Delaspre相关文献与解析，生知库 | 链接生命科学的每一步

Pazos-Gil Maria, Medina-Carbonero Marta, Sanz-AlcÃ¡zar Arabela, Portillo-Carrasquer Marta, Oliveira-Jorge Luiza, HernÃ¡ndez Gonzalo, SÃ¡nchez Mayka, Delaspre Fabien, Cabiscol Elisa, Ros Joaquim, Tamarit Jordi

发表日期：2026

文献求助收藏

Corrigendum to "Deciphering the ferroptosis pathways in dorsal root ganglia of Friedreich ataxia models. The role of LKB1/AMPK, KEAP1, and GSK3β in the impairment of the NRF2 response" [Redox Biol. 76 (2024) 103339]

对“解读弗里德赖希共济失调模型背根神经节中的铁死亡通路。LKB1/AMPK、KEAP1 和 GSK3β 在 NRF2 反应受损中的作用”[Redox Biol. 76 (2024) 103339]的更正

期刊:Redox Biology

影响因子:11.9

doi:10.1016/j.redox.2025.103583

Sanz-Alcázar, Arabela; Portillo-Carrasquer, Marta; Delaspre, Fabien; Pazos-Gil, Maria; Tamarit, Jordi; Ros, Joaquim; Cabiscol, Elisa

Correction: Mitochondrial impairment, decreased Sirtuin activity and protein acetylation in dorsal root ganglia in Friedreich ataxia models

更正：弗里德赖希共济失调模型中背根神经节线粒体功能障碍、Sirtuin活性降低和蛋白质乙酰化

期刊:Cellular and Molecular Life Sciences

影响因子:6.2

doi:10.1007/s00018-025-05948-7

Sanz-Alcázar, Arabela; Britti, Elena; Delaspre, Fabien; Medina-Carbonero, Marta; Pazos-Gil, Maria; Tamarit, Jordi; Ros, Joaquim; Cabiscol, Elisa

Deciphering the ferroptosis pathways in dorsal root ganglia of Friedreich ataxia models. The role of LKB1/AMPK, KEAP1, and GSK3β in the impairment of the NRF2 response

解读弗里德赖希共济失调模型背根神经节中的铁死亡途径。LKB1/AMPK、KEAP1 和 GSK3β 在 NRF2 反应受损中的作用

期刊:Redox Biology

影响因子:10.7

doi:10.1016/j.redox.2024.103339

Arabela Sanz-Alcázar, Marta Portillo-Carrasquer, Fabien Delaspre, Maria Pazos-Gil, Jordi Tamarit, Joaquim Ros, Elisa Cabiscol

Mitochondrial impairment, decreased sirtuin activity and protein acetylation in dorsal root ganglia in Friedreich Ataxia models

弗里德赖希共济失调模型中的线粒体损伤、sirtuin 活性降低和背根神经节中的蛋白质乙酰化

期刊:Cellular and Molecular Life Sciences

影响因子:6.2

doi:10.1007/s00018-023-05064-4

Arabela Sanz-Alcázar, Elena Britti, Fabien Delaspre, Marta Medina-Carbonero, Maria Pazos-Gil, Jordi Tamarit, Joaquim Ros, Elisa Cabiscol

Mice harboring the FXN I151F pathological point mutation present decreased frataxin levels, a Friedreich ataxia-like phenotype, and mitochondrial alterations

携带 FXN I151F 病理点突变的小鼠表现出 frataxin 水平降低、弗里德赖希共济失调样表型和线粒体改变

期刊:Cellular and Molecular Life Sciences

影响因子:6.2

doi:10.1007/s00018-021-04100-5

Marta Medina-Carbonero, Arabela Sanz-Alcázar, Elena Britti, Fabien Delaspre, Elisa Cabiscol, Joaquim Ros, Jordi Tamarit

信号转导

发表日期：2022

文献求助收藏

PPAR gamma agonist leriglitazone improves frataxin-loss impairments in cellular and animal models of Friedreich Ataxia

PPARγ 激动剂 leriglitazone 可改善弗里德赖希共济失调细胞和动物模型中的 frataxin 丢失障碍

期刊:Neurobiology of Disease

影响因子:5.1

doi:10.1016/j.nbd.2020.105162

Laura Rodríguez-Pascau, Elena Britti, Pablo Calap-Quintana, Yi Na Dong, Cristina Vergara, Fabien Delaspre, Marta Medina-Carbonero, Jordi Tamarit, Federico V Pallardó, Pilar Gonzalez-Cabo, Joaquim Ros, David R Lynch, Marc Martinell, Pilar Pizcueta

