Publications by authors named "M Cottee"
Article Synopsis
- BFL1, an antiapoptotic protein from the BCL2 family, is linked to hematological cancers but hasn't been extensively researched.
- Two articles present the development of selective BFL1 inhibitors, starting from hit identification using a covalent fragment library and leading to optimized compounds.
- One compound not only induced cell death in specific cancer cell lines but also stabilized the BFL1 protein, significantly increasing its half-life to 10.8 hours while activating cellular apoptosis markers.
Background: A significant burden of atherosclerotic disease is driven by inflammation. Recently, microRNAs (miRNAs) have emerged as important factors driving and protecting from atherosclerosis. miR-223 regulates cholesterol metabolism and inflammation via targeting both cholesterol biosynthesis pathway and NFB signaling pathways; however, its role in atherosclerosis has not been investigated.
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- - Recent research highlights the need for innovative cancer treatments, particularly through the use of oncolytic viruses (OVs) that can attack tumors in multiple ways.
- - The study discovers a specific amiRNA, called amiR-4, that enhances the effectiveness of a type of oncolytic virus, revealing ARID1A as a key factor in tumor resistance.
- - Combining virus targeting of ARID1A with small-molecule inhibitors like EZH2 leads to effective killing of both infected and uninfected cancer cells, suggesting a new therapeutic strategy involving amiRNA and traditional treatments.
Excessive replication of Saccharomyces cerevisiae Ty1 retrotransposons is regulated by Copy Number Control, a process requiring the p22/p18 protein produced from a sub-genomic transcript initiated within Ty1 GAG. In retrotransposition, Gag performs the capsid functions required for replication and re-integration. To minimize genomic damage, p22/p18 interrupts virus-like particle function by interaction with Gag.
View Article and Find Full Text PDFObjectives: During the advancement of atherosclerosis, plaque cellularity is governed by the influx of monocyte-derived macrophages and their turnover via apoptotic and nonapoptotic forms of cell death. Previous reports have demonstrated that programmed necrosis, or necroptosis, of plaque macrophages contribute to necrotic core formation. Knockdown or inhibition of the necrosome components RIPK1 (receptor-interacting protein kinase 1) and RIPK3 (receptor-interacting protein kinase 3) slow atherogenesis, and activation of the terminal step of necroptosis, MLKL (mixed lineage kinase domain-like protein), has been demonstrated in advanced human atherosclerotic plaques.
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