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Truncation of Ube3a-ATS Unsilences Paternal Ube3a and Ameliorates Behavioral Defects in the Angelman...

Truncation of Ube3a-ATS Unsilences Paternal Ube3a and Ameliorates Behavioral Defects in the Angelman...

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_plos_journals_1477954437

Truncation of Ube3a-ATS Unsilences Paternal Ube3a and Ameliorates Behavioral Defects in the Angelman Syndrome Mouse Model

About this item

Full title

Truncation of Ube3a-ATS Unsilences Paternal Ube3a and Ameliorates Behavioral Defects in the Angelman Syndrome Mouse Model

Publisher

United States: Public Library of Science

Journal title

PLoS genetics, 2013-12, Vol.9 (12), p.e1004039-e1004039

Language

English

Formats

Publication information

Publisher

United States: Public Library of Science

More information

Scope and Contents

Contents

Angelman syndrome (AS) is a severe neurodevelopmental disorder caused by maternal deficiency of the imprinted gene UBE3A. Individuals with AS suffer from intellectual disability, speech impairment, and motor dysfunction. Currently there is no cure for the disease. Here, we evaluated the phenotypic effect of activating the silenced paternal allele o...

Alternative Titles

Full title

Truncation of Ube3a-ATS Unsilences Paternal Ube3a and Ameliorates Behavioral Defects in the Angelman Syndrome Mouse Model

Identifiers

Primary Identifiers

Record Identifier

TN_cdi_plos_journals_1477954437

Permalink

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_plos_journals_1477954437

Other Identifiers

ISSN

1553-7404,1553-7390

E-ISSN

1553-7404

DOI

10.1371/journal.pgen.1004039

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