Sharon Ronit相关文献与解析，生知库 | 链接生命科学的每一步

Î±-Synuclein structural features inhibit harmful polyunsaturated fatty acid oxidation, suggesting roles in neuroprotection.

α-突触核蛋白的结构特征抑制有害的多不饱和脂肪酸氧化，表明其在神经保护中发挥作用

doi:10.1074/jbc.M116.765149

De Franceschi Giorgia, Fecchio Chiara, Sharon Ronit, Schapira Anthony H V, Proukakis Christos, Bellotti Vittorio, de Laureto Patrizia Polverino

神经科学

发表日期：2017

文献求助收藏

Î-synuclein neuropathology is controlled by nuclear hormone receptors and enhanced by docosahexaenoic acid in a mouse model for Parkinson's disease.

在帕金森病小鼠模型中，α-突触核蛋白神经病理学受核激素受体控制，并受二十二碳六烯酸增强

期刊:Brain Pathology

影响因子:6.2

doi:10.1111/j.1750-3639.2011.00530.x

Yakunin Eugenia, Loeb Virginie, Kisos Haya, Biala Yoav, Yehuda Shlomo, Yaari Yoel, Selkoe Dennis J, Sharon Ronit

Increased neuronal Î±-synuclein pathology associates with its accumulation in oligodendrocytes in mice modeling Î±-synucleinopathies.

在模拟α-突触核蛋白病的鼠模型中，神经元α-突触核蛋白病理的增加与其在少突胶质细胞中的积累有关

期刊:PLoS One

影响因子:2.6

doi:10.1371/journal.pone.0046817

Kisos Haya, PukaÃ Katharina, Ben-Hur Tamir, Richter-Landsberg Christiane, Sharon Ronit

神经科学

发表日期：2012

文献求助收藏

α-Synuclein expression selectively affects tumorigenesis in mice modeling Parkinson's disease

α-突触核蛋白表达选择性地影响帕金森病小鼠模型中的肿瘤发生

期刊:PLoS One

影响因子:2.6

doi:10.1371/journal.pone.0019622

Israeli, Eitan; Yakunin, Eugenia; Zarbiv, Yonaton; Hacohen-Solovich, Amir; Kisos, Haya; Loeb, Virginie; Lichtenstein, Michal; Ben-Gedalya, Tziona; Sabag, Ofra; Pikarsky, Eli; Lorberboum-Galski, Haya; Sharon, Ronit

The transgenic overexpression of alpha-synuclein and not its related pathology associates with complex I inhibition.

α-突触核蛋白的转基因过表达及其相关病理与复合物I抑制有关

期刊:Journal of Biological Chemistry

影响因子:3.9

doi:10.1074/jbc.M109.061051

Loeb Virginie, Yakunin Eugenia, Saada Ann, Sharon Ronit

免疫/内分泌

发表日期：2010

文献求助收藏

Alpha-synuclein and polyunsaturated fatty acids promote clathrin-mediated endocytosis and synaptic vesicle recycling.

α-突触核蛋白和多不饱和脂肪酸促进网格蛋白介导的内吞作用和突触小泡循环

期刊:Traffic

影响因子:2.5

doi:10.1111/j.1600-0854.2008.00853.x

Ben Gedalya Tziona, Loeb Virginie, Israeli Eitan, Altschuler Yoram, Selkoe Dennis J, Sharon Ronit

免疫/内分泌

发表日期：2009

文献求助收藏

Polyunsaturated fatty acids induce alpha-synuclein-related pathogenic changes in neuronal cells

多不饱和脂肪酸可诱导神经元细胞中与α-突触核蛋白相关的病理变化。

期刊:American Journal of Pathology

影响因子:3.6

doi:10.2353/ajpath.2007.070373

Assayag, Karen; Yakunin, Evgenia; Loeb, Virginie; Selkoe, Dennis J; Sharon, Ronit

An Emerging Role for Phosphoinositides in the Pathophysiology of Parkinson's Disease

磷脂酰肌醇在帕金森病病理生理学中的新兴作用

α-Synuclein Translocates to the Nucleus to Activate Retinoic-Acid-Dependent Gene Transcription

α-突触核蛋白转位至细胞核以激活视黄酸依赖性基因转录

α-Synuclein in blood cells differentiates Parkinson's disease from healthy controls

血液细胞中的α-突触核蛋白可区分帕金森病患者和健康对照组。

Î±-Synuclein structural features inhibit harmful polyunsaturated fatty acid oxidation, suggesting roles in neuroprotection.

