Tuning Apoptosis and Neuroinflammation: TBK1 Restrains RIPK1

Haiyang Yu; Don W Cleveland

doi:10.1016/j.cell.2018.08.035

Tuning Apoptosis and Neuroinflammation: TBK1 Restrains RIPK1

Cell. 2018 Sep 6;174(6):1339-1341. doi: 10.1016/j.cell.2018.08.035.

Authors

Haiyang Yu¹, Don W Cleveland²

Affiliations

¹ Ludwig Institute for Cancer Research, University of California at San Diego, La Jolla, CA 92093, USA.
² Ludwig Institute for Cancer Research, University of California at San Diego, La Jolla, CA 92093, USA; Department of Cellular and Molecular Medicine, University of California at San Diego, La Jolla, CA 92093, USA. Electronic address: dcleveland@ucsd.edu.

PMID: 30193106
DOI: 10.1016/j.cell.2018.08.035

Abstract

Partial loss of TANK-binding kinase 1 (TBK1) causes amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Xu et al. identify the role of TBK1 in suppressing neuroinflammation and apoptosis by its inhibition of the receptor-interacting serine/threonine-protein kinase 1 (RIPK1) and elucidate how aging and genetic susceptibility together cause neuroinflammation.

Publication types

Comment

MeSH terms

Amyotrophic Lateral Sclerosis*
Apoptosis
Frontotemporal Dementia*
Humans
Inflammation
Mutation
Protein Serine-Threonine Kinases
Receptor-Interacting Protein Serine-Threonine Kinases

Substances

Protein Serine-Threonine Kinases
RIPK1 protein, human
Receptor-Interacting Protein Serine-Threonine Kinases
TBK1 protein, human

Grants and funding

F32 AG059358/AG/NIA NIH HHS/United States