The role of Ctr1 and Ctr2 in mammalian copper homeostasis and platinum-based chemotherapy.

Published

Journal Article (Review)

Copper (Cu) is an essential metal for growth and development that has the potential to be toxic if levels accumulate beyond the ability of cells to homeostatically balance uptake with detoxification. One system for Cu acquisition is the integral membrane Cu(+) transporter, Ctr1, which has been quite well characterized in terms of its function and physiology. The mammalian Ctr2 protein has been a conundrum for the copper field, as it is structurally closely related to the high affinity Cu transporter Ctr1, sharing important motifs for Cu transport activity. However, in contrast to mammalian Ctr1, Ctr2 fails to suppress the Cu-dependent growth phenotype of yeast cells defective in Cu(+) import, nor does it appreciably stimulate Cu acquisition when over-expressed in mammalian cells, underscoring important functional dissimilarities between the two proteins. Several roles for the mammalian Ctr2 have been suggested both in vitro and in vivo. Here, we summarize and discuss current insights into the Ctr2 protein and its interaction with Ctr1, its functions in mammalian Cu homeostasis and platinum-based chemotherapy.

Full Text

Duke Authors

Cited Authors

  • Öhrvik, H; Thiele, DJ

Published Date

  • January 2015

Published In

Volume / Issue

  • 31 /

Start / End Page

  • 178 - 182

PubMed ID

  • 24703712

Pubmed Central ID

  • 24703712

Electronic International Standard Serial Number (EISSN)

  • 1878-3252

International Standard Serial Number (ISSN)

  • 0946-672X

Digital Object Identifier (DOI)

  • 10.1016/j.jtemb.2014.03.006

Language

  • eng