HAX1 is a novel binding partner of Che-1/AATF. Implications in oxidative stress cell response.


Journal

Biochimica et biophysica acta. Molecular cell research
ISSN: 1879-2596
Titre abrégé: Biochim Biophys Acta Mol Cell Res
Pays: Netherlands
ID NLM: 101731731

Informations de publication

Date de publication:
01 2024
Historique:
received: 18 05 2023
revised: 31 08 2023
accepted: 14 09 2023
medline: 20 11 2023
pubmed: 25 9 2023
entrez: 24 9 2023
Statut: ppublish

Résumé

HAX1 is a multifunctional protein involved in the antagonism of apoptosis in cellular response to oxidative stress. In the present study we identified HAX1 as a novel binding partner for Che-1/AATF, a pro-survival factor which plays a crucial role in fundamental processes, including response to multiple stresses and apoptosis. HAX1 and Che-1 proteins show extensive colocalization in mitochondria and we demonstrated that their association is strengthened after oxidative stress stimuli. Interestingly, in MCF-7 cells, resembling luminal estrogen receptor (ER) positive breast cancer, we found that Che-1 depletion correlates with decreased HAX1 mRNA and protein levels, and this event is not significantly affected by oxidative stress induction. Furthermore, we observed an enhancement of the previously reported interaction between HAX1 and estrogen receptor alpha (ERα) upon H

Identifiants

pubmed: 37742722
pii: S0167-4889(23)00160-X
doi: 10.1016/j.bbamcr.2023.119587
pii:
doi:

Substances chimiques

Hydrogen Peroxide BBX060AN9V
Apoptosis Regulatory Proteins 0
AATF protein, human 0
Repressor Proteins 0
HAX1 protein, human 0
Adaptor Proteins, Signal Transducing 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

119587

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Cinzia Pisani (C)

CNR-Institute of Molecular Biology and Pathology, Department of Molecular Medicine, Sapienza University of Rome, Viale Regina Elena 291, 00161 Rome, Italy. Electronic address: cinzia.pisani@cnr.it.

Annalisa Onori (A)

CNR-Institute of Molecular Biology and Pathology, Department of Molecular Medicine, Sapienza University of Rome, Viale Regina Elena 291, 00161 Rome, Italy.

Francesca Gabanella (F)

CNR-Institute of Biochemistry and Cell Biology, Department of Sense Organs, Sapienza University of Rome, Viale del Policlinico 155, 00161 Rome, Italy.

Simona Iezzi (S)

SAFU Unit, Department of Research and Advanced Technologies, Translational Research Area, IRCCS Regina Elena National Cancer Institute, Via Elio Chianesi 53, 00144 Rome, Italy.

Roberta De Angelis (R)

ISPRA, Italian National Institute for Environmental Protection and Research, Via Vitaliano Brancati 48, 00144 Rome, Italy.

Maurizio Fanciulli (M)

SAFU Unit, Department of Research and Advanced Technologies, Translational Research Area, IRCCS Regina Elena National Cancer Institute, Via Elio Chianesi 53, 00144 Rome, Italy.

Andrea Colizza (A)

Department of Sense Organs, Sapienza University of Rome, Viale del Policlinico 155, 00161 Rome, Italy.

Marco de Vincentiis (M)

Department of Sense Organs, Sapienza University of Rome, Viale del Policlinico 155, 00161 Rome, Italy.

Maria Grazia Di Certo (MG)

CNR-Institute of Biochemistry and Cell Biology, Department of Sense Organs, Sapienza University of Rome, Viale del Policlinico 155, 00161 Rome, Italy.

Claudio Passananti (C)

CNR-Institute of Molecular Biology and Pathology, Department of Molecular Medicine, Sapienza University of Rome, Viale Regina Elena 291, 00161 Rome, Italy. Electronic address: claudio.passananti@cnr.it.

Nicoletta Corbi (N)

CNR-Institute of Molecular Biology and Pathology, Department of Molecular Medicine, Sapienza University of Rome, Viale Regina Elena 291, 00161 Rome, Italy. Electronic address: nicoletta.corbi@cnr.it.

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Classifications MeSH