STeerING PI4P for innate immune activation

Chao Qin; Shu Feng; Pinghui Feng

doi:10.1016/j.immuni.2023.02.012

STeerING PI4P for innate immune activation

Immunity. 2023 Mar 14;56(3):463-465. doi: 10.1016/j.immuni.2023.02.012.

Authors

Chao Qin¹, Shu Feng², Pinghui Feng³

Affiliations

¹ Section of Infection and Immunity, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA.
² Department of Diabetes & Cancer Metabolism, Beckman Research Institute, City of Hope, Duarte, CA, USA.
³ Section of Infection and Immunity, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA; Department of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Los Angeles, CA, USA. Electronic address: pinghuif@usc.edu.

PMID: 36921569
DOI: 10.1016/j.immuni.2023.02.012

Abstract

STING transverses the endoplasmic reticulum (ER), Golgi, and endosomal compartments before its degradation within the lysosomes. In this issue of Immunity, Fang et al. demonstrate that the enrichment of cholesterol and sphingomyelin in the trans-Golgi network and endosomes mediated by the ARMH3-PI4KB-PI4P pathway plays a pivotal role in STING activation under cGAS-dependent and -independent conditions.

Publication types

Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural
Comment

MeSH terms

Endosomes / metabolism
Golgi Apparatus* / metabolism
Immunity, Innate
Lysosomes / metabolism
Nucleotidyltransferases* / metabolism

Substances

Nucleotidyltransferases

Abstract

Publication types

MeSH terms

Substances

Grants and funding