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Monoclonal antibodies have been considered promising therapeutic entities due to their highly specific binding to antigens. For oncology in particular, the tumor specific binding of an antibody, without affecting normal tissue, is considered an ideal cancer therapy. Although the proposed mechanism of action of antibody therapeutics varies by targets and indications, antibody-dependent cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), ligand neutralization and inhibition of the signaling pathway are commonly used. Recent advances in genomic information, genetic engineering, and transgenic technology have greatly accelerated drug development processes. It is also possible to add new functions to antibody molecules through molecular engineering. For example, antibody-drug conjugates (ADC), which combine a monoclonal antibody and a small-molecule cytotoxic drug, have been successfully used for cancer treatment. It has been more than 20 years since the first therapeutic antibody was approved in Japan, and there are now more than 30 antibodies on the market, with many new molecules under development. Despite some drawbacks and challenges, antibody therapeutics hold great promise as we advance our knowledge and technologies in the coming years.
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http://dx.doi.org/10.1248/yakushi.16-00252-1 | DOI Listing |
Transplant Proc
March 2025
Department of Surgery, School of Medicine, Kyungpook National University, Daegu, South Korea.
Background: The conventional lymphocyte crossmatch (XM) assay necessitates mononuclear cell isolation. In our previous work, we introduced a novel 3-laser, 4-color flow cytometric (FC) XM protocol utilizing whole blood lysis (WBL) and CD45 fluorescence-triggered acquisition to detect human leukocyte antigen (HLA) antibody binding. Building on this, we aimed to adapt these advancements for complement-dependent cytotoxicity (CDC) XM using FC (FCCDC).
View Article and Find Full Text PDFMol Cell Probes
March 2025
Human and Neurobiology, Department of Chemistry and Biology, University of Siegen, Siegen, Germany. Electronic address:
Huntington's disease (HD) arises from the abnormal expansion of a CAG repeat in the HTT gene. The mutant CAG repeat triggers aberrant RNA-protein interactions and translates into toxic aggregate-prone polyglutamine protein. These aberrant RNA-protein ineractions also seed the formation of cytoplasmic liquid-like granules, such as stress granules.
View Article and Find Full Text PDFJ Biol Chem
March 2025
Department of Pharmacology and Therapeutics, McGill University, Montréal, Quebec, Canada; Department of Anatomy and Cell Biology, McGill University, Montréal, Quebec, Canada; Integrated Program in Neuroscience, McGill University; Montréal, Québec, Canada. Electronic address:
Follicle-stimulating hormone (FSH), a product of pituitary gonadotrope cells, regulates gonadal function and fertility. FSH production is stimulated by gonadotropin-releasing hormone (GnRH) and activin-class ligands of the TGFβ family. Inhibin A and B are TGFβ proteins that suppress FSH synthesis by competitively binding activin type II receptors in concert with the co-receptors betaglycan (TGFBR3) and TGFBR3L.
View Article and Find Full Text PDFExp Cell Res
March 2025
Department of Ophthalmology, Tong Ren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China. Electronic address:
Our study aimed to elucidate the mechanism by which circTHADA competitively adsorbs miR-494-3p to regulate CASP1-mediated endothelial cell (EC) pyroptosis in diabetic retinopathy (DR). To be specific, we used high glucose (HG)-induced human retinal microvascular endothelial cells (HRMECs) as DR cell models and streptozotocin (STZ)-treated mice as DR mouse models. The expression levels of circTHADA, miR-494-3p, CASP1, NLRP3, GSDMD-N and IL-1β were detected and flow cytrometry was applied to measure cell pyroptosis rate and dual luciferase reporter assays were utilized to determine the direct binding sites.
View Article and Find Full Text PDFGene
March 2025
Department of Ophthalmology, The Second Hospital of Jilin University, Changchun 130000 Jilin, China. Electronic address:
Background: Following injury and disruption of the retinal barrier, retinal pigment epithelium can differentiate into a fibroblastic phenotype, leading to proliferation and migration, thereby resulting in pathological conditions such as proliferative vitreoretinopathy and diabetic retinopathy. Previous studies have detected the specific expression of serine/arginine-rich splicing factor 10 (SRSF10) in the retina; however, its specific function has not been thoroughly studied. SRSF10 has been hypothesized to play an important role in retinal function.
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