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Laura Martorano

Researcher at University of Padua

Publications -  6
Citations -  88

Laura Martorano is an academic researcher from University of Padua. The author has contributed to research in topics: Zebrafish & Mitochondrial DNA. The author has an hindex of 3, co-authored 6 publications receiving 45 citations.

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The zebrafish orthologue of the human hepatocerebral disease gene MPV17 plays pleiotropic roles in mitochondria

TL;DR: The zebrafish mpv17−/− mutant shows a severe mitochondrial phenotype with ultrastructural alterations and oxidative phosphorylation impairment, linking the loss of Mpv17 to pyrimidine de novo synthesis and opening a new simple therapeutic approach for MPV17-related MDS.
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The stem-like Stat3-responsive cells of zebrafish intestine are Wnt/β-catenin dependent.

TL;DR: The findings indicate that Jak/Stat3 signalling is needed for intestinal stem cell maintenance and possibly crucial in controlling Wnt/β-catenin-dependent colorectal cancer cell proliferation.
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Y705 and S727 are required for the mitochondrial import and transcriptional activities of STAT3, and for regulation of stem cell proliferation.

TL;DR: In this paper, it was shown that import of STAT3 inside mitochondria requires Y705 phosphorylation by Jak, whereas its mitochondrial transcriptional activity, as well as its effect on proliferation, depends on the MAPK target S727.
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Efficient clofilium tosylate-mediated rescue of POLG-related disease phenotypes in zebrafish.

TL;DR: In this paper, the DNA polymerase gamma (Polg) is a nuclear-encoded enzyme involved in DNA replication in animal mitochondria and mutations in the POLG gene underlie a set of mitochondrial diseases characterized by mtDNA depletion or deletion and multiorgan defects, for which an effective therapy is still needed.
Posted ContentDOI

Mitochondrial STAT3 regulates proliferation of tissue stem cells

TL;DR: It is determined in vivo that mitochondrial STAT3 regulates mtDNA transcription in embryonic and larval stem cell niches and that this activity determines their proliferation rates, and that STAT3-dependent increase of mitochondrial transcription seems independent from STAT3 binding to DNA and does not originate fromSTAT3 regulation of mtDNA replication.