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Protective effect of neurofilament heavy gene overexpression in motor neuron disease induced by mutant superoxide dismutase.神经丝重链基因过表达对突变型超氧化物歧化酶诱导的运动神经元疾病的保护作用。
Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9626-30. doi: 10.1073/pnas.95.16.9626.
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Extra axonal neurofilaments do not exacerbate disease caused by mutant Cu,Zn superoxide dismutase.额外的轴突神经丝不会加剧由突变型铜锌超氧化物歧化酶引起的疾病。
Neurobiol Dis. 2000 Aug;7(4):462-70. doi: 10.1006/nbdi.2000.0296.
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Human Cu/Zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mutant SOD1.人类铜/锌超氧化物歧化酶（SOD1）在小鼠体内的过表达会导致线粒体空泡化、轴突变性和运动神经元过早死亡，并加速表达家族性肌萎缩侧索硬化突变型SOD1的小鼠的运动神经元疾病进程。
Neurobiol Dis. 2000 Dec;7(6 Pt B):623-43. doi: 10.1006/nbdi.2000.0299.
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Cell cycle regulators in the neuronal death pathway of amyotrophic lateral sclerosis caused by mutant superoxide dismutase 1.由突变型超氧化物歧化酶1引起的肌萎缩侧索硬化症神经元死亡途径中的细胞周期调节因子。
J Neurosci. 2003 Mar 15;23(6):2131-40. doi: 10.1523/JNEUROSCI.23-06-02131.2003.
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Absence of neurofilaments reduces the selective vulnerability of motor neurons and slows disease caused by a familial amyotrophic lateral sclerosis-linked superoxide dismutase 1 mutant.神经丝的缺失降低了运动神经元的选择性易损性，并减缓了由家族性肌萎缩侧索硬化症相关的超氧化物歧化酶1突变体引起的疾病进程。
Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9631-6. doi: 10.1073/pnas.95.16.9631.
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Transgenic mice in the study of ALS: the role of neurofilaments.肌萎缩侧索硬化症研究中的转基因小鼠：神经丝的作用
Brain Pathol. 1998 Oct;8(4):759-69. doi: 10.1111/j.1750-3639.1998.tb00199.x.
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Selective loss of neurofilament expression in Cu/Zn superoxide dismutase (SOD1) linked amyotrophic lateral sclerosis.与铜/锌超氧化物歧化酶（SOD1）相关的肌萎缩侧索硬化症中神经丝表达的选择性丧失。
J Neurochem. 2002 Sep;82(5):1118-28. doi: 10.1046/j.1471-4159.2002.01045.x.
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Overexpression of neurofilament subunit NF-L and NF-H extends survival of a mouse model for amyotrophic lateral sclerosis.神经丝亚基NF-L和NF-H的过表达延长了肌萎缩侧索硬化小鼠模型的生存期。
Neurosci Lett. 2000 Mar 3;281(1):72-4. doi: 10.1016/s0304-3940(00)00808-9.
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The neuronal Golgi apparatus is fragmented in transgenic mice expressing a mutant human SOD1, but not in mice expressing the human NF-H gene.在表达突变型人类超氧化物歧化酶1（SOD1）的转基因小鼠中，神经元高尔基体发生碎片化，但在表达人类神经丝重链（NF-H）基因的小鼠中则不会。
J Neurol Sci. 2000 Feb 1;173(1):63-72. doi: 10.1016/s0022-510x(99)00301-9.
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Axonal transport of mutant superoxide dismutase 1 and focal axonal abnormalities in the proximal axons of transgenic mice.突变型超氧化物歧化酶1的轴突运输与转基因小鼠近端轴突中的局灶性轴突异常
Neurobiol Dis. 1998 Jul;5(1):27-35. doi: 10.1006/nbdi.1998.0178.
引用本文的文献
1
The usage and advantages of several common amyotrophic lateral sclerosis animal models.几种常见肌萎缩侧索硬化症动物模型的应用及优势
Front Neurosci. 2024 Feb 26;18:1341109. doi: 10.3389/fnins.2024.1341109. eCollection 2024.
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The 2022 Lady Estelle Wolfson lectureship on neurofilaments.2022 年埃斯特尔·沃尔夫森夫人神经丝讲座。
J Neurochem. 2022 Nov;163(3):179-219. doi: 10.1111/jnc.15682. Epub 2022 Sep 19.
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Microglia Influence Neurofilament Deposition in ALS iPSC-Derived Motor Neurons.小胶质细胞影响肌萎缩侧索硬化症 iPSC 衍生运动神经元中的神经丝沉积。
Genes (Basel). 2022 Jan 27;13(2):241. doi: 10.3390/genes13020241.
