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V

Victoria E. von Saucken

University System of Ohio

H指数:8

被引数:1,416

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Postsynaptic BMP signaling regulates myonuclear properties in Drosophila larval muscles

JOURNAL OF CELL BIOLOGY

IF6.4

2024-10-300

PRE

Muscle cofilin alters neuromuscular junction postsynaptic development to strengthen functional neurotransmission

IF3.6

2024-07-082

OA

A good gut feeling on Sarm1-mediated axon degeneration

IF12.8

2021-04-260

OAAI

The effect of amyloid on microglia-neuron interactions before plaque onset occurs independently of TREM2 in a mouse model of Alzheimer's disease

NEUROBIOLOGY OF DISEASE

IF5.6

2020-11-0116

OAAI

TREM2 is required for microglial instruction of astrocytic synaptic engulfment in neurodevelopment

IF5.1

2019-07-0272

OAAI

The Trem2 R47H variant confers loss-of-function-like phenotypes in Alzheimer's disease

Trem2 R47H变体在阿尔茨海默氏病中赋予功能丧失样表型

MOLECULAR NEURODEGENERATION

IF17.5

2018-06-01164

OAAI

TREM2 in Neurodegenerative Diseases

MOLECULAR NEURODEGENERATION

IF17.5

2017-08-02313

OAAI

Loss of native α-synuclein multimerization by strategically mutating its amphipathic helix causes abnormal vesicle interactions in neuronal cells

HUMAN MOLECULAR GENETICS

IF3.2

2017-06-1977

OAAI

Parkinson-causing α-synuclein missense mutations shift native tetramers to monomers as a mechanism for disease initiation (vol 6, 7314, 2015)

NATURE COMMUNICATIONS

IF15.7

2015-07-308

OAAI

KTKEGV repeat motifs are key mediators of normal α-synuclein tetramerization: Their mutation causes excess monomers and neurotoxicity

KTKEGV重复基序是正常 α-突触核蛋白四聚化的关键介质: 它们的突变导致过量单体和神经毒性

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

IF9.1

2015-07-07146

OAAI

Parkinson-causing α-synuclein missense mutations shift native tetramers to monomers as a mechanism for disease initiation

NATURE COMMUNICATIONS

IF15.7

2015-06-16260

OAAI