SnapShot: CGAS-STING Signaling

Lorenzo Galluzzi; Claire Vanpouille-Box; Samuel F Bakhoum; Sandra Demaria

doi:10.1016/j.cell.2018.03.015

SnapShot: CGAS-STING Signaling

Cell. 2018 Mar 22;173(1):276-276.e1. doi: 10.1016/j.cell.2018.03.015.

Authors

Lorenzo Galluzzi¹, Claire Vanpouille-Box², Samuel F Bakhoum³, Sandra Demaria⁴

Affiliations

¹ Department of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA; Sandra and Edward Meyer Cancer Center, New York, NY, USA; Université Paris Descartes/Paris V, Paris, France.
² Department of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA.
³ Sandra and Edward Meyer Cancer Center, New York, NY, USA; Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
⁴ Department of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA; Sandra and Edward Meyer Cancer Center, New York, NY, USA; Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, NY, USA.

PMID: 29570996
DOI: 10.1016/j.cell.2018.03.015

Abstract

CGAS responds to cytosolic DNA by initiating a STING-dependent response that ultimately engages innate immune effectors to ensure the preservation of organismal homeostasis.

Publication types

Review

MeSH terms

Cellular Microenvironment
Humans
Immunity, Innate
Membrane Proteins / metabolism*
NF-kappa B / metabolism
NF-kappaB-Inducing Kinase
Nucleotidyltransferases / metabolism*
Protein Serine-Threonine Kinases / metabolism
Signal Transduction

Substances

Membrane Proteins
NF-kappa B
STING1 protein, human
Protein Serine-Threonine Kinases
TBK1 protein, human
Nucleotidyltransferases
cGAS protein, human