Directory
Marta Llovera Tomas

Marta Llovera Tomas

Degree: PhD

973 702 949
marta.llovera(ELIMINAR)@udl.cat

ResearcherID: http://www.researcherid.com/rid/B-5585-2009

Publications

  • Llovera, M; Gouveia, L; Zorzano, A; Sanchis, D

    The effects of ENDOG on lipid metabolism may be tissue-dependent and may not require its translocation from mitochondria

    Nature Communications 15 -. .

    [doi:10.1038/s41467-024-51447-x]

  • Beà A; García Valero J; Irazoki A; Lana C; López-Lluch G; Portero-Otín M; Pérez-Galán P; Inserte J; Ruiz-Meana M; Zorzano A; Llovera M; Sanchis D

    Cardiac fibroblasts display endurance to ischemia, high ROS control and elevated respiration regulated by the JAK2/STAT pathway.

    FEBS Journal 289 2540-2561. .

    [doi:10.1111/febs.16283]

  • Barés G; Beà A; Hernández L; Navaridas R; Felip I; Megino C; Blasco N; Nadeu F; Campo E; Llovera M; Dolcet X; Sanchis D

    ENDOG Impacts on Tumor Cell Proliferation and Tumor Prognosis in the Context of PI3K/PTEN Pathway Status.

    Cancers 13 -. .

    [doi:10.3390/cancers13153803]

  • Britti E; Delaspre F; Sanz A; Medina-Carbonero M; Llovera M; Purroy R; Mincheva-Tasheva S; Tamarit J; Ros J

    Calcitriol increases frataxin levels and restores mitochondrial function in cell models of Friedreich Ataxia.

    BIOCHEMICAL JOURNAL 478 1-20. .

    [doi:10.1042/BCJ20200331]

  • Blasco N; Beà A; Barés G; Girón C; Navaridas R; Irazoki A; López-Lluch G; Zorzano A; Dolcet X; Llovera M; Sanchis D

    Involvement of the mitochondrial nuclease EndoG in the regulation of cell proliferation through the control of reactive oxygen species

    Redox Biology 37 101736-101736. .

    [doi:10.1016/j.redox.2020.101736]

  • Britti, E; Delaspre, F; Mincheva, S; Llovera, M; Tamarit, J; Ros, J

    Calcitriol as a supplement for Friedreich ataxia

    FEBS Open Bio 8 213-213. .

  • Blasco, N; Camara, Y; Núñez E.; Bea, A; Bares, G; Forne, C; Ruiz-Meana, M; Giron, C; Barba, I; Garcia-Arumi, E; Garcia-Dorado, D; Vazquez, J; Marti, R; Llovera, M; Sanchis, D

    Cardiomyocyte hypertrophy induced by Endonuclease G deficiency requires reactive oxygen radicals accumulation and is inhibitable by the micropeptide humanin

    Redox Biology 16 146-156. .

    [doi:10.1016/j.redox.2018.02.021]

  • Cardona M; López JA; Serafín A; Rongvaux A; Inserte J; García-Dorado D; Flavell R; Llovera M; Cañas X; Vázquez J; Sanchis D

    Executioner Caspase-3 and 7 Deficiency Reduces Myocyte Number in the Developing Mouse Heart

    PLOS ONE 10 -. .

    [doi:10.1371/journal.pone.0131411]

  • Cornago M; Garcia-Alberich C; Blasco-Angulo N; Vall-Llaura N; Nager M; Herreros J; Comella JX; Sanchis D; Llovera M

    Histone deacetylase inhibitors promote glioma cell death by G2 checkpoint abrogation leading to mitotic catastrophe

    CELL DEATH & DISEASE 5 -. .

    [doi:10.1038/cddis.2014.412]

  • Ye, Junmei; Cardona, Maria; Llovera, Marta; Comella, Joan X.; Sanchis, Daniel

    Translation of Myocyte Enhancer Factor-2 is induced by hypertrophic stimuli in cardiomyocytes through a Calcineurin-dependent pathway

    Journal Of Molecular And Cellular Cardiology 53 578-587. .

    [doi:10.1016/j.yjmcc.2012.07.013]

  • Georgieva, Maya V.; de Pablo, Yolanda; Sanchis, Daniel; Comella, Joan X.; Llovera, Marta

    Ubiquitination of TrkA by Nedd4-2 regulates receptor lysosomal targeting and mediates receptor signaling.

    JOURNAL OF NEUROCHEMISTRY 117 479-493. .

    [doi:10.1111/j.1471-4159.2011.07218.x]

  • Zhang, Jisheng; Ye, Junmei; Altafaj, Albert; Cardona, Maria; Bahi, Nuria; Llovera, Marta; Canas, Xavier; Cook, Stuart A.; Comella, Joan X.; Sanchis, Daniel

    EndoG links Bnip3-induced mitochondrial damage and caspase-independent DNA fragmentation in ischemic cardiomyocytes.

    PLOS ONE 6 -. .

    [doi:10.1371/journal.pone.0017998]

Projects

  • INVESTIGO 2022: Senyalització cel·lular i apoptosi
  • New molecular functions of apoptotic genes in cardiac development and stress
  • ANALISIS DEL POTENCIAL DE LOS INHBIDORES DE LAS HISTONA DESACETILASAS EN LA SENSIBILIZACION A LA MUERTE POR TRAIL DE BIOBLASTOMAS HUMANOS