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The ubiquitously expressed MURR1 protein is absent in canine copper toxicosis.

Abstract：

BACKGROUND/AIMS:Copper toxicosis (CT) in Bedlington terriers is an autosomal recessive disorder characterized by massive lysosomal copper accumulation in livers of affected dogs, and a defect in the biliary excretion of this metal. We propose that MURR1, the gene defective in canine CT, has a role in the regulation of copper excretion into bile during copper overload. METHODS:Polyclonal antibodies raised against full-length recombinant human MURR1 were used for immunoblot analysis and indirect immunofluorescence studies. RESULTS:Using Western blot analysis, these antibodies abundantly detected MURR1 as a 23 kDa protein in liver extracts of mice and dogs, but MURR1 was undetectable in the livers of affected Bedlington terriers. MURR1 was also detected in different tissues and cell lines; in cell lines the protein was found both in cytosol and membrane preparations. Consistent with this observation, indirect immunofluorescence staining revealed that in some cells MURR1 was associated with a vesicular compartment diffusely localized throughout the cell. CONCLUSIONS:The genomic deletion in MURR1 results in complete absence of MURR1 protein. Based on the unanticipated subcellular localization, our results suggest a role for MURR1 in the regulation of vesicular copper sequestration during copper overload.

journal_name

J Hepatol

journal_title

Journal of hepatology

authors

Klomp AE,van de Sluis B,Klomp LW,Wijmenga C

doi

10.1016/s0168-8278(03)00380-5

subject

Has Abstract

pub_date

2003-11-01 00:00:00

pages

703-9

issue

5

eissn

0168-8278

issn

1600-0641

pii

S0168827803003805

journal_volume

39

pub_type

杂志文章

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