brindled mice
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2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Sukru Gulec ◽  
James F. Collins


1996 ◽  
Vol 271 (1) ◽  
pp. 283-288 ◽  
Author(s):  
Andrey V. Kuznetsov ◽  
Joseph F. Clark ◽  
Kirstin Winkler ◽  
Wolfram S. Kunz
Keyword(s):  


1995 ◽  
Vol 45 (1) ◽  
pp. 10-18 ◽  
Author(s):  
Noriaki Yoshimura ◽  
Kazuyuki Kida ◽  
Saburo Usutani ◽  
Masahiko Nishimura


1994 ◽  
Vol 14 (2) ◽  
pp. 81-89
Author(s):  
Noriaki Yoshimura ◽  
Ichiro Hatayama ◽  
Kiyomi Sato ◽  
Kazuyuki Kida ◽  
Saburo Usutani




1990 ◽  
Vol 267 (2) ◽  
pp. 417-422 ◽  
Author(s):  
G L Waldrop ◽  
M J Ettinger

Fibroblasts from the brindled mouse model of Menkes disease are known to accumulate excess copper. Most of the copper in the cytosol of these fibroblasts is bound to metallothionein (MT), which is elevated in Menkes or brindled mouse fibroblasts. Copper accumulation by normal fibroblasts containing excess MT was examined to determine if the excess copper accumulation phenotype was secondary to excess MT or associated with the primary defect in fibroblasts from the brindled mice. MT was induced in normal fibroblasts by copper, zinc or dexamethasone to levels comparable with those in brindled mice fibroblasts, as determined by radioimmunoassays. Normal fibroblasts containing excess MT accumulate copper normally, i.e. they do not exhibit the excess copper accumulation phenotype. Consistent with this result, copper efflux from normal fibroblasts containing excess MT was also normal. The data suggest that one function of the protein associated with the primary defect is to help determine how much copper is taken up and retained by fibroblasts and other cell types exhibiting the excess copper phenotype in Menkes disease. The capacity of this protein is apparently exceeded in normal fibroblasts if serum or albumin is not present extracellularly to limit total copper uptake. Consistent with a defect in an intracellular protein, the kinetics of copper transport by brindled mice fibroblasts were found to be normal.



1989 ◽  
Vol 62 (1) ◽  
pp. 177-184
Author(s):  
Joseph R. Prohaska

Female C57BL mice heterozygous for the brindled gene were mated to normal males and fed on a purified diet low in copper throughout gestation and lactation with (+ Cu) or without (−Cu) Cu-supplemented drinking water. Male offspring of two genotypes (control, + /y and brindled, Mobr/y) were compared when 10–12 d old. Brindled mice from dams on the – Cu treatment were smaller and had lower packed cell volumes than brindled mice from dams on the + Cu treatment. The −Cu brindled mice were smaller than their littermate brothers (+/y) but had equivalent biochemical features consistent with severe Cu deficiency. Compared with control mice from dams on the +Cu treatment, caeruloplasmin (EC1.16.3.1) activity was lower in offspring of all three other groups including Mobr/y mice who were not anaemic. Iron levels were similar in organs and bone marrow from all four groups of offspring. When dietary Cu is limiting in brindled mice a more severe Cu deficiency ensues. Thus, appropriate Cu nutriture is important to the management of Menkes' disease in humans, a genetic analogue of the brindled mouse.



1989 ◽  
Vol 9 (3) ◽  
pp. 353-356 ◽  
Author(s):  
Joseph R. Prohaska
Keyword(s):  




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