131574-92-0Relevant academic research and scientific papers
Disruption of glycolytic flux is a signal for inflammasome signaling and pyroptotic cell death
Sanman, Laura E.,Qian, Yu,Eisele, Nicholas A.,Ng, Tessie M.,van der Linden, Wouter A.,Monack, Denise M.,Weerapana, Eranthie,Bogyo, Matthew
, (2016/06/01)
When innate immune cells such as macrophages are challenged with environmental stresses or infection by pathogens, they trigger the rapid assembly of multi-protein complexes called inflammasomes that are responsible for initiating pro-inflammatory responses and a form of cell death termed pyroptosis. We describe here the identification of an intracellular trigger of NLRP3-mediated inflammatory signaling, IL-1b production and pyroptosis in primed murine bone marrow-derived macrophages that is mediated by the disruption of glycolytic flux. This signal results from a drop of NADH levels and induction of mitochondrial ROS production and can be rescued by addition of products that restore NADH production. This signal is also important for host-cell response to the intracellular pathogen Salmonella typhimurium, which can disrupt metabolism by uptake of host-cell glucose. These results reveal an important inflammatory signaling network used by immune cells to sense metabolic dysfunction or infection by intracellular pathogens.
Convenient synthesis of C-terminal di- and tri-peptide amides from N-protected dipeptidoylbenzotriazoles
Celik, Ilhami,Abdel-Fattah, Ashraf A.A.
experimental part, p. 4923 - 4929 (2009/10/09)
N-Protected dipeptidoylbenzotriazoles react with aqueous ammonia to give dipeptide primary amides (77-98%) and with N-unprotected α-amino amides to afford tripeptide primary amides (82-86%).
