Publicaciones en colaboración con investigadores/as de Universidad de Salamanca (14)

2024

  1. Identification of PRMT5 as a therapeutic target in cholangiocarcinoma

    Gut

  2. New insights into the regulation of bile acids synthesis during the early stages of liver regeneration: A human and experimental study

    Biochimica et Biophysica Acta - Molecular Basis of Disease, Vol. 1870, Núm. 5

  3. Non-mitogenic FGF19 mRNA-based therapy for the treatment of experimental metabolic dysfunction-associated steatotic liver disease (MASLD)

    Clinical science (London, England : 1979), Vol. 138, Núm. 20, pp. 1265-1284

2023

  1. Identification and experimental validation of druggable epigenetic targets in hepatoblastoma

    Journal of Hepatology, Vol. 79, Núm. 4, pp. 989-1005

2022

  1. Metabolic-associated fatty liver disease: From simple steatosis toward liver cirrhosis and potential complications. Proceedings of the Third Translational Hepatology Meeting, organized by the Spanish Association for the Study of the Liver (AEEH)

    Gastroenterologia y Hepatologia, Vol. 45, Núm. 9, pp. 724-734

  2. New molecular mechanisms in cholangiocarcinoma: signals triggering interleukin-6 production in tumor cells and KRAS co-opted epigenetic mediators driving metabolic reprogramming

    Journal of Experimental and Clinical Cancer Research, Vol. 41, Núm. 1

2021

  1. Dual Targeting of G9a and DNA Methyltransferase-1 for the Treatment of Experimental Cholangiocarcinoma

    Hepatology, Vol. 73, Núm. 6, pp. 2380-2396

2020

  1. C3G is upregulated in hepatocarcinoma, contributing to tumor growth and progression and to HGF/MET pathway activation

    Cancers, Vol. 12, Núm. 8, pp. 1-22

  2. Dual pharmacological targeting of hdacs and pde5 inhibits liver disease progression in a mouse model of biliary inflammation and fibrosis

    Cancers, Vol. 12, Núm. 12, pp. 1-27

  3. Pilot multi-omic analysis of human bile from benign and malignant biliary strictures: A machine-learning approach

    Cancers, Vol. 12, Núm. 6, pp. 1-30

2016

  1. C3G knock-down enhances migration and invasion by increasing Rap1-mediated p38α activation, while it impairs tumor growth through p38α-independent mechanisms

    Oncotarget, Vol. 7, Núm. 29, pp. 45060-45078

2013

  1. Met signaling in cardiomyocytes is required for normal cardiac function in adult mice

    Biochimica et Biophysica Acta - Molecular Basis of Disease, Vol. 1832, Núm. 12, pp. 2204-2215

2012

  1. C3G transgenic mouse models with specific expression in platelets reveal a new role for C3G in platelet clotting through its GEF activity

    Biochimica et Biophysica Acta - Molecular Cell Research, Vol. 1823, Núm. 8, pp. 1366-1377

2010

  1. C3G down-regulates p38 MAPK activity in response to stress by Rap-1 independent mechanisms: Involvement in cell death

    Cellular Signalling, Vol. 22, Núm. 3, pp. 533-542