UAB Digital Repository of Documents 11 records found  1 - 10next  jump to record: Search took 0.03 seconds. 
1.
19 p, 5.0 MB SIVA-1 regulates apoptosis and synaptic function by modulating XIAP interaction with the death receptor antagonist FAIM-L / Coccia, Elena (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Planells-Ferrer, Laura (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Badillos-Rodríguez, Raquel (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Pascual, Marta (Universitat Autònoma de Barcelona. Departament de Biologia Cel·lular, de Fisiologia i d'Immunologia) ; Segura, Miguel F. (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Fernández-Hernández, Rita (Institut de Recerca Biomèdica de Lleida) ; López-Soriano, Joaquin (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Garí, Eloi (Institut de Recerca Biomèdica de Lleida) ; Soriano García, Eduardo (Institució Catalana de Recerca i Estudis Avançats (ICREA)) ; Barneda-Zahonero, Bruna (Universitat Autònoma de Barcelona. Institut de Neurociències) ; Moubarak, Rana S. (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Pérez-García, M. Jose (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Comella i Carnicé, Joan Xavier (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Universitat Autònoma de Barcelona.Institut de Neurociències
The long isoform of Fas apoptosis inhibitory molecule (FAIM-L) is a neuron-specific death receptor antagonist that modulates apoptotic cell death and mechanisms of neuronal plasticity. FAIM-L exerts its antiapoptotic action by binding to X-linked inhibitor of apoptosis protein (XIAP), an inhibitor of caspases, which are the main effectors of apoptosis. [...]
2020 - 10.1038/s41419-020-2282-x
Cell death and disease, Vol. 11 (february 2020)  
2.
12 p, 3.1 MB Survivin, a key player in cancer progression, increases in obesity and protects adipose tissue stem cells from apoptosis / Ejarque, Miriam (Hospital Universitari Joan XXIII de Tarragona) ; Ceperuelo Mallafré, Victòria (Hospital Universitari Joan XXIII de Tarragona) ; Serena, Carolina (Hospital Universitari Joan XXIII de Tarragona) ; Pachón, Gisela (CIBER de Diabetes y Enfermedades Metabólicas Asociadas, Instituto de Salud Carlos III, Madrid) ; Núñez Álvarez, Yaiza (Institut Germans Trias i Pujol. Institut de Medicina Predictiva i Personalitzada del Càncer) ; Terrón Puig, Margarida (Hospital Universitari Joan XXIII de Tarragona) ; Calvo, Enrique (Hospital Universitari Joan XXIII de Tarragona) ; Núñez Roa, Catalina (Hospital Universitari Joan XXIII de Tarragona) ; Oliva Olivera, Wilfredo (Centro de Investigación Biomédica en Red de Fisiopatología de la Obesidad y Nutrición) ; Tinahones, Francisco J (Centro de Investigación Biomédica en Red de Fisiopatología de la Obesidad y Nutrición) ; Peinado, Miguel Angel (Institut Germans Trias i Pujol. Institut de Medicina Predictiva i Personalitzada del Càncer) ; Vendrell, Joan (Hospital Universitari Joan XXIII de Tarragona) ; Fernández Veledo, Sonia (Hospital Universitari Joan XXIII de Tarragona) ; Universitat Autònoma de Barcelona
Adipose tissue (AT) has a central role in obesity-related metabolic imbalance through the dysregulated production of cytokines and adipokines. In addition to its known risk for cardiovascular disease and diabetes, obesity is also a major risk for cancer. [...]
2017 - 10.1038/cddis.2017.209
Cell Death and Disease, Núm. 8 (2017) , p. 1-12  
3.
14 p, 1.9 MB Low doses of LPS exacerbate the inflammatory response and trigger death on TLR3-primed human monocytes / Monguió Tortajada, Marta (Institut Germans Trias i Pujol) ; Franquesa, Marcella (Institut Germans Trias i Pujol) ; Sarrias, Maria-Rosa (Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas) ; Borràs, Francesc E (Institut Germans Trias i Pujol) ; Universitat Autònoma de Barcelona. Departament de Biologia Cel·lular, de Fisiologia i d'Immunologia
TLR sensing of pathogens triggers monocyte activation to initiate the host innate immune response to infection. Monocytes can dynamically adapt to different TLR agonists inducing different patterns of inflammatory response, and the sequence of exposure to TLRs can dramatically modulate cell activation. [...]
2018 - 10.1038/s41419-018-0520-2
Cell death and disease, Vol. 9 (May 2018) , art. 499  
4.
