
NCBI . NLM . NIH . GOV {
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Title[redir]:
Copper induces cell death by targeting lipoylated TCA cycle proteins - PMC
Description:
Copper is an essential co-factor for all organisms, and yet it becomes toxic if concentrations exceed a threshold maintained by evolutionarily conserved homeostatic mechanisms. How excess copper induces cell death, however, is unknown. Here, we show ...
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Keywords {🔍}
copper, fig, cell, death, cells, doi, google, scholar, pubmed, fdx, pmc, free, article, elesclomol, protein, proteins, lipoylation, treatment, ionophores, lipoylated, cancer, mechanisms, table, mitochondrial, viability, dlat, abc, ionophore, acid, copperinduced, intracellular, toxicity, tca, induced, lipoic, deletion, chem, concentrations, respiration, apoptosis, disease, stress, levels, genes, data, cycle, pathway, distinct, binding, cluster,
