Tina Pekec
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Tina Pekec has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
Abhishek Anil Dubey
Laboratory of Protein Metabolism, International Institute of Molecular and Cell Biology in Warsaw, Warsaw, Poland
1 shared publication- Alicja A. Komur
Institute of Bioorganic Chemistry, Polish Academy of Sciences, Poznan, Poland
1 shared publication - Daria Sobańska
Institute of Bioorganic Chemistry, Polish Academy of Sciences, Poznan, Poland
1 shared publication - Jarosław Lewandowski
Institute of Bioorganic Chemistry, Polish Academy of Sciences, Poznan, Poland
1 shared publication - Jędrzej Małecki
Department of Biosciences, Faculty of Mathematics and Natural Sciences, University of Oslo, 0316 Oslo, Norway; CRESCO - Centre for Embryology and Healthy Development, University of Oslo and Oslo University Hospital, Oslo, Norway
1 shared publication - Karolina Świtońska-Kurkowska
Institute of Bioorganic Chemistry, Polish Academy of Sciences, Poznan, Poland
1 shared publication
Latest Publications
- Open Access
- 19 August 2022
- Published by Springer Nature in Nature Communications
- Vol. 13 (1) , 1-19
Ferritin-mediated iron detoxification promotes hypothermia survival in Caenorhabditis elegans and murine neurons
How animals rewire cellular programs to survive cold is a fascinating problem with potential biomedical implications, ranging from emergency medicine to space travel. Studying a hibernation-like response in the free-living nematode Caenorhabditis elegans, we uncovered a regulatory axis that enhances the natural resistance of nematodes to severe cold. This axis involves conserved transcription factors, DAF-16/FoxO and PQM-1, which jointly promote cold survival by upregulating FTN-1, a protein related to mammalian ferritin heavy chain (FTH1). Moreover, we show that inducing expression of FTH1 also promotes cold survival of mammalian neurons, a cell type particularly sensitive to deterioration in hypothermia. Our findings in both animals and cells suggest that FTN-1/FTH1 facilitates cold survival by detoxifying ROS-generating iron species. We finally show that mimicking the effects of FTN-1/FTH1 with drugs protects neurons from cold-induced degeneration, opening a potential avenue to improved treatments of hypothermia.
- 19 August 2022
- Published by Springer Nature in Nature Communications
- Vol. 13 (1) , 1-19
Open AccessFerritin-mediated iron detoxification promotes hypothermia survival in Caenorhabditis elegans and murine neurons
How animals rewire cellular programs to survive cold is a fascinating problem with potential biomedical implications, ranging from emergency medicine to space travel. Studying a hibernation-like response in the free-living nematode Caenorhabditis elegans, we uncovered a regulatory axis that enhances the natural resistance of nematodes to severe cold. This axis involves conserved transcription factors, DAF-16/FoxO and PQM-1, which jointly promote cold survival by upregulating FTN-1, a protein related to mammalian ferritin heavy chain (FTH1). Moreover, we show that inducing expression of FTH1 also promotes cold survival of mammalian neurons, a cell type particularly sensitive to deterioration in hypothermia. Our findings in both animals and cells suggest that FTN-1/FTH1 facilitates cold survival by detoxifying ROS-generating iron species. We finally show that mimicking the effects of FTN-1/FTH1 with drugs protects neurons from cold-induced degeneration, opening a potential avenue to improved treatments of hypothermia.