12 p, 2.7 MB Development of a neuroprotective peptide that preserves survival pathways by preventing Kidins220/ARMS calpain processing induced by excitotoxicity / Gamir-Morralla, A (CIBERNED, Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, Instituto de Salud Carlos III) ; López-Menéndez, C (CIBERNED, Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, Instituto de Salud Carlos III) ; Ayuso-Dolado, S (Universidad Autónoma de Madrid. Instituto de Investigaciones Biomédicas "Alberto Sols") ; Tejeda, G S (Universidad Autónoma de Madrid. Instituto de Investigaciones Biomédicas "Alberto Sols") ; Montaner, J (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Rosell, A (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Iglesias, T (CIBERNED, Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, Instituto de Salud Carlos III) ; Díaz-Guerra, M (Universidad Autónoma de Madrid. Instituto de Investigaciones Biomédicas "Alberto Sols") ; Universitat Autònoma de Barcelona
Kinase D-interacting substrate of 220 kDa (Kidins220), also known as ankyrin repeat-rich membrane spanning (ARMS), has a central role in the coordination of receptor crosstalk and the integration of signaling pathways essential for neuronal differentiation, survival and function. [...]
2015 - 10.1038/cddis.2015.307
Cell death and disease, Vol. 6 (october 2015) , p. e1939  
5.
13 p, 2.4 MB Amyloid- β reduces the expression of neuronal FAIM-L, thereby shifting the inflammatory response mediated by TNF α from neuronal protection to death / Carriba, P (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Jimenez, S (Universidad de Sevilla. Departamento Bioquimica y Biologia Molecular) ; Navarro, V (Universidad de Sevilla. Departamento Bioquimica y Biologia Molecular) ; Moreno-Gonzalez, I (Universidad de Malaga. Departamento de Biologia Celular, Genetica y Fisiologia) ; Barneda-Zahonero, B (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Moubarak, Rana S (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Lopez-Soriano, J (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Gutierrez, A (Universidad de Malaga. Departamento de Biologia Celular, Genetica y Fisiologia) ; Vitorica, J (Universidad de Sevilla. Departamento Bioquimica y Biologia Molecular) ; Comella, J X (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Universitat Autònoma de Barcelona
The brains of patients with Alzheimer's disease (AD) present elevated levels of tumor necrosis factor- α (TNF α), a cytokine that has a dual function in neuronal cells. On one hand, TNF α can activate neuronal apoptosis, and on the other hand, it can protect these cells against amyloid- β (A β) toxicity. [...]
2015 - 10.1038/cddis.2015.6
Cell death and disease, Vol. 6 (02 2015) , p. e1639  
6.
15 p, 2.3 MB Defective sarcoplasmic reticulum-mitochondria calcium exchange in aged mouse myocardium / Fernandez-Sanz, C (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Ruiz-Meana, M (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Miro-Casas, E (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Nuñez, E (Centro Nacional de Investigaciones Cardiovasculares) ; Castellano, J (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Loureiro, M (Centro Nacional de Investigaciones Cardiovasculares) ; Barba, I (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Poncelas, M (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Rodriguez-Sinovas, A (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Vázquez, J (Centro Nacional de Investigaciones Cardiovasculares) ; Garcia-Dorado, D (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Universitat Autònoma de Barcelona
Mitochondrial alterations are critically involved in increased vulnerability to disease during aging. We investigated the contribution of mitochondria-sarcoplasmic reticulum (SR) communication in cardiomyocyte functional alterations during aging. [...]
2014 - 10.1038/cddis.2014.526
Cell death and disease, Vol. 5 (december 2014) , p. e1573  
7.
13 p, 3.7 MB Histone deacetylase inhibitors promote glioma cell death by G2 checkpoint abrogation leading to mitotic catastrophe / Cornago, M (Institut de Recerca Biomèdica de Lleida) ; Garcia-Alberich, C (Institut de Recerca Biomèdica de Lleida) ; Blasco-Angulo, N (Institut de Recerca Biomèdica de Lleida) ; Vall-llaura, N (Institut de Recerca Biomèdica de Lleida) ; Nager, M (Institut de Recerca Biomèdica de Lleida) ; Herreros, J (Institut de Recerca Biomèdica de Lleida) ; Comella, J X (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Sanchis, D (Institut de Recerca Biomèdica de Lleida) ; Llovera, M (Institut de Recerca Biomèdica de Lleida) ; Universitat Autònoma de Barcelona
Glioblastoma multiforme is resistant to conventional anti-tumoral treatments due to its infiltrative nature and capability of relapse; therefore, research efforts focus on characterizing gliomagenesis and identifying molecular targets useful on therapy. [...]
