the transcriptional activity of MYC. We find B cells selectively deficient in ARF-BP1 have many defects in developing and mature B cells associated with increased expression of p53 and reduced expression of Myc. Overexpression of Myc results in suppression of p53 and complete reversal of defects induced by ARF-BP1 deficiency. These findings indicate that the dynamic balance between MYC and p53 required for normal B cell maturation and function is finely tuned and critically dependent on the activities of ARF-BP1.
摘要
E3 连接酶 ARF-BP1 通过指导 p53 的降解和增强 MYC 的转录活性来控制生死决定的平衡。我们发现 ARF-BP1 选择性缺乏的 B 细胞在发育和成熟 B 细胞中存在许多缺陷，这些缺陷与 p53 表达增加和 Myc 表达减少有关。Myc 的过表达导致 p53 抑制和 ARF-BP1 缺乏引起的缺陷完全逆转。这些发现表明，正常 B 细胞成熟和功能所需的 MYC 和 p53 之间的动态平衡是精细调节的，并且严重依赖于 ARF-BP1 的活性。
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