Pedersengiles2961

Furthermore, IL-1β-induced activation of the IL-1R1/IκB/IKK/NF-κB signaling pathway in HepG2 cells was proved to be inhibited by TOGA. Taken together, TOGA effectively prevents the support of TAMs from fueling tumorigenesis through a mechanism related to the NF-κB pathway, and it may be a promising GA-modified drug for the treatment of HCC.Molecularly imprinted polymers (MIPs) emerged half a century ago have now attracted tremendous attention as artificial receptors or plastic antibodies. Although the preparation of MIPs targeting small molecules, peptides, or even proteins is straightforward and well-developed, the molecular imprinting of microorganisms still remains a big challenge. This review highlights the preparation of MIPs that reveal biomimetic specificity and selectivity towards microorganisms by creating the well-defined cell recognition sites. We present the state-of-the-art strategies for the expeditious synthesis of MIPs targeting microorganism including surface components imprinting, cell mediated lithography, and microcontact stamping. These receptor-like biomimetic materials have garnered increasing attention in different fields. In this review, we also describe the diverse applications of microorganism-imprinted polymers such as microbial activation, microbial fuel cells, and microorganism detection and sensing. The major challenges and further prospects on the design of microorganism-imprinted polymers is also outlined.

Bacterial surface proteins act as potential adhesins or invasins. The GroEL is a signal peptide-free surface expressed protein that aids adhesion in Escherichia coli by binding to LOX-1 receptor of the host cells. Mycobacterium tuberculosis (Mtb) expresses GroEL2 protein, having high level sequence identity with E. coli GroEL. This study investigates the interaction mechanism of GroEL2 protein of Mtb with LOX-1 of macrophages using integrated computational and experimental approach.

Mtb GroEL2 protein was purified as histidine tagged protein using Ni-NTA chromatography. Confocal and scanning electron microscopies were used to study the uptake of GroEL2 coated fluorescent latex beads through the LOX-1 receptor in RAW264.7 macrophage cell line. Docking studies were performed to understand the interaction between the GroEL2 and LOX-1 proteins. Polyinosinic acid (PIA) was used as a LOX-1 inhibitor in both in silico and in vitro experiments.

GroEL2 protein coating enhances uptake of latex beads into macrophages through LOX-1 receptor. LOX-1 inhibitor PIA decreased the uptake of GroEL2 coated latex beads. GroEL2 interacts with the key ligand binding regions of the LOX-1 receptor, such as the basic spine and the saddle hydrophobic patch. PIA molecule destabilized the LOX-1-GroEL2 docked complex.

Surface associated GroEL2 protein of Mtb is a potential ligand for macrophage LOX-1 receptor. Interaction between GroEL2 and LOX-1 receptor may be utilized by Mtb to gain its intracellular access.

Surface associated GroEL2 of Mtb may bind to the macrophage LOX-1 receptor, enabling the internalization of the bacteria and progression of the infection.

Surface associated GroEL2 of Mtb may bind to the macrophage LOX-1 receptor, enabling the internalization of the bacteria and progression of the infection.Breast cancer is the most common cancer affecting women and one of the leading causes of cancer-related deaths worldwide. In existing studies, some long non-coding RNAs (lncRNAs) are considered to have important regulatory roles in the development of cancers. However, the pathogenic significance of LINC00511 in breast cancer is unclear. In this study, LINC00511 was significantly up-regulated in breast cancer, and its expression level was correlated to poor prognosis of patients with breast cancer. To further study the role of LINC00511 in breast cancer, we knocked down the expression of LINC00511 using siRNAs. Cells transfected with siRNA-2 proliferated, and its metastasis was suppressed. RNA-seq analysis revealed 182 potential targets for LINC00511. Daurisoline The in-silico analysis revealed that differently expressed genes were closely related to signaling mediated by p38-alpha and p38-beta. Subcellular localization showed that LINC00511 was mainly located in the cytoplasm, and knocking down the LINC00511 gene could down-regulate the expression of MMP13. Using bioinformatics analysis combined with dual-luciferase report assay, we finally determined that miR-150 was the direct target of LINC00511. The dual-luciferase report assays also showed that MMP13 was the target of miR-150. LINC00511 knockdown significantly reduced MMP13 protein levels, and miR-150 gene knockdown significantly rescued the down-regulation of MMP13 caused by LINC00511 gene silencing. Moreover, silencing MMP13 and overexpression of miR-150 could reduce the proliferation of breast cancer cells. In conclusion, our data show that LINC00511 is a breast cancer promoter, and the LINC00511/miR-150/MMP13 axis may be a new therapeutic strategy for breast cancer patients.Cadmium (Cd), a heavy metal produced by various industries, contaminates the environment and seriously damages the skeletal system of humans and animals. Recent studies have reported that Cd can affect the viability of cells, including osteoblasts, both in vivo and in vitro. However, the mechanism of Cd-induced apoptosis remains unclear. In the present study, primary rat osteoblasts were used to investigate the Cd-induced apoptotic mechanism. We found that treatment with 2 and 5 μM Cd for 12 h decreased osteoblast viability and increased apoptosis. Furthermore, Cd increased the generation of reactive oxygen species (ROS), and, thus, DNA damage measured via p-H2AX. The level of the nuclear transcription factor p53 was significantly increased, which upregulated the expression of PUMA, Noxa, Bax, and mitochondrial cytochrome c, downregulated the expression of Bcl-2, and increased the level of cleaved caspase-3. However, pretreatment with the ROS scavenger N-acetyl-l-cysteine (NAC) or the p53 transcription specific inhibitor PFT-α suppressed Cd-induced apoptosis. Our results indicate that Cd can induce apoptosis in osteoblasts by increasing the generation of ROS and activating the mitochondrial p53 signaling pathway, and this mechanism requires the transcriptional activation of p53.