Thiophene-2 (TP2) is an inhibitor of polyketide synthase 13 (Pks13), which plays a critical role in the biosynthesis of mycolic acid, an essential component of the cell wall in M. tuberculosis, and is a potential new target for tuberculosis treatment. TP2 inhibits FadD32-dependent loading of the mycolic acid precursor meromycoloyl chain onto acyl carrier protein (ACP) domains located at the N terminus of Pks13, preventing synthesis of mycolic acid and resulting in mycobacterial cell death. TP2 bacteriosidal activity is equivalent to treatment with the first-line drug isoniazid, and enhances its activity, but is less likely to cause resistance. The minimal inhibitory concentration (MIC) values of TP2 against drug-susceptible multidrug-resistant M. tuberculosis strains is approximately 1 μM.
Thiophene-2 (TP2) is an inhibitor of polyketide synthase 13 (Pks13).
The outbreak and spread of Tembusu virus (TMUV) has caused very large losses in the waterfowl-breeding industry since 2010. The viral envelope (E) protein, the principal surface protein of viral particles, plays a vital role in viral entry and fusion.
Over 50% of genes in Plasmodium falciparum, the deadliest human malaria parasite, contain predicted introns, yet experimental characterization of splicing in this organism remains incomplete. We present here a transcriptome-wide characterization of intraerythrocytic splicing events, as captured by RNA-Seq data
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Valentina Serra et al.
Frontiers in microbiology, 7, 1704-1704 (2016-11-22)
Journal of lipid research, 61(8), 1168-1179 (2020-06-28)
Cholesteryl ester transfer protein (CETP) facilitates the net transfer of cholesteryl esters (CEs) and TGs between lipoproteins, impacting the metabolic fate of these lipoproteins. Previous studies have shown that a CETP antibody can alter CETP's preference for CE versus TG
The number and functional activity of circulating progenitor cells (CPCs) is altered in diabetic patients. Furthermore, reduced CPC count has been shown to independently predict cardiovascular events. Validation of CPCs as a biomarker for cardiovascular risk stratification requires rigorous methodology.
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