Atp13a2-deficient mice exhibit neuronal ceroid lipofuscinosis, limited α-synuclein accumulation and age-dependent sensorimotor deficits-Reference-Cited by-同舟云学术

Atp13a2-deficient mice exhibit neuronal ceroid lipofuscinosis, limited α-synuclein accumulation and age-dependent sensorimotor deficits

Published:2013-02-07 Issue:10 Volume:22 Page:2067-2082
ISSN:1460-2083
Container-title:Human Molecular Genetics
language:en
Short-container-title:

Author:

Schultheis Patrick J.,Fleming Sheila M.,Clippinger Amy K.,Lewis Jada,Tsunemi Taiji,Giasson Benoit,Dickson Dennis W.,Mazzulli Joseph R.,Bardgett Mark E.,Haik Kristi L.,Ekhator Osunde,Chava Anil Kumar,Howard John,Gannon Matt,Hoffman Elizabeth,Chen Yinhuai,Prasad Vikram,Linn Stephen C.,Tamargo Rafael J.,Westbroek Wendy,Sidransky Ellen,Krainc Dimitri,Shull Gary E.

Publisher

Oxford University Press (OUP)

Subject

Genetics(clinical),Genetics,Molecular Biology,General Medicine

Link

http://academic.oup.com/hmg/article-pdf/22/10/2067/17258956/ddt057.pdf

Reference84 articles.

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2. Structural divergence between the two subgroups of P5 ATPases;Sørensen;Biochim. Biophys. Acta,2010

3. Hereditary parkinsonism with dementia is caused by mutations in ATP13A2, encoding a lysosomal type 5 P-type ATPase;Ramirez;Nature Genet.,2006

4. A truncating mutation in ATP13A2 is responsible for adult-onset neuronal ceroid lipofuscinosis in Tibetan terriers;Farias;Neurobiol. Dis.,2011

5. A one base pair deletion in the canine ATP13A2 gene causes exon skipping and Late-onset Neuronal Ceroid Lipofusccinosis in the Tibetan Terrier;Wohlke;PLoS Genet.,2001

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