Publicaciones en colaboración con investigadores/as de Universidad Complutense de Madrid (16)

2024

  1. Identification of PRMT5 as a therapeutic target in cholangiocarcinoma

    Gut

  2. Proceedings of the 5th Meeting of Translational Hepatology, organized by the Spanish Association for the Study of the Liver (AEEH)

    Gastroenterologia y Hepatologia

2022

  1. Activation of the unfolded protein response (Upr) is associated with cholangiocellular injury, fibrosis and carcinogenesis in an experimental model of fibropolycystic liver disease

    Cancers, Vol. 14, Núm. 1

  2. 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

  3. 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

  4. Next-generation sequencing of bile cell-free DNA for the early detection of patients with malignant biliary strictures

    Gut, Vol. 71, Núm. 6, pp. 1141-1151

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. 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

2018

  1. TWEAK promotes migration and invasion in MEFs through a mechanism dependent on ERKs activation and Fibulin 3 down-regulation

    Journal of Cellular Physiology, Vol. 233, Núm. 2, pp. 968-978

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

2015

  1. p38 MAPK down-regulates fibulin 3 expression through methylation of gene regulatory sequences: Role in migration and invasion

    Journal of Biological Chemistry, Vol. 290, Núm. 7, pp. 4383-4397

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

  2. p38α mediates cell survival in response to oxidative stress via induction of antioxidant genes: Effect on the p70S6K pathway

    Journal of Biological Chemistry, Vol. 287, Núm. 4, pp. 2632-2642

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