Zinc deficiency-induced cell death

Michael S. Clegg, Lynn A. Hanna, Brad J. Niles, Tony Y. Momma, Carl L Keen

Research output: Contribution to journalArticle

88 Scopus citations

Abstract

Zinc deficiency is characterized by an attenuation of growth factor signaling pathways and an amplification of p53 pathways. This outcome is facilitated by hypo-phosphorylation of AKT and ERK secondary to zinc deficiency, which are permissive events to the activation of the intrinsic cell death pathway. Low zinc concentrations provide an environment that is also conducive to the production of reactive oxygen/reactive nitrogen species (ROS/ RNS) and caspase activation. Additionally, during zinc deficiency endogenous survival pathways such as NF-κB are inhibited in their transactivation potential. The above factors contribute to the irreversible commitment of the zinc deficient cell to death.

Original languageEnglish (US)
Pages (from-to)661-669
Number of pages9
JournalIUBMB Life
Volume57
Issue number10
DOIs
StatePublished - Oct 2005

Keywords

  • AKT
  • Apoptosis
  • Caspase
  • ERK
  • Growth factors
  • IGF
  • NF-κB
  • Nutrition
  • p53
  • Reactive nitrogen species
  • Reactive oxygen species
  • Signal transduction
  • Zinc
  • Zinc deficiency

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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  • Cite this

    Clegg, M. S., Hanna, L. A., Niles, B. J., Momma, T. Y., & Keen, C. L. (2005). Zinc deficiency-induced cell death. IUBMB Life, 57(10), 661-669. https://doi.org/10.1080/15216540500264554