2014 - 10.1038/cddis.2014.412
Cell death and disease, Vol. 5 (october 2014) , p. e1435  
8.
12 p, 1.8 MB MYCN repression of Lifeguard/FAIM2 enhances neuroblastoma aggressiveness / Planells-Ferrer, L (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Urresti, J (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Soriano, A (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Reix, S (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Murphy, D M (Royal College of Surgeons and National Children's Research Centre Our Lady's Children's Hospital) ; Ferreres, J C (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Borràs, F (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Gallego, S (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Stallings, R L (Royal College of Surgeons and National Children's Research Centre Our Lady's Children's Hospital) ; Moubarak, Rana S (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Segura, M F (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Comella, J X (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Universitat Autònoma de Barcelona
Neuroblastoma (NBL) is the most common solid tumor in infants and accounts for 15% of all pediatric cancer deaths. Several risk factors predict NBL outcome: age at the time of diagnosis, stage, chromosome alterations and MYCN (V-Myc Avian Myelocytomatosis Viral Oncogene Neuroblastoma-Derived Homolog) amplification, which characterizes the subset of the most aggressive NBLs with an overall survival below 30%. [...]
2014 - 10.1038/cddis.2014.356
Cell death and disease, Vol. 5 (09 2014) , p. e1401  
9.
10 p, 2.8 MB DYRK1A promotes dopaminergic neuron survival in the developing brain and in a mouse model of Parkinson's disease / Barallobre, M J (Instituto de Biología Molecular de Barcelona, CSIC) ; Perier, C (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Bové, Jordi (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Laguna, Ariadna (Department of Developmental Biology, Instituto de Biología Molecular de Barcelona, CSIC) ; Delabar, J M (Université Paris Diderot. Unité de Biologie Fonctionnelle et Adaptative) ; Vila, M (Institució Catalana de Recerca i Estudis Avançats) ; Arbonés, M L (Instituto de Biología Molecular de Barcelona, CSIC) ; Universitat Autònoma de Barcelona
In the brain, programmed cell death (PCD) serves to adjust the numbers of the different types of neurons during development, and its pathological reactivation in the adult leads to neurodegeneration. [...]
2014 - 10.1038/cddis.2014.253
Cell death and disease, Vol. 5 (06 2014) , p. e1289  
10.
11 p, 1.5 MB PDR-1/hParkin negatively regulates the phagocytosis of apoptotic cell corpses in Caenorhabditis elegans / Cabello, J (CIBIR (Centre for Biomedical Research of La Rioja)) ; Sämann, J (Bioinformatics and Molecular Genetics (Faculty of Biology), Center for Biochemistry and Molecular Cell Research (Faculty of Medicine)) ; Gómez-Orte, E (CIBIR (Centre for Biomedical Research of La Rioja)) ; Erazo, Tatiana (Universitat Autònoma de Barcelona. Institut de Neurociències) ; Coppa, A (Institut d'Investigació Biomèdica de Bellvitge) ; Pujol, A (Centro de Investigación Biomédica en Red de Enfermedades Raras) ; Büssing, I (Bioinformatics and Molecular Genetics (Faculty of Biology), Center for Biochemistry and Molecular Cell Research (Faculty of Medicine)) ; Schulze, B (Bioinformatics and Molecular Genetics (Faculty of Biology), Center for Biochemistry and Molecular Cell Research (Faculty of Medicine)) ; Lizcano de Vega, José Miguel (Universitat Autònoma de Barcelona. Institut de Neurociències) ; Ferrer, I (Institut d'Investigació Biomèdica de Bellvitge) ; Baumeister, R (FRIAS Freiburg Institute for Advanced Studies, Section Life Sciences (LIFENET), University of Freiburg) ; Lizcano de Vega, José Miguel (Universitat Autònoma de Barcelona. Institut de Neurociències) ; Dalfo, E (Centro de Investigación Biomédica en Red de Enfermedades Raras)
Apoptotic cell death is an integral part of cell turnover in many tissues, and proper corpse clearance is vital to maintaining tissue homeostasis in all multicellular organisms. Even in tissues with high cellular turnover, apoptotic cells are rarely seen because of efficient clearance mechanisms in healthy individuals. [...]
2014 - 10.1038/cddis.2014.57
Cell death and disease, Vol. 5 (03 2014) , p. e1120  

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