RAP1通过兼职功能激活端粒延长替代途径（ALT）中的NF-κB和Notch信号通路。

RAP1 moonlights to activate NF-κB and Notch in ALT.

作者信息

Churikov Dmitri, Géli Vincent

机构信息

Marseille Cancer Research Centre (CRCM), U1068 INSERM, UMR7258 CNRS, UM105 Aix-Marseille University, Institut Paoli-Calmettes, 13273 Marseille, France.

Ligue Nationale Contre le Cancer (Equipe labellisée), 75103 Paris, France.

出版信息

Sci Signal. 2021 Jun 29;14(689):eabj1166. doi: 10.1126/scisignal.abj1166.

DOI:10.1126/scisignal.abj1166

PMID:34187904

Abstract

Cancer cells activate either telomerase or telomere recombination (ALT) to maintain telomere length and achieve immortalization. In this issue of , Robinson reveal an unanticipated role of the protein SLX4IP in the SUMOylation of RAP1, which enhances its extratelomeric function in activating an NF-κB-Notch signaling axis that favors ALT.

摘要

癌细胞激活端粒酶或端粒重组（ALT）以维持端粒长度并实现永生化。在本期杂志中，罗宾逊等人揭示了蛋白质SLX4IP在RAP1的SUMO化中的意外作用，这增强了其在激活有利于ALT的NF-κB-Notch信号轴中的端粒外功能。