Cell senescence,loss of splicing,and lipid metabolism in TDP-43-related neurodegenerative processes  

作　　者：Pascual Torres Reinald Pamplona Manuel Portero-Otin 

机构地区：[1]Metabolic Pathophysiology Research Group,Department of Experimental Medicine,University of Lleida-IRBLleida,Lleida,Spain

出　　处：《Neural Regeneration Research》2023年第8期1725-1726,共2页中国神经再生研究（英文版）

基　　金：the Instituto de Salud CarlosⅢ(PI 17-000134,PI 20-0155)to MPO;the Generalitat de Catalunya 2017SGR696 to RP;a"Margarita Salas"fellow from the Spanish Ministry of Universities[Financed by European Union-NextGenerationEl funds];a FUNDELA Grant,RedELA-Plataforma Investigación and the FundacióMiquel Valls(Jack Van den Hoek donation)(to MPO);FEDER funds are acknowledged("A way to make Europe")(to MPO)。

摘　　要：In recent work,we have shown that cell senescence of mouse fibroblasts in vitro associates with a build-up of cryptic exons in selected mRNAs,whose level is usually controlled by the activity of TAR DNA binding protein of 43 kDa(Tdp-43)(Torres et al.,2022).In vivo,we also found traits of cell senescence in the motor neuron disease model achieved by overexpressing SOD-G93A,the SOD1 gene(harboring a single amino acid substitution of glycine to alanine at codon 93).

关 键 词：METABOLISM DEGENERATIVE 

分 类 号：R741[医药卫生—神经病学与精神病学]