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

作     者：Pascual Torres Reinald Pamplona Manuel Portero-Otin Pascual Torres;Reinald Pamplona;Manuel Portero-Otin

作者机构：Metabolic Pathophysiology Research GroupDepartment of Experimental MedicineUniversity of Lleida-IRBLleidaLleidaSpain 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2023年第18卷第8期

页      面：1725-1726页

核心收录：

学科分类：0710[理学-生物学] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100204[医学-神经病学] 10[医学] 

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)。 

主　　题：metabolism degenerative 

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).