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Impairment of mitochondria in adult mouse brain overexpressing predominantly full-length, N-terminal...

Impairment of mitochondria in adult mouse brain overexpressing predominantly full-length, N-terminal...

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_plos_journals_1350968764

Impairment of mitochondria in adult mouse brain overexpressing predominantly full-length, N-terminally acetylated human α-synuclein

About this item

Full title

Impairment of mitochondria in adult mouse brain overexpressing predominantly full-length, N-terminally acetylated human α-synuclein

Publisher

United States: Public Library of Science

Journal title

PloS one, 2013-05, Vol.8 (5), p.e63557-e63557

Language

English

Formats

Publication information

Publisher

United States: Public Library of Science

More information

Scope and Contents

Contents

While most forms of Parkinson's Disease (PD) are sporadic in nature, a small percentage of PD have genetic causes as first described for dominant, single base pair changes as well as duplication and triplication in the α-synuclein gene. The α-synuclein gene encodes a 140 amino acid residue protein that interacts with a variety of organelles includi...

Alternative Titles

Full title

Impairment of mitochondria in adult mouse brain overexpressing predominantly full-length, N-terminally acetylated human α-synuclein

Identifiers

Primary Identifiers

Record Identifier

TN_cdi_plos_journals_1350968764

Permalink

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_plos_journals_1350968764

Other Identifiers

ISSN

1932-6203

E-ISSN

1932-6203

DOI

10.1371/journal.pone.0063557

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