Browsing by Author "Barake Sabbagh, M. Francisca"

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    Bases biológicas del cáncer: una propuesta de contenidos mínimos para las carreras de la salud
    (2021) Garrido Cisterna, Francisco Javier; Ríos Leal, Juvenal Antonio; Zavala, Valentina; Zolezzi, Juan; Labbé, Tomás; Roje, Dunja; García Bloj, Benjamín; Barake Sabbagh, M. Francisca; Universidad San Sebastián; University of California, Davis; Universidad de Magallanes; Universidad de Santiago; Fundación Nuestros Hijos; Universidad Mayor
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    GALECTIN-8 Is a Neuroprotective Factor in the Brain that Can Be Neutralized by Human Autoantibodies
    (2019) Pardo Huguet, Evelyn Cristina; Barake Sabbagh, M. Francisca; Godoy Zeballos, Juan Alejandro; Oyanadel, C.; Espinoza, S.; Metz Baer, Claudia Andrea; Retamal, C.; Massardo Vega, Loreto; Tapia-Rojas, Cheril; Inestrosa Cantín, Nibaldo; Soza, Alejandro; Gonzalez, A.
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    Galectin-8 mediates fibrogenesis induced by cyclosporine in human gingival fibroblasts
    (2020) Patricio C. Smith; Metz Baer, Claudia Andrea; Peña, Adely de la; Oyanadel, Claudia; Ávila, Patricio; Arancibia, Rodrigo; Vicuña, Lucas; Retamal Villarroel, Claudio Enrique; Barake Sabbagh, M. Francisca; González de la Rosa, Alfonso; Soza Gajardo, Andrea
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    Immune System Alterations by Aldosterone During Hypertension : From Clinical Observations to Genomic and Non-Genomic Mechanisms Leading to Vascular Damage
    (2013) Muñoz Durango, Natalia; Barake Sabbagh, M. Francisca; Letelier, N.; Campino Johnson, María del Carmen; Fardella B., Carlos; Kalergis Parra, Alexis Mikes
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    Neuronal surface P antigen (NSPA) modulates postsynaptic NMDAR stability through ubiquitination of tyrosine phosphatase PTPMEG
    (2020) Espinoza, Sofía; Barake Sabbagh, M. Francisca; Carvajal Cachaña, Francisco Javier; Segovia Miranda, Fabián Josué; Cerpa Nebott, Waldo Francisco; González de la Rosa, Alfonso; Arredondo, Sebastián B.; Guerrero, Fernanda G.; Valenzuela, David M.; Wyneken, Ursula
    Abstract Background Cognitive dysfunction (CD) is common among patients with the autoimmune disease systemic lupus erythematosus (SLE). Anti-ribosomal P autoantibodies associate with this dysfunction and have neuropathogenic effects that are mediated by cross-reacting with neuronal surface P antigen (NSPA) protein. Elucidating the function of NSPA can then reveal CD pathogenic mechanisms and treatment opportunities. In the brain, NSPA somehow contributes to glutamatergic NMDA receptor (NMDAR) activity in synaptic plasticity and memory. Here we analyze the consequences of NSPA absence in KO mice considering its structural features shared with E3 ubiquitin ligases and the crucial role of ubiquitination in synaptic plasticity. Results Electrophysiological studies revealed a decreased long-term potentiation in CA3-CA1 and medial perforant pathway-dentate gyrus (MPP-DG) hippocampal circuits, reflecting glutamatergic synaptic plasticity impairment in NSPA-KO mice. The hippocampal dentate gyrus of these mice showed a lower number of Arc-positive cells indicative of decreased synaptic activity and also showed proliferation defects of neural progenitors underlying less adult neurogenesis. All this translates into poor spatial and recognition memory when NSPA is absent. A cell-based assay demonstrated ubiquitination of NSPA as a property of RBR-type E3 ligases, while biochemical analysis of synaptic regions disclosed the tyrosine phosphatase PTPMEG as a potential substrate. Mice lacking NSPA have increased levels of PTPMEG due to its reduced ubiquitination and proteasomal degradation, which correlated with lower levels of GluN2A and GluN2B NMDAR subunits only at postsynaptic densities (PSDs), indicating selective trafficking of these proteins out of PSDs. As both GluN2A and GluN2B interact with PTPMEG, tyrosine (Tyr) dephosphorylation likely drives their endocytic removal from the PSD. Actually, immunoblot analysis showed reduced phosphorylation of the GluN2B endocytic signal Tyr1472 in NSPA-KO mice. Conclusions NSPA contributes to hippocampal plasticity and memory processes ensuring appropriate levels of adult neurogenesis and PSD-located NMDAR. PTPMEG qualifies as NSPA ubiquitination substrate that regulates Tyr phosphorylation-dependent NMDAR stability at PSDs. The NSPA/PTPMEG pathway emerges as a new regulator of glutamatergic transmission and plasticity and may provide mechanistic clues and therapeutic opportunities for anti-P-mediated pathogenicity in SLE, a still unmet need.
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    Situación actual del cáncer de colon en Chile : Una mirada traslacional
    (2020) Ríos Leal, Juvenal Antonio; Barake Sabbagh, M. Francisca; Arce, M. J.; Francisco, López-Köstner; Labbe, T. P.; Villena, J.; Becerra, S.