Trafficking mechanisms of P-type ATPase copper transporters

被引：50

作者：

Hartwig, Cortnie ^{[1
]}

Zlatic, Stephanie A. ^{[1
]}

Wallin, Melissa ^{[2
]}

Vrailas-Mortimer, Alysia ^{[3
]}

Fahrni, Christoph J. ^{[4
,5
]}

Faundez, Victor ^{[1
]}

机构：

[1] Emory Univ, Dept Cell Biol, Atlanta, GA 30322 USA

[2] Augusta Univ, Med Illustrat Grad Program, Augusta, GA 30912 USA

[3] Illinois State Univ, Sch Biol Sci, Normal, IL 61790 USA

[4] Georgia Inst Technol, Sch Chem & Biochem, Atlanta, GA 30332 USA

[5] Georgia Inst Technol, Petit Inst Bioengn & Biosci, Atlanta, GA 30332 USA

来源：

CURRENT OPINION IN CELL BIOLOGY | 2019年 / 59卷

基金：

美国国家卫生研究院;

关键词：

CYTOCHROME-C-OXIDASE; KINKY-HAIR DISEASE; MITOCHONDRIAL METALLOCHAPERONE SCO1; SPINAL MUSCULAR-ATROPHY; MENKES-DISEASE; WASH COMPLEX; DEPENDENT TRAFFICKING; REGULATED TRAFFICKING; FUNCTIONAL-ANALYSIS; PARKINSONS-DISEASE;

D O I：

10.1016/j.ceb.2019.02.009

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Copper is an essential micronutrient required for oxygen-dependent enzymes, yet excess of the metal is a toxicant. The tug-of-war between these copper activities is balanced by chaperones and membrane transporters, which control copper distribution and availability. The P-type ATPase transporters, ATP7A and ATP7B, regulate cytoplasmic copper by pumping copper out of cells or into the endomembrane system. Mutations in ATP7A and ATP7B cause diseases that share neuropsychiatric phenotypes, which are similar to phenotypes observed in mutations affecting cytoplasmic trafficking complexes required for ATP7A/B dynamics. Here, we discuss evidence indicating that phenotypes associated to genetic defects in trafficking complexes, such as retromer and the adaptor complex AP-1, result in part from copper dyshomeostasis due to mislocalized ATP7A and ATP7B.

引用

收藏

页码：24 / 33

页数：10

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