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作 者:Camilla Aurora Franchino Elisa Motori Matteo Bergami
机构地区:[1]Institute for Biochemistry,University of Cologne,50674 Cologne,Germany [2]Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases(CECAD),Faculty of Medicine and University Hospital Cologne,University of Cologne,50931 Cologne,Germany [3]Center for Molecular Medicine,50931 Cologne,Germany
出 处:《Signal Transduction and Targeted Therapy》2024年第2期341-342,共2页信号转导与靶向治疗(英文)
基 金:supported by the Deutsche Forschungsgemeinschaft(SFB1218-Grant No.269925409 and CECAD EXC 2030-Grant No.390661388 to E.M.and M.B.,SFB1451-Grant No.431549029 to M.B.).
摘 要:In a recently published study in Science,Naòn et al.report two uncharacterized splice variants of Mitofusin 2(MFN2)that specifically shape and tether the endoplasmic reticulum(ER)to mitochondria.1 This work sheds new light on the pleiotropic effects previously ascribed to MFN2 loss-of-function mutations,and has important implications for associated metabolic and neurological diseases.
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