Massive Open Online Courses (MOOCs) with Open Educational Resources for toxicology learning \u2013 Drugs and pollutants as xenobiotics

Due to the lack of European Massive Open Online Courses (MOOCs) in the field of the Toxicology and the major differences in the styles of teaching and learning of this important subject in amongst various European life science-oriented institutions, the European Erasmus+ project \u201cLearning Toxicology through Open Educational Resources (TOX-OER)\u201d was developed and implemented. Considering the complexity and heterogeneity of the toxicology field, the TOX-OER project main objective was to develop and share toxicology-related knowledge and skills among students/ earners from seven countries, which promote the internationalization of Higher Education Institutions in Europe but also in countries from other continents. The project was coordinated by Universidad de Salamanca (Spain), and the partners were: Space Research and Technology Institute (Bulgaria), Univerzita Karlova V Praze (Czech Republic), South-Eastern Finland University of Applied Sciences (Finland), Universit\ue0 di Bologna (Italy), Universidade do Porto (Portugal) and Universitatea Transilvania din Brasov (Romania). One of the goals/ objectives of the project is the dissemination, popularizing the information and reaching potentially interested people who can benefit from the offered courses. The aim of this paper is to present and analyze part of the TOX-OER\u2019s outcomes developed by the project\u2019s partnership, especially the modules/ topics related to the drugs, gaseous and persistent organic pollutants, as the principal groups of xenobiotics

Kinome analysis of receptor-induced phosphorylation in human natural killer cells.

BACKGROUND: Natural killer (NK) cells contribute to the defense against infected and transformed cells through the engagement of multiple germline-encoded activation receptors. Stimulation of the Fc receptor CD16 alone is sufficient for NK cell activation, whereas other receptors, such as 2B4 (CD244) and DNAM-1 (CD226), act synergistically. After receptor engagement, protein kinases play a major role in signaling networks controlling NK cell effector functions. However, it has not been characterized systematically which of all kinases encoded by the human genome (kinome) are involved in NK cell activation. RESULTS: A kinase-selective phosphoproteome approach enabled the determination of 188 kinases expressed in human NK cells. Crosslinking of CD16 as well as 2B4 and DNAM-1 revealed a total of 313 distinct kinase phosphorylation sites on 109 different kinases. Phosphorylation sites on 21 kinases were similarly regulated after engagement of either CD16 or co-engagement of 2B4 and DNAM-1. Among those, increased phosphorylation of FYN, KCC2G (CAMK2), FES, and AAK1, as well as the reduced phosphorylation of MARK2, were reproducibly observed both after engagement of CD16 and co-engagement of 2B4 and DNAM-1. Notably, only one phosphorylation on PAK4 was differentally regulated. CONCLUSIONS: The present study has identified a significant portion of the NK cell kinome and defined novel phosphorylation sites in primary lymphocytes. Regulated phosphorylations observed in the early phase of NK cell activation imply these kinases are involved in NK cell signaling. Taken together, this study suggests a largely shared signaling pathway downstream of distinct activation receptors and constitutes a valuable resource for further elucidating the regulation of NK cell effector responses