Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Tumor cell phenotype is sustained by selective MAPK oxidation in mitochondria.

PloS one - 11 Jun 2008

Galli Soledad, Antico Arciuch Valeria Gabriela, Poderoso Cecilia, Converso Daniela Paola, Zhou Qiongqiong, Bal de Kier Joffé Elisa, Cadenas Enrique, Boczkowski Jorge, Carreras María Cecilia, Poderoso Juan José

Abstract excerpt

Mitochondria are major cellular sources of hydrogen peroxide (H(2)O(2)), the production of which is modulated by oxygen availability and the mitochondrial energy state. An increase of steady-state cell H(2)O(2) concentration is able to control the transition from proliferating to quiescent phenot...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Catalysis
Share to Cell Cycle
Share to Cell Nucleus

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mitochondria

Share to Mitogen-Activated Protein Kinases

Share to Oxidation-Reduction

Share to Phosphorylation

Share to Protein Transport

Source

Open in PubMed Open full text

Identifiers

PMID: 18545666
DOI: 10.1371/journal.pone.0002379
PMCID: PMC2398776

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-18545666-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Tumor cell phenotype is sustained by selective MAPK oxidation in mitochondria.PMID 18545666Read ↗

Mechanisms associated with mitochondrial-generated reactive oxygen species in cancer.Semantic proximity Read ↗

The Hallmarks of Cancer from a Redox Perspective.Semantic proximity Read ↗

Mitochondrial ROS in cancer: initiators, amplifiers or an Achilles' heel?Semantic proximity Read ↗

Epithelial-mesenchymal transition and H<sub>2</sub>O<sub>2</sub> signaling – a driver of disease progression and a vulnerability in cancersSemantic proximity Read ↗

Oxidative Stress, Tumor Microenvironment, and Metabolic Reprogramming: A Diabolic LiaisonSemantic proximity Read ↗

Microenvironment-Cell Nucleus Relationship in the Context of Oxidative StressSemantic proximity Read ↗

Mitochondrial H <sub>2</sub> O <sub>2</sub> release does not directly cause genomic DNA damageSemantic proximity Read ↗

Hydrogen peroxide formation by Nox4 limits malignant transformationSemantic proximity Read ↗

A cell state-specific metabolic vulnerability to GPX4-dependent ferroptosis in glioblastomaSemantic proximity Read ↗

An unexpected friend − ROS in apoptosis-induced compensatory proliferation: Implications for regeneration and cancerSemantic proximity Read ↗

Targeting extracellular ROS signaling of tumor cells.Semantic proximity Read ↗

A Peroxiredoxin-P38 MAPK scaffold increases MAPK activity by MAP3K-independent mechanismsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.