10 research outputs found
Regulatory T Cells Inhibit Protein Kinase Cθ Recruitment to the Immune Synapse of Naive T Cells with the Same Antigen Specificity
Fe de errores de “Evaluation of the TRPM2 channel as a biomarker in breast cancer using public databases analysis”
Background: Breast cancer is one of the most common malignancies affecting women. Recent
investigations have revealed a major role of ion channels in cancer. The transient receptor
potential melastatin-2 (TRPM2) is a plasma membrane and lysosomal channel with important
roles in cell migration and cell death in immune cells and tumor cells.
Methods: In this study, we investigated the prognostic value of TRPM2 channel in breast cancer,
analyzing public databases compiled in OncomineTM (Thermo Fisher, Ann Arbor, MI) and online
Kaplan-Meier Plotter platforms.
Results: The results revealed that TRPM2 mRNA overexpression is significant in situ and invasive
breast carcinoma compared to normal breast tissue. Furthermore, multi-gene validation using
OncomineTM showed that this channel is coexpressed with proteins related to cellular migration,
transformation, and apoptosis. On the other hand, Kaplan-Meier analysis exhibited that low
expression of TRPM2 could be used to predict poor outcome in ER- and HER2+ breast carcinoma
patients.
Conclusions: TRPM2 is a promising biomarkerfor aggressiveness of breast cancer, and a potential
target for the development of new therapies
Chemotaxis of Mouse Bone Marrow Neutrophils and Dendritic Cells Is Controlled by ADP-Ribose, the Major Product Generated by the CD38 Enzyme Reaction
Identification of immunogenic T-cell peptides of Mycobacterium tuberculosis PE_PGRS33 protein
Meeting report from the 2nd International Symposium on New Frontiers in Cardiovascular Research. Protecting the cardiovascular system from ischemia: between bench and bedside
Recent advances in basic cardiovascular research as well as their translation into the clinical situation were the focus at the last “New Frontiers in Cardiovascular Research meeting”. Major topics included the characterization of new targets and procedures in cardioprotection, deciphering new players and inflammatory mechanisms in ischemic heart disease as well as uncovering microRNAs and other biomarkers as versatile and possibly causal factors in cardiovascular pathogenesis. Although a number of pathological situations such as ischemia–reperfusion injury or atherosclerosis can be simulated and manipulated in diverse animal models, also to challenge new drugs for intervention, patient studies are the ultimate litmus test to obtain unequivocal information about the validity of biomedical concepts and their application in the clinics. Thus, the open and bidirectional exchange between bench and bedside is crucial to advance the field of ischemic heart disease with a particular emphasis of understanding long-lasting approaches in cardioprotection
Plasma-activated medium induces A549 cell injury via a spiral apoptotic cascade involving the mitochondrial–nuclear network
TRPM2: a multifunctional ion channel for calcium signalling
The transient potential receptor melastatin-2 (TRPM2) channel has emerged as an important Ca2+ signalling mechanism in a variety of cells, contributing to cellular functions that include cytokine production, insulin release, cell motility and cell death. Its ability to respond to reactive oxygen species has made TRPM2 a potential therapeutic target for chronic inflammation, neurodegenerative diseases, and oxidative stress-related pathologies. TRPM2 is a non-selective, calcium (Ca2+)-permeable cation channel of the melastatin-related transient receptor potential (TRPM) ion channel subfamily. It is activated by intracellular adenosine diphosphate ribose (ADPR) through a diphosphoribose hydrolase domain in its C-terminus and regulated through a variety of factors, including synergistic facilitation by [Ca2+]i, cyclic ADPR, H2O2, NAADP, and negative feedback regulation by AMP and permeating protons (pH). In addition to its role mediating Ca2+ influx into the cells, TRPM2 can also function as a lysosomal Ca2+ release channel, contributing to cell death. The physiological and pathophysiological context of ROS-mediated events makes TRPM2 a promising target for the development of therapeutic tools of inflammatory and degenerative diseases