The hepatocyte growth factor receptor (MET) is a receptor tyrosine kinase (RTK) that mediates the activity of a variety of downstream pathways upon its activation. These pathways regulate various physiological processes within the cell, including growth, survival, proliferation, and motility. Under normal physiological conditions, this allows MET to regulate various development and regenerative processes; however, mutations resulting in aberrant MET activity and the consequent dysregulation of downstream signaling can contribute to cellular pathophysiology.
View Article and Find Full Text PDFThe eastern equatorial Atlantic hosts a productive marine ecosystem that depends on upward supply of nitrate, the primary limiting nutrient in this region. The annual productivity peak, indicated by elevated surface chlorophyll levels, occurs in the Northern Hemisphere summer, roughly coinciding with strengthened easterly winds. For enhanced productivity in the equatorial Atlantic, nitrate-rich water must rise into the turbulent layer above the Equatorial Undercurrent.
View Article and Find Full Text PDFObjective: To evaluate the effect of administering postpartum heparin-based pharmacologic thromboprophylaxis on the incidence of postpartum venous thromboembolism (VTE) and complications.
Methods: This was a multicenter retrospective cohort study of all individuals delivering at more than 20 weeks of gestation at four U.S.
: The COVID-19 pandemic prompted unprecedented vaccine development efforts against SARS-CoV-2. India, which was one of the countries most impacted by COVID-19, developed its indigenous vaccine in addition to utilizing the ones developed by other countries. While antibody levels and neutralizing antibody titres are considered initial correlates of immune protection, long-term protection from the pathogen relies on memory B and T cells and their recall responses.
View Article and Find Full Text PDFAugmenting the portfolio of therapeutics for type 2-driven diseases is crucial to address unmet clinical needs and to design personalized treatment schemes. An attractive therapy for such diseases would consist in targeting the recruitment of T helper 2 (Th2) lymphocytes to inflammatory sites. Herein, we show the degradation of filamins (FLN) a and b by the ASB2α E3 ubiquitin ligase as a mechanism sustaining Th2 lymphocyte functions.
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