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LACE1 interacts with p53 and mediates its mitochondrial translocation and apoptosis
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SYSNO ASEP 0469444 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title LACE1 interacts with p53 and mediates its mitochondrial translocation and apoptosis Author(s) Česneková, J. (CZ)
Spáčilová, J. (CZ)
Hansíková, H. (CZ)
Houštěk, Josef (FGU-C) RID, ORCID
Zeman, J. (CZ)
Stibůrek, L. (CZ)Source Title OncoTarget. - : Impact Journals LLC - ISSN 1949-2553
Roč. 7, č. 30 (2016), s. 47687-47698Number of pages 12 s. Language eng - English Country US - United States Keywords p53 ; LACE1 ; mitochondria ; apoptosis ; translocation Subject RIV EB - Genetics ; Molecular Biology R&D Projects GA13-07223S GA ČR - Czech Science Foundation (CSF) Institutional support FGU-C - RVO:67985823 UT WOS 000385413000067 EID SCOPUS 84982836612 DOI https://doi.org/10.18632/oncotarget.9959 Annotation p53 is a major cellular tumor suppressor that in addition to its nuclear, transcription-dependent activity is also known to function extranuclearly. Cellular stressors such as reactive oxygen species can promote translocation of p53 into mitochondria where it acts to protect mitochondrial genome or trigger cell death via transcription-independent manner. Here we report that the mammalian homologue of yeast mitochondrial Afg1 ATPase (LACE1) promotes translocation of p53 into mitochondria. We further show that LACE1 exhibits significant pro-apoptotic activity, which is dependent on p53, and that the protein is required for normal mitochondrial respiratory function. LACE1 physically interacts with p53 and is necessary for mitomycin c-induced translocation of p53 into mitochondria. Conversely, increased expression of LACE1 partitions p53 to mitochondria, causes reduction in nuclear p53 content and induces apoptosis. Thus, LACE1 mediates mitochondrial translocation of p53 and its transcription-independent apoptosis. Workplace Institute of Physiology Contact Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Year of Publishing 2017
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