The phospho-barcode of RIPK1: complementarity or redundancy?

Wenxian Wu; Björn Stork

doi:10.1080/23723556.2020.1776085

The phospho-barcode of RIPK1: complementarity or redundancy?

Mol Cell Oncol. 2020 Jul 16;7(5):1776085. doi: 10.1080/23723556.2020.1776085. eCollection 2020.

Authors

Wenxian Wu¹, Björn Stork¹

Affiliation

¹ Institute of Molecular Medicine I, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.

Abstract

Receptor interacting serine/threonine kinase 1 (RIPK1) is the central mediator of tumor necrosis factor (TNF) signaling. It regulates both pro-survival/pro-inflammatory and cell death pathways. In order to fulfill this complex regulation, RIPK1 is regulated by several post-translational modifications, including ubiquitination, acetylation, and phosphorylation. In our recent work, we show that the unc-51-like autophagy activating kinase 1 (ULK1) phosphorylates RIPK1 at Ser357 and thus blocks TNF-induced cell death.

Keywords: Autophagy; RIPK1; TNF; Ulk1; necroptosis.

Grants and funding

This work was supported by the Deutsche Forschungsgemeinschaft STO 864/4-1, STO 864/5-1 and GRK 2158 (to BS), and the Düsseldorf School of Oncology (to BS; funded by the Comprehensive Cancer Center Düsseldorf/Deutsche Krebshilfe and the Medical Faculty of the Heinrich Heine University Düsseldorf).