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Issue 6, 2015
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Copper homeostasis in Mycobacterium tuberculosis

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Copper (Cu) is a trace element essential for the growth and development of almost all organisms, including bacteria. However, Cu overload in most systems is toxic. Studies show Cu accumulates in macrophage phagosomes infected with bacteria, suggesting Cu provides an innate immune mechanism to combat invading pathogens. To counteract the host-supplied Cu, increasing evidence suggests that bacteria have evolved Cu resistance mechanisms to facilitate their pathogenesis. In particular, Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis, has evolved multiple pathways to respond to Cu. Here, we summarize what is currently known about Cu homeostasis in Mtb and discuss potential sources of Cu encountered by this and other pathogens in a mammalian host.

Graphical abstract: Copper homeostasis in Mycobacterium tuberculosis

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Publication details

The article was received on 24 Nov 2014, accepted on 24 Dec 2014 and first published on 14 Jan 2015

Article type: Minireview
DOI: 10.1039/C4MT00305E
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Citation: Metallomics, 2015,7, 929-934

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    Copper homeostasis in Mycobacterium tuberculosis

    X. Shi and K. H. Darwin, Metallomics, 2015, 7, 929
    DOI: 10.1039/C4MT00305E

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