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Cabozantinib Selectively Induces Proteasomal Degradation of p53 Somatic Mutant Y220C and Impedes Tumor Growth.
J Biol Chem
January 2025
Department of Hepatopancreatobiliary Surgery, Suzhou Ninth Hospital Affiliated to Soochow University; Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University; Jiangsu, China. Electronic address:
Inactivation of p53 by mutations commonly occurs in human cancer. The mutated p53 proteins may escape proteolytic degradation and exhibit high expression in tumors, and acquire gain-of-function activity that promotes tumor progression and chemo-resistance. Therefore, selectively targeting of the gain-of-function p53 mutants may serve as a promising therapeutic strategy for cancer prevention and treatment.
View Article and Find Full Text PDFSystematically developing a registry of splice-site creating variants utilizing massive publicly available transcriptome sequence data.
Nat Commun
January 2025
Division of Genome Analysis Platform Development, National Cancer Center Research Institute, Tokyo, Japan.
Genomic variants causing abnormal splicing play important roles in genetic disorders and cancer development. Among them, variants that cause the formation of novel splice-sites (splice-site creating variants, SSCVs) are particularly difficult to identify and often overlooked in genomic studies. Additionally, these SSCVs are frequently considered promising candidates for treatment with splice-switching antisense oligonucleotides (ASOs).
View Article and Find Full Text PDFA Novel Microbe, Immunization Deaths, and Vaccination on Trial: BCG and the Lübeck Disaster of 1930.
Am Surg
January 2025
Mercer University School of Medicine, Columbus, GA, USA.
Today's controversies of gain-of-function virological research and mRNA COVID vaccination policies had an antecedent nearly a century ago in an event often referred to as "the Lübeck disaster." From April through September 1930, 77 newborn infants in Lübeck, Germany, died after receiving oral BCG immunizations tainted with active human . The tragedy threatened to end BCG immunizations.
View Article and Find Full Text PDFLGR4 is essential for maintaining β-cell homeostasis through suppression of RANK.
Mol Metab
January 2025
Arthur Riggs Diabetes and Metabolism Research Institute, City of Hope, Duarte, CA 91010, USA; Department of Translational Research and Cellular Therapeutics, City of Hope, Duarte, CA 91010, USA. Electronic address:
Objective: Loss of functional β-cell mass is a major cause of diabetes. Thus, identifying regulators of β-cell health is crucial for treating this disease. The In this study, we assessed the regulation of Lgr4 in islets, and the role of LGR4 and LGR4/RANK stoichiometry in β-cell health under basal and stress-induced conditions, in vitro and in vivo.
View Article and Find Full Text PDFNeuroligin-3 R451C induces gain-of-function gene expression in astroglia in an astroglia-enriched brain organoid model.
Cell Regen
January 2025
Department of Cell Biology and Neuroscience, Rutgers University, 604 Allison Road, Piscataway, NJ, 08854, USA.
Astroglia are integral to brain development and the emergence of neurodevelopmental disorders. However, studying the pathophysiology of human astroglia using brain organoid models has been hindered by inefficient astrogliogenesis. In this study, we introduce a robust method for generating astroglia-enriched organoids through BMP4 treatment during the neural differentiation phase of organoid development.
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