Sarrabeth相关文献与解析，生知库 | 链接生命科学的每一步

Mouse microglia express unique miRNA-mRNA networks to facilitate age-specific functions in the developing central nervous system

小鼠小胶质细胞表达独特的 miRNA-mRNA 网络，以促进中枢神经系统发育中年龄特异性的功能

doi:10.1038/s42003-023-04926-8

Alexander D Walsh, Sarrabeth Stone, Saskia Freytag, Andrea Aprico, Trevor J Kilpatrick, Brendan R E Ansell, Michele D Binder

Endoplasmic reticulum associated degradation is required for maintaining endoplasmic reticulum homeostasis and viability of mature Schwann cells in adults

内质网相关降解是维持成人内质网稳态和成熟雪旺细胞活力所必需的

期刊:Glia

影响因子:5.4

doi:10.1002/glia.23910

Shuangchan Wu, Sarrabeth Stone, Yuan Yue, Wensheng Lin

The UPR preserves mature oligodendrocyte viability and function in adults by regulating autophagy of PLP

UPR 通过调节 PLP 的自噬来维持成人成熟少突胶质细胞的活力和功能

期刊:JCI Insight

影响因子:6.3

doi:10.1172/jci.insight.132364

Sarrabeth Stone, Shuangchan Wu, Klaus-Armin Nave, Wensheng Lin

The Integrated UPR and ERAD in Oligodendrocytes Maintain Myelin Thickness in Adults by Regulating Myelin Protein Translation

少突胶质细胞中整合的 UPR 和 ERAD 通过调节髓鞘蛋白翻译来维持成人髓鞘厚度

期刊:Journal of Neuroscience

影响因子:4.4

doi:10.1523/JNEUROSCI.0604-20.2020

Shuangchan Wu, Sarrabeth Stone, Klaus-Armin Nave, Wensheng Lin

NF-κB Activation Accounts for the Cytoprotective Effects of PERK Activation on Oligodendrocytes during EAE

NF-κB激活是PERK激活在EAE模型中对少突胶质细胞发挥细胞保护作用的原因。

期刊:Journal of Neuroscience

影响因子:4.4

doi:10.1523/JNEUROSCI.1156-20.2020

Zhixin Lei ，Yuan Yue ，Sarrabeth Stone ，Shuangchan Wu ，Wensheng Lin

Neuron-specific PERK inactivation exacerbates neurodegeneration during experimental autoimmune encephalomyelitis

神经元特异性 PERK 失活加剧实验性自身免疫性脑脊髓炎期间的神经退行性

期刊:JCI Insight

影响因子:6.3

doi:10.1172/jci.insight.124232

Sarrabeth Stone, Yuan Yue, Milos Stanojlovic, Shuangchan Wu, Gerard Karsenty, Wensheng Lin

Role of nuclear factor κB in multiple sclerosis and experimental autoimmune encephalomyelitis

核因子κB在多发性硬化症和实验性自身免疫性脑脊髓炎中的作用

期刊:Neural Regeneration Research

影响因子:6.7

doi:10.4103/1673-5374.237109

Yue, Yuan; Stone, Sarrabeth; Lin, Wensheng

Activating transcription factor 6α deficiency exacerbates oligodendrocyte death and myelin damage in immune-mediated demyelinating diseases

激活转录因子 6α 缺乏会加剧免疫介导的脱髓鞘疾病中的少突胶质细胞死亡和髓鞘损伤

期刊:Glia

影响因子:5.4

doi:10.1002/glia.23307

Sarrabeth Stone, Shuangchan Wu, Stephanie Jamison, Wilaiwan Durose, Jean Pierre Pallais, Wensheng Lin

Type II Activation of Macrophages and Microglia by Immune Complexes Enhances Th17 Biasing in an IL-6-Independent Manner

免疫复合物对巨噬细胞和小胶质细胞的 II 型激活以 IL-6 非依赖的方式增强 Th17 偏向

期刊:PLoS One

影响因子:2.9

doi:10.1371/journal.pone.0164454

Sarrabeth Stone, Anne Camille La Flamme

Tyro3 deletion is protective in experimental autoimmune encephalomyelitis

Tyro3 缺失在实验性自身免疫性脑脊髓炎中具有保护作用

Mouse microglia express unique miRNA-mRNA networks to facilitate age-specific functions in the developing central nervous system

小鼠小胶质细胞表达独特的 miRNA-mRNA 网络，以促进中枢神经系统发育中年龄特异性的功能

Endoplasmic reticulum associated degradation is required for maintaining endoplasmic reticulum homeostasis and viability of mature Schwann cells in adults

内质网相关降解是维持成人内质网稳态和成熟雪旺细胞活力所必需的

The UPR preserves mature oligodendrocyte viability and function in adults by regulating autophagy of PLP

UPR 通过调节 PLP 的自噬来维持成人成熟少突胶质细胞的活力和功能

The Integrated UPR and ERAD in Oligodendrocytes Maintain Myelin Thickness in Adults by Regulating Myelin Protein Translation

少突胶质细胞中整合的 UPR 和 ERAD 通过调节髓鞘蛋白翻译来维持成人髓鞘厚度

NF-κB Activation Accounts for the Cytoprotective Effects of PERK Activation on Oligodendrocytes during EAE

NF-κB激活是PERK激活在EAE模型中对少突胶质细胞发挥细胞保护作用的原因。

Neuron-specific PERK inactivation exacerbates neurodegeneration during experimental autoimmune encephalomyelitis

神经元特异性 PERK 失活加剧实验性自身免疫性脑脊髓炎期间的神经退行性

Role of nuclear factor κB in multiple sclerosis and experimental autoimmune encephalomyelitis

核因子κB在多发性硬化症和实验性自身免疫性脑脊髓炎中的作用

Activating transcription factor 6α deficiency exacerbates oligodendrocyte death and myelin damage in immune-mediated demyelinating diseases

激活转录因子 6α 缺乏会加剧免疫介导的脱髓鞘疾病中的少突胶质细胞死亡和髓鞘损伤

Type II Activation of Macrophages and Microglia by Immune Complexes Enhances Th17 Biasing in an IL-6-Independent Manner

免疫复合物对巨噬细胞和小胶质细胞的 II 型激活以 IL-6 非依赖的方式增强 Th17 偏向