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The Neglected Genes of ALS: Cytoskeletal Dynamics Impact Synaptic Degeneration in ALS.渐冻症中被忽视的基因：细胞骨架动力学影响渐冻症中的突触退化
Front Cell Neurosci. 2020 Nov 13;14:594975. doi: 10.3389/fncel.2020.594975. eCollection 2020.
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Cross talk between SOD1 and the mitochondrial UPR in cancer and neurodegeneration.SOD1 与线粒体 UPR 在癌症和神经退行性变中的对话。
Mol Cell Neurosci. 2019 Jul;98:12-18. doi: 10.1016/j.mcn.2019.04.003. Epub 2019 Apr 24.
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Diagnostic and Prognostic Performance of Neurofilaments in ALS.神经丝蛋白在肌萎缩侧索硬化症中的诊断和预后价值
Front Neurol. 2019 Jan 18;9:1167. doi: 10.3389/fneur.2018.01167. eCollection 2018.
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Meta-analysis of Genetic Modifiers Reveals Candidate Dysregulated Pathways in Amyotrophic Lateral Sclerosis.遗传修饰体的荟萃分析揭示了肌萎缩侧索硬化症中候选失调的途径。
Neuroscience. 2019 Jan 1;396:A3-A20. doi: 10.1016/j.neuroscience.2018.10.033.
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A motor neuron strategy to save time and energy in neurodegeneration: adaptive protein stoichiometry.一种在神经退行性疾病中节省时间和能量的运动神经元策略：适应性蛋白质化学计量。
J Neurochem. 2018 Sep;146(5):631-641. doi: 10.1111/jnc.14542.
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SOD1, an unexpected novel target for cancer therapy.超氧化物歧化酶1（SOD1），一种出人意料的癌症治疗新靶点。
Genes Cancer. 2014 Apr;5(1-2):15-21. doi: 10.18632/genesandcancer.4.
本文引用的文献
1
Neurofilaments and motor neuron disease.神经丝与运动神经元病。
Trends Cell Biol. 1997 Jun;7(6):243-9. doi: 10.1016/S0962-8924(97)01049-0.
2
Absence of neurofilaments reduces the selective vulnerability of motor neurons and slows disease caused by a familial amyotrophic lateral sclerosis-linked superoxide dismutase 1 mutant.神经丝的缺失降低了运动神经元的选择性易损性，并减缓了由家族性肌萎缩侧索硬化症相关的超氧化物歧化酶1突变体引起的疾病进程。
Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9631-6. doi: 10.1073/pnas.95.16.9631.
3
Pathogenesis of two axonopathies does not require axonal neurofilaments.两种轴索性神经病的发病机制不需要轴突神经丝。
Nature. 1998 Feb 5;391(6667):584-7. doi: 10.1038/35378.
4
Delayed maturation of regenerating myelinated axons in mice lacking neurofilaments.缺乏神经丝的小鼠中再生有髓轴突的延迟成熟。
Exp Neurol. 1997 Nov;148(1):299-316. doi: 10.1006/exnr.1997.6654.
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Evidence of increased oxidative damage in both sporadic and familial amyotrophic lateral sclerosis.散发性和家族性肌萎缩侧索硬化症中氧化损伤增加的证据。
J Neurochem. 1997 Nov;69(5):2064-74. doi: 10.1046/j.1471-4159.1997.69052064.x.
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Mutant superoxide dismutase-1-linked familial amyotrophic lateral sclerosis: molecular mechanisms of neuronal death and protection.突变型超氧化物歧化酶-1相关的家族性肌萎缩侧索硬化症：神经元死亡与保护的分子机制
J Neurosci. 1997 Nov 15;17(22):8756-66. doi: 10.1523/JNEUROSCI.17-22-08756.1997.
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The copper chelator d-penicillamine delays onset of disease and extends survival in a transgenic mouse model of familial amyotrophic lateral sclerosis.
Eur J Neurosci. 1997 Jul;9(7):1548-51. doi: 10.1111/j.1460-9568.1997.tb01511.x.
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Bcl-2: prolonging life in a transgenic mouse model of familial amyotrophic lateral sclerosis.Bcl-2：在家族性肌萎缩侧索硬化转基因小鼠模型中延长寿命
Science. 1997 Jul 25;277(5325):559-62. doi: 10.1126/science.277.5325.559.
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Elevated free nitrotyrosine levels, but not protein-bound nitrotyrosine or hydroxyl radicals, throughout amyotrophic lateral sclerosis (ALS)-like disease implicate tyrosine nitration as an aberrant in vivo property of one familial ALS-linked superoxide dismutase 1 mutant.在整个肌萎缩侧索硬化症（ALS）样疾病中，游离硝基酪氨酸水平升高，但蛋白质结合的硝基酪氨酸或羟基自由基水平未升高，这表明酪氨酸硝化是一种家族性ALS相关超氧化物歧化酶1突变体在体内的异常特性。
Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7606-11. doi: 10.1073/pnas.94.14.7606.
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