Helicobacter pylori (H. pylori) is a gram-negative bacterium living in the human gastrointestinal tract considered as the most common cause of gastritis. H. pylori was listed as the main risk factor for gastric cancer. Triple therapy consisting of a proton pump inhibitor and combinations of antibiotics is the main treatment used. However, this line of therapy has proven less effective mainly due to biofilm formation. Bacteria can regulate and synchronize the expression of multiple genes involved in virulence, toxin production, motility, chemotaxis, and biofilm formation by quorum sensing (QS), thus contributing to antimicrobial resistance. Henceforth, the inhibition of QS called quorum quenching (QQ) is a promising target and alternative to fight H. pylori resistance to antimicrobials. Many phytochemicals as well as synthetic compounds acting as quorum quenchers in H. pylori were described in vitro and in vivo. Otherwise, many other compounds known as quorum quenchers in other species and inhibitors of biofilm formation in H. pylori could act as quorum quenchers in H. pylori. Here, we summarize and discuss the latest findings on H. pylori’s biofilm formation, QS sensing, and QQ mechanisms.
The YAP oncogene is a known cancer target. Therefore, it is of interest to understand the molecular docking interaction of verteporfin
(a derivative of benzo-porphyrin) with the WW domain of YAP (clinically used for photo-dynamic therapy in macular degeneration)
as a potential WW domain-ligand modulator by inhibition. A homology protein SWISS MODEL of the human YAP protein was
constructed to dock (using AutoDock vina) with the PubChem verteporfin structure for interaction analysis. The docking result shows
the possibilities of verteporfin interaction with the oncogenic transcription cofactor YAP having WW1 and WW2 domains. Thus, the
ability of verteporfin to bind with the YAP WW domain having modulator activity is implied in this analysis.
signaling pathway (AKT1 and LMTK3). These elements are considered as major factors of tumorigenesis (Hsu et al. 2002; Page et al., 2000). They contribute to the progression of different types of cancer by promoting cell survival
Introduction: Since the COVID-19 pandemic began in December 2019, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has continuously evolved with many variants of concern emerging across the world.
Methodology: In order to monitor the evolution of these variants in Morocco, we analyzed a total of 2130 genomes of the delta variant circulating around the world. We also included 164 Moroccan delta variant sequences in our analysis.
Results: Our findings suggest at least four introductions from multiple international sources and a rise of a dominant delta sub-lineage AY.33 in Morocco. Moreover, we report three mutations in the N-terminal domain of the S protein specific to the Moroccan AY.33 isolates, T29A, T250I and T299I. The effect of these mutations on the secondary structure and the dynamic behavior of the S protein N-terminal domain was further determined.
Conclusions: We conclude that these mutations might have functional consequences on the S protein of SARS-CoV-2.
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