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Low-expressing synucleinopathy mouse models based on oligomer formation and C-terminal truncation of α-synuclein

ABSTRACT: Two mouse models were developed that expressed mutated human alpha synuclein under the control of endogenous murine αSyn (mαSyn) regulatory regions. The expression of the mαSyn was thereby abolished. The genetically ingeneered mice expressed either human αSyn (hαSyn) with a C-terminal deletion ending hαSyn at amino acid 119 or hαSyn with 3 alanine to proline substitutions at residues 30, 56, and 76. Here we tested the expression of different αSyn variants in the hippocampus of respective mouse models and their parental lines.

INSTRUMENT(S): TSQ Quantiva

ORGANISM(S): Homo Sapiens (human) Mus Musculus (mouse)

TISSUE(S): Brain

DISEASE(S): Parkinson's Disease

SUBMITTER: Ivan Silbern

LAB HEAD: Prof. Dr. Henning Urlaub

PROVIDER: PXD022314 | Pride | 2021-05-28

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	20171227_aSyn15N_Dilutions_TransitionResults.tsv	Tabular
	20171227_aSyn15N_Dilutions_WTBrain.sky.zip	Other
	20180330_Hippocampus_aSyn_SRM_trypsin.sky.zip	Other
	20180403_Hippocamp_aSyn_SRM_trypsin_TransitionResults.tsv	Tabular
	20180522_Hippocamp_aSyn_SRM_LysN_TransitionResults.tsv	Tabular

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