A mitochondrial checkpoint to NF-κB signaling

Emma Guilbaud; Lorenzo Galluzzi

doi:10.1038/s41419-024-06868-3

A mitochondrial checkpoint to NF-κB signaling

Emma Guilbaud, Lorenzo Galluzzi

Cornell University

Research output: Contribution to journal › Comment/debate

Abstract

Mitochondrial dysfunction can elicit multiple inflammatory pathways, especially when apoptotic caspases are inhibited. Such an inflammatory program is negatively regulated by the autophagic disposal of permeabilized mitochondria. Recent data demonstrate that the ubiquitination of mitochondrial proteins is essential for NEMO-driven NF-kB activation downstream of mitochondrial permeabilization.

Original language	English
Article number	477
Journal	Cell Death and Disease
Volume	15
Issue number	7
DOIs	https://doi.org/10.1038/s41419-024-06868-3
State	Published - Jul 2024
Externally published	Yes

Keywords

Animals
Apoptosis
Autophagy
Humans
I-kappa B Kinase/metabolism
Mitochondria/metabolism
Mitochondrial Proteins/metabolism
NF-kappa B/metabolism
Signal Transduction
Ubiquitination

UN SDGs

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

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10.1038/s41419-024-06868-3

Cite this

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title = "A mitochondrial checkpoint to NF-κB signaling",

abstract = "Mitochondrial dysfunction can elicit multiple inflammatory pathways, especially when apoptotic caspases are inhibited. Such an inflammatory program is negatively regulated by the autophagic disposal of permeabilized mitochondria. Recent data demonstrate that the ubiquitination of mitochondrial proteins is essential for NEMO-driven NF-kB activation downstream of mitochondrial permeabilization.",

keywords = "Animals, Apoptosis, Autophagy, Humans, I-kappa B Kinase/metabolism, Mitochondria/metabolism, Mitochondrial Proteins/metabolism, NF-kappa B/metabolism, Signal Transduction, Ubiquitination",

author = "Emma Guilbaud and Lorenzo Galluzzi",

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doi = "10.1038/s41419-024-06868-3",

language = "English",

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journal = "Cell Death and Disease",

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AU - Guilbaud, Emma

AU - Galluzzi, Lorenzo

N1 - Publisher Copyright: © The Author(s) 2024.

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N2 - Mitochondrial dysfunction can elicit multiple inflammatory pathways, especially when apoptotic caspases are inhibited. Such an inflammatory program is negatively regulated by the autophagic disposal of permeabilized mitochondria. Recent data demonstrate that the ubiquitination of mitochondrial proteins is essential for NEMO-driven NF-kB activation downstream of mitochondrial permeabilization.

AB - Mitochondrial dysfunction can elicit multiple inflammatory pathways, especially when apoptotic caspases are inhibited. Such an inflammatory program is negatively regulated by the autophagic disposal of permeabilized mitochondria. Recent data demonstrate that the ubiquitination of mitochondrial proteins is essential for NEMO-driven NF-kB activation downstream of mitochondrial permeabilization.

KW - Animals

KW - Apoptosis

KW - Autophagy

KW - Humans

KW - I-kappa B Kinase/metabolism

KW - Mitochondria/metabolism

KW - Mitochondrial Proteins/metabolism

KW - NF-kappa B/metabolism

KW - Signal Transduction

KW - Ubiquitination

UR - http://www.scopus.com/inward/record.url?scp=85197514392&partnerID=8YFLogxK

U2 - 10.1038/s41419-024-06868-3

DO - 10.1038/s41419-024-06868-3

M3 - Comment/debate

C2 - 38961079

AN - SCOPUS:85197514392

SN - 2041-4889

VL - 15

JO - Cell Death and Disease

JF - Cell Death and Disease

IS - 7

M1 - 477

ER -

A mitochondrial checkpoint to NF-κB signaling

Abstract

Keywords

UN SDGs

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