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Magnetically Responsive Nanomedicine
Published in Lin Zhu, Stimuli-Responsive Nanomedicine, 2021
Meng Zhang, Ergang Liu, Yongzhuo Huang
Moreover, magnetic nanoparticles can be used to control the death of cancer cells by modulating apoptosis. Extrinsic apoptosis signaling pathways initiated by death receptors are widely investigated to treat cancers. Clustering of death receptors is the main activator of extrinsic apoptosis signaling pathways. For example, TNF-related apoptosis inducing ligand (TRAIL) can significantly induce the formation of death receptor clusters and cell apoptosis. Anti-death receptor 4 (DR4) antibody conjugated zinc-doped iron oxide magnetic nanoparticles could effectively turn on the apoptosis signaling in the DR4-overexpressed DLD-1 colon cancer cells, and under an external magnetic field they could as well induce morphologic changes in a zebrafish model expressing zebrafish ovarian TNF receptor, which functioned similarly to human DR4 [144, 145]. In this system, the antibody-modified magnetic nanoparticles could bind to DR4 on the cancer cells, and DR4 thus formed the receptor clusters under the applied magnetic field to activate the apoptosis signaling of cancer cells.
Anti-Arthritic Potential of Gold Nanoparticle
Published in Klaus D. Sattler, st Century Nanoscience – A Handbook, 2020
Jayeeta Sengupta, Sourav Ghosh, Antony Gomes
It is thought that the main risk factor for rheumatoid arthritis is the genetic factors. Antigen-presenting cells of the immune system possess major histocompatibility (MHC) antigens (class II) at the cell surface, encoded by a gene HLA-DR4. It is estimated that a conserved sequence in HLA-DR4 gene contributes around 30% of total genetic risks for rheumatoid arthritis. This conserved and specific sequence in HLA-DR4 gene causes a slight change in class II MHC antigens, leading to the activation of T lymphocytes. The other genetic risk factors contributing to the initiation of the pathogenesis of rheumatoid arthritis include peptidyl arginine deiminase-4, STAT4, PTNP22, and CTLA4. Peptidyl argi-nine deiminase-4 causes increased citrullination of peptides, which unfolds the peptide (change in 3D structure) due to the loss of positively charged arginine residues. It makes the self-protein an antigen, producing specific anti-citrullinated peptide antibodies (rheumatoid arthritis-specific autoantibody). A polymorphism in peptidyl argi-nine deiminase-4 gene causes increased citrullination of peptides. Anti-citrullinated peptide antibodies can be identified up to 12–15 years before the commencement of clinical symptoms of rheumatoid arthritis, indicating a preclinical period of the pathogenesis of the disease. STAT4, PTNP22, and CTLA4 are involved in the activation of tumor necrosis factor receptor and T-cell activation, leading to the initiation of rheumatoid arthritis pathogenesis.
Terpenoids: The Biological Key Molecules
Published in Dijendra Nath Roy, Terpenoids Against Human Diseases, 2019
Moumita Majumdar, Dijendra Nath Roy
Apoptosis or type-1 programmed cell death is initiated by the activation of death receptor (DR) signalling through the binding of the Fas receptor (FasR), TNF receptor (TNFR), DR3, DR4 and DR5 with their respective ligands, resulting in conformational change. After oligomerisation of the receptor via ligands, specialized adaptor proteins activate the caspase cascades. Trimerisation of Fas by binding with FasI recruits adaptor protein Fas-associated death domain (FADD), which activates caspase-8. After oligomerisation, caspase-8 initiates the signalling that stimulates apoptosis via two parallel pathways. In the absence of the caspase cascade, death receptors activate another alternative signalling system designated as necroptosis via formation of the IIb complex. As the largest group of natural products, plant terpenoids have a promising effect on death domain signalling.
Cytochrome P450 1B1 promotes cancer cell survival via specificity protein 1 (Sp1)-mediated suppression of death receptor 4
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Yeo-Jung Kwon, Nam-Hyeon Cho, Dong-Jin Ye, Hyoung-Seok Baek, Yeon-Sang Ryu, Young-Jin Chun
Hypermethylation on decoy receptors of TRAIL in multiple types of tumors was reported by Shivapurkar et al. (2004) who postulated that promotion of aberrant DNA methylation and subsequent silencing of decoy receptors was the basis for tumor-selective apoptotic effects of TRAIL. Because DR4 has close homology to decoy receptors, hypermethylation on DR4 genes also may occur in cancer cells (LeBlanc and Ashkenazi 2003). Further, hypermethylation on the DR4 promoter in TRAIL-resistant ovarian cancer tissues was observed and the consequent loss of DR4 protein expression in patients was detected by Horak et al. (2005). Based upon these findings, the possibility of DR4 suppression by oncoprotein CYP1B1 through epigenetic regulation in cancer cells was suggested and data indicated that CYP1B1 may induce methylation of DR4 genes.