The original version of this article unfortunately contained an error in acknowledgment text. The authors would like to include a statement: "Moumita Dasgupta is supported by Junior Research Fellowship from University Grant Commission, India." in acknowledgment section.
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http://dx.doi.org/10.1007/s10495-019-01534-y | DOI Listing |
Acta Pharmacol Sin
January 2025
Laboratory of Molecular Target Therapy of Cancer, Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan, 442000, China.
Stem Cell Res
December 2024
Murdoch Children's Research Institute, Parkville, Victoria, Australia; Department of Paediatrics, University of Melbourne, Parkville, Victoria, Australia. Electronic address:
A rare neurodevelopmental disorder has been linked to a well-conserved splice site variant in the TRAPPC4 gene (c.454 + 3A > G), which causes mis-splicing of TRAPPC4 transcripts and reduced levels of TRAPPC4 protein. Patients present with severe progressive neurological symptoms including seizures, microcephaly, intellectual disability and facial dysmorphism.
View Article and Find Full Text PDFMol Med
January 2025
Department of Gastrointestinal Surgery, Taizhou Hospital, Wenzhou Medical University, No.105 Westgate Street, Linhai, 317000, China.
Plant Cell Rep
January 2025
Hainan Key Laboratory for Sustainable Utilization of Tropical Bioresources and College of Biology, Institute of Tropical Agriculture and Forestry, Hainan University, Haikou, 570228, China.
Antioxidants (Basel)
December 2024
Department of Nutrition, Chung Shan Medical University, Taichung 402, Taiwan.
Spinocerebellar ataxia type 3 (SCA3), caused by the abnormal expansion of polyglutamine (polyQ) in the ataxin-3 protein, is one of the inherited polyQ neurodegenerative diseases that share similar genetic and molecular features. Mutant polyQ-expanded ataxin-3 protein is prone to aggregation in affected neurons and is predominantly degraded by autophagy, which is beneficial for neurodegenerative disease treatment. Not only does mutant polyQ-expanded ataxin-3 increase susceptibility to oxidative cytotoxicity, but it also hampers antioxidant potency in neuronal cells.
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