α-突触核蛋白的结构特征抑制有害的多不饱和脂肪酸氧化，表明其在神经保护中发挥作用

Î-synuclein neuropathology is controlled by nuclear hormone receptors and enhanced by docosahexaenoic acid in a mouse model for Parkinson's disease.

在帕金森病小鼠模型中，α-突触核蛋白神经病理学受核激素受体控制，并受二十二碳六烯酸增强

Increased neuronal Î±-synuclein pathology associates with its accumulation in oligodendrocytes in mice modeling Î±-synucleinopathies.

在模拟α-突触核蛋白病的鼠模型中，神经元α-突触核蛋白病理的增加与其在少突胶质细胞中的积累有关

α-Synuclein expression selectively affects tumorigenesis in mice modeling Parkinson's disease

α-突触核蛋白表达选择性地影响帕金森病小鼠模型中的肿瘤发生

The transgenic overexpression of alpha-synuclein and not its related pathology associates with complex I inhibition.

α-突触核蛋白的转基因过表达及其相关病理与复合物I抑制有关

Alpha-synuclein and polyunsaturated fatty acids promote clathrin-mediated endocytosis and synaptic vesicle recycling.

α-突触核蛋白和多不饱和脂肪酸促进网格蛋白介导的内吞作用和突触小泡循环

Polyunsaturated fatty acids induce alpha-synuclein-related pathogenic changes in neuronal cells

多不饱和脂肪酸可诱导神经元细胞中与α-突触核蛋白相关的病理变化。

An Emerging Role for Phosphoinositides in the Pathophysiology of Parkinson's Disease

磷脂酰肌醇在帕金森病病理生理学中的新兴作用

α-Synuclein Translocates to the Nucleus to Activate Retinoic-Acid-Dependent Gene Transcription

α-突触核蛋白转位至细胞核以激活视黄酸依赖性基因转录

α-Synuclein in blood cells differentiates Parkinson's disease from healthy controls

血液细胞中的α-突触核蛋白可区分帕金森病患者和健康对照组。

Î±-Synuclein structural features inhibit harmful polyunsaturated fatty acid oxidation, suggesting roles in neuroprotection.

α-突触核蛋白的结构特征抑制有害的多不饱和脂肪酸氧化，表明其在神经保护中发挥作用

Î-synuclein neuropathology is controlled by nuclear hormone receptors and enhanced by docosahexaenoic acid in a mouse model for Parkinson's disease.

在帕金森病小鼠模型中，α-突触核蛋白神经病理学受核激素受体控制，并受二十二碳六烯酸增强

Increased neuronal Î±-synuclein pathology associates with its accumulation in oligodendrocytes in mice modeling Î±-synucleinopathies.

在模拟α-突触核蛋白病的鼠模型中，神经元α-突触核蛋白病理的增加与其在少突胶质细胞中的积累有关

α-Synuclein expression selectively affects tumorigenesis in mice modeling Parkinson's disease

α-突触核蛋白表达选择性地影响帕金森病小鼠模型中的肿瘤发生

The transgenic overexpression of alpha-synuclein and not its related pathology associates with complex I inhibition.

α-突触核蛋白的转基因过表达及其相关病理与复合物I抑制有关

Alpha-synuclein and polyunsaturated fatty acids promote clathrin-mediated endocytosis and synaptic vesicle recycling.

α-突触核蛋白和多不饱和脂肪酸促进网格蛋白介导的内吞作用和突触小泡循环

Polyunsaturated fatty acids induce alpha-synuclein-related pathogenic changes in neuronal cells

多不饱和脂肪酸可诱导神经元细胞中与α-突触核蛋白相关的病理变化。

Î-synuclein neuropathology is controlled by nuclear hormone receptors and enhanced by docosahexaenoic acid in a mouse model for Parkinson's disease.