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  1. Article

    Open Access

    VE-Cadherin modulates β-catenin/TCF-4 to enhance Vasculogenic Mimicry

    Vasculogenic Mimicry (VM) refers to the capacity to form a blood network from aggressive cancer cells in an independent way of endothelial cells, to provide nutrients and oxygen leading to enhanced microenviro...

    Daniel Delgado-Bellido, Esteban Zamudio-Martínez in Cell Death & Disease (2023)

  2. No Access

    Protocol

    Co-immunoprecipitation of Protein Complexes from Different Subcellular Compartments in Vasculogenic Mimicry Studies

    Aberrant extravascular expression of has been observed in associated with ; we have recently shown that in VM prone cells (mainly in the form of phospho-VE-cadherin in Y658) is in part located in the c...

    Daniel Delgado-Bellido, Angel Garcia-Diaz, Francisco Javier Oliver in Vasculogenic Mimicry (2022)

  3. No Access

    Article

    VE-cadherin promotes vasculogenic mimicry by modulating kaiso-dependent gene expression

    Aberrant extra-vascular expression of VE-cadherin (VEC) has been observed in metastasis associated with vasculogenic mimicry (VM); however, the ultimate reason why non-endothelial VEC favors the acquisition of...

    Daniel Delgado-Bellido, Mónica Fernández-Cortés in Cell Death & Differentiation (2019)

  4. Article

    Open Access

    PIM kinases mediate resistance of glioblastoma cells to TRAIL by a p62/SQSTM1-dependent mechanism

    Glioblastoma (GBM) is the most common and aggressive brain tumor and is associated with poor prognosis. GBM cells are frequently resistant to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and...

    Santiago Serrano-Saenz, Carmen Palacios, Daniel Delgado-Bellido in Cell Death & Disease (2019)

  5. Article

    Open Access

    Autophagy requires poly(adp-ribosyl)ation-dependent AMPK nuclear export

    AMPK is a central energy sensor linking extracellular milieu fluctuations with the autophagic machinery. In the current study we uncover that Poly(ADP-ribosyl)ation (PARylation), a post-translational modificat...

    José M Rodríguez-Vargas, María I Rodríguez in Cell Death & Differentiation (2016)

  6. Article

    Open Access

    Innate resistance of PD-1 blockade through loss of function mutations in JAK resulting in inability to express PD-L1 upon interferon exposure

    Daniel Shin, Angel Garcia-Diaz, Jesse Zaretsky in Journal for ImmunoTherapy of Cancer (2015)