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Zinc deficiency‐induced cell death
Author(s) -
Clegg Michael S.,
Hanna Lynn A.,
Niles Brad J.,
Momma Tony Y.,
Keen Carl L.
Publication year - 2005
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216540500264554
Subject(s) - transactivation , zinc deficiency (plant disorder) , programmed cell death , zinc , reactive oxygen species , reactive nitrogen species , microbiology and biotechnology , mapk/erk pathway , signal transduction , apoptosis , protein kinase b , phosphorylation , chemistry , biology , biochemistry , transcription factor , organic chemistry , gene
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.IUBMB Life, 57: 661‐670, 2005