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Overexpression of CCS in G93A-SOD1 mice leads to accelerated neurological deficits with severe mitoc...

Overexpression of CCS in G93A-SOD1 mice leads to accelerated neurological deficits with severe mitoc...

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_jstor_primary_25427328

Overexpression of CCS in G93A-SOD1 mice leads to accelerated neurological deficits with severe mitochondrial pathology

About this item

Full title

Overexpression of CCS in G93A-SOD1 mice leads to accelerated neurological deficits with severe mitochondrial pathology

Publisher

United States: National Academy of Sciences

Journal title

Proceedings of the National Academy of Sciences - PNAS, 2007-04, Vol.104 (14), p.6072-6077

Language

English

Formats

Publication information

Publisher

United States: National Academy of Sciences

More information

Scope and Contents

Contents

Cu, Zn superoxide dismutase (SOD1) has been detected within spinal cord mitochondria of mutant SOD1 transgenic mice, a model of familial ALS. The copper chaperone for SOD1 (CCS) provides SOD1 with copper, facilitates the conversion of immature apo-SOD1 to a mature holoform, and influences in yeast the cytosolic/mitochondrial partitioning of SOD1. T...

Alternative Titles

Full title

Overexpression of CCS in G93A-SOD1 mice leads to accelerated neurological deficits with severe mitochondrial pathology

Identifiers

Primary Identifiers

Record Identifier

TN_cdi_jstor_primary_25427328

Permalink

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_jstor_primary_25427328

Other Identifiers

ISSN

0027-8424

E-ISSN

1091-6490

DOI

10.1073/pnas.0610923104

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