Como va la investigacion/Abstract

Durante este semestre he tenido el problema de que he estado asistiendo a entrevistas para empezar escuela graduada en agosto. Debido a esto he estado ausente varias veces impidiéndome asistir al laboratorio como de costumbre. Además, he estado intentando unos experimentos que no me están saliendo como esperaba. Para esto, voy a hacer unas modificaciones al protocolo y ver si obtengo resultados. Debido a esto pienso que he logrado solo un 10% de los objetivos para este semestre, pero espero ir avanzando para al final del semestre lograr todas las metas establecidas. Aquí les presento el “abstract” del poster que voy a presentar durante el Anual Poster Day de Bio-MINDS:

The immune system is in charge of protecting the body against pathogens but sometimes it fails and produces an immune response against its own cells. When this happens it is known as an autoimmune disease. These conditions are a major threat to the health of all Americans. At least ten million people (mostly women) in the United States suffer from an illness caused by autoimmunity. In addition, various autoimmune diseases have markedly higher incidence in Puerto Ricans, such as diabetes mellitus type 1. It is readily apparent that more knowledge of the patho-physiology of autoimmune diseases is needed. There is a process by which the immune system does not attack an antigen called immunological tolerance, and B-cells that participate in this process are called anergic. Several autoimmune diseases such as rheumatoid arthritis and diabetes are associated with loss of immunological tolerance. Therefore, understanding how immunological tolerance is maintained for self-antigens is important to understand how autoimmunity is triggered. Previous studies have shown that anergic B-cells from an anti-insulin mouse model have impaired calcium (Ca²⁺) mobilization from the endoplasmic reticulum (ER), reduced basal levels of nuclear factor of activated T cells (NFATc1) and reduced NFATc1 mobilization following B-cell receptor (BCR) stimulation. These processes are crucial in the activation of B-cells. BCR signals lead to the production of inositol 1,4,5-triphosphatate (IP₃) that interacts with a Ca²⁺ channel in the ER, IP₃ receptor (IP₃R), that induces the release of Ca²⁺ from the ER. Since the impaired Ca²⁺ mobilization is due to intracellular Ca²⁺ stores, we hypothesized that the IP₃R function is impaired in anergic B-cells leading to disrupted mobilization of Ca²⁺. For this reason, our aim is to characterize IP₃R in order to compare this protein with its counterpart in anergic B-cells. Since all human cells have the IP₃R we are currently using HeLa cells and hFOB cells for our experiments. We have successfully detected the IP₃R in HeLa cells via immunobloting. Future experiments will assess the phosphorylation status of IP₃R and potential IP₃R interactions with other proteins.

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