Adaptive inhibition of CGAS signaling by TREX1

María Cecilia Lira; Claire Vanpouille-Box; Lorenzo Galluzzi

doi:10.1016/j.trecan.2024.02.001

Adaptive inhibition of CGAS signaling by TREX1

María Cecilia Lira
, Claire Vanpouille-Box
, Lorenzo Galluzzi

Cornell University

Research output: Contribution to journal › Article › peer-review

7 Scopus citations

Abstract

Mammalian cells react to the accumulation of double-stranded (ds)DNA in the cytosol by secreting antiviral and proinflammatory cytokines, notably type I interferon (IFN). Recent data reported by Tani et al. demonstrate that overactivation of this pathway is prevented by an adaptive feedback mechanism elicited by type I IFN receptors and executed by the exonuclease three prime repair exonuclease 1 (TREX1).

Original language	English
Pages (from-to)	177-179
Number of pages	3
Journal	Trends in Cancer
Volume	10
Issue number	3
DOIs	https://doi.org/10.1016/j.trecan.2024.02.001
State	Published - Mar 2024
Externally published	Yes

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

autophagy
immune checkpoint inhibitors
NK cells
PD-1
STAT1
STING1
Nucleotidyltransferases/genetics
Cytokines
Mammals/genetics
Phosphoproteins/genetics
Animals
DNA
Exodeoxyribonucleases

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10.1016/j.trecan.2024.02.001

Cite this

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title = "Adaptive inhibition of CGAS signaling by TREX1",

abstract = "Mammalian cells react to the accumulation of double-stranded (ds)DNA in the cytosol by secreting antiviral and proinflammatory cytokines, notably type I interferon (IFN). Recent data reported by Tani et al. demonstrate that overactivation of this pathway is prevented by an adaptive feedback mechanism elicited by type I IFN receptors and executed by the exonuclease three prime repair exonuclease 1 (TREX1).",

keywords = "autophagy, immune checkpoint inhibitors, NK cells, PD-1, STAT1, STING1, Nucleotidyltransferases/genetics, Cytokines, Mammals/genetics, Phosphoproteins/genetics, Animals, DNA, Exodeoxyribonucleases",

author = "Lira, \{Mar{\'i}a Cecilia\} and Claire Vanpouille-Box and Lorenzo Galluzzi",

note = "Publisher Copyright: {\textcopyright} 2024 Elsevier Inc.",

year = "2024",

month = mar,

doi = "10.1016/j.trecan.2024.02.001",

language = "English",

volume = "10",

pages = "177--179",

journal = "Trends in Cancer",

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number = "3",

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TY - JOUR

T1 - Adaptive inhibition of CGAS signaling by TREX1

AU - Lira, María Cecilia

AU - Vanpouille-Box, Claire

AU - Galluzzi, Lorenzo

PY - 2024/3

Y1 - 2024/3

N2 - Mammalian cells react to the accumulation of double-stranded (ds)DNA in the cytosol by secreting antiviral and proinflammatory cytokines, notably type I interferon (IFN). Recent data reported by Tani et al. demonstrate that overactivation of this pathway is prevented by an adaptive feedback mechanism elicited by type I IFN receptors and executed by the exonuclease three prime repair exonuclease 1 (TREX1).

AB - Mammalian cells react to the accumulation of double-stranded (ds)DNA in the cytosol by secreting antiviral and proinflammatory cytokines, notably type I interferon (IFN). Recent data reported by Tani et al. demonstrate that overactivation of this pathway is prevented by an adaptive feedback mechanism elicited by type I IFN receptors and executed by the exonuclease three prime repair exonuclease 1 (TREX1).

KW - autophagy

KW - immune checkpoint inhibitors

KW - NK cells

KW - PD-1

KW - STAT1

KW - STING1

KW - Nucleotidyltransferases/genetics

KW - Cytokines

KW - Mammals/genetics

KW - Phosphoproteins/genetics

KW - Animals

KW - DNA

KW - Exodeoxyribonucleases

UR - https://www.scopus.com/pages/publications/85186433130

U2 - 10.1016/j.trecan.2024.02.001

DO - 10.1016/j.trecan.2024.02.001

M3 - Article

C2 - 38355355

AN - SCOPUS:85186433130

SN - 2405-8033

VL - 10

SP - 177

EP - 179

JO - Trends in Cancer

JF - Trends in Cancer

IS - 3

ER -

Adaptive inhibition of CGAS signaling by TREX1

Abstract

UN SDGs

Keywords

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