Calcitriol increases frataxin levels and restores mitochondrial function in cell models of Friedreich Ataxia

骨化三醇可提高 Frataxin 水平并恢复弗里德赖希共济失调细胞模型中的线粒体功能

期刊:Biochemical Journal

影响因子:4.4

doi:10.1042/BCJ20200331

Elena Britti, Fabien Delaspre, A Sanz-Alcázar, Marta Medina-Carbonero, Marta Llovera, Rosa Purroy, Stefka Mincheva-Tasheva, Jordi Tamarit, Joaquim Ros

Calpain-Inhibitors Protect Frataxin-Deficient Dorsal Root Ganglia Neurons from Loss of Mitochondrial Na+/Ca2+ Exchanger, NCLX, and Apoptosis

钙蛋白酶抑制剂可保护 Frataxin 缺乏的背根神经节神经元免于线粒体 Na+/Ca2+ 交换器的丧失、NCLX 和细胞凋亡

期刊:Neurochemical Research

影响因子:3.7

doi:10.1007/s11064-020-03020-3

Elena Britti, Fabien Delaspre, Jordi Tamarit, Joaquim Ros

Frataxin-deficient neurons and mice models of Friedreich ataxia are improved by TAT-MTScs-FXN treatment

TAT-MTScs-FXN 治疗可改善 Frataxin 缺陷神经元和弗里德赖希共济失调小鼠模型

期刊:Journal of Cellular and Molecular Medicine

影响因子:4.3

doi:10.1111/jcmm.13365

Elena Britti, Fabien Delaspre, Anat Feldman, Melissa Osborne, Hagar Greif, Jordi Tamarit, Joaquim Ros

Pathological frataxin deficiency in mice causes tissue-specific alterations in iron homeostasis.

小鼠病理性弗拉塔辛缺乏会导致组织特异性的铁稳态改变。

Corrigendum to "Deciphering the ferroptosis pathways in dorsal root ganglia of Friedreich ataxia models. The role of LKB1/AMPK, KEAP1, and GSK3β in the impairment of the NRF2 response" [Redox Biol. 76 (2024) 103339]

对“解读弗里德赖希共济失调模型背根神经节中的铁死亡通路。LKB1/AMPK、KEAP1 和 GSK3β 在 NRF2 反应受损中的作用”[Redox Biol. 76 (2024) 103339]的更正

Correction: Mitochondrial impairment, decreased Sirtuin activity and protein acetylation in dorsal root ganglia in Friedreich ataxia models

更正：弗里德赖希共济失调模型中背根神经节线粒体功能障碍、Sirtuin活性降低和蛋白质乙酰化

Deciphering the ferroptosis pathways in dorsal root ganglia of Friedreich ataxia models. The role of LKB1/AMPK, KEAP1, and GSK3β in the impairment of the NRF2 response

解读弗里德赖希共济失调模型背根神经节中的铁死亡途径。LKB1/AMPK、KEAP1 和 GSK3β 在 NRF2 反应受损中的作用

Mitochondrial impairment, decreased sirtuin activity and protein acetylation in dorsal root ganglia in Friedreich Ataxia models

弗里德赖希共济失调模型中的线粒体损伤、sirtuin 活性降低和背根神经节中的蛋白质乙酰化

Mice harboring the FXN I151F pathological point mutation present decreased frataxin levels, a Friedreich ataxia-like phenotype, and mitochondrial alterations

携带 FXN I151F 病理点突变的小鼠表现出 frataxin 水平降低、弗里德赖希共济失调样表型和线粒体改变

PPAR gamma agonist leriglitazone improves frataxin-loss impairments in cellular and animal models of Friedreich Ataxia

PPARγ 激动剂 leriglitazone 可改善弗里德赖希共济失调细胞和动物模型中的 frataxin 丢失障碍

Calcitriol increases frataxin levels and restores mitochondrial function in cell models of Friedreich Ataxia

骨化三醇可提高 Frataxin 水平并恢复弗里德赖希共济失调细胞模型中的线粒体功能

Calpain-Inhibitors Protect Frataxin-Deficient Dorsal Root Ganglia Neurons from Loss of Mitochondrial Na+/Ca2+ Exchanger, NCLX, and Apoptosis

钙蛋白酶抑制剂可保护 Frataxin 缺乏的背根神经节神经元免于线粒体 Na+/Ca2+ 交换器的丧失、NCLX 和细胞凋亡

Frataxin-deficient neurons and mice models of Friedreich ataxia are improved by TAT-MTScs-FXN treatment

TAT-MTScs-FXN 治疗可改善 Frataxin 缺陷神经元和弗里德赖希共济失调小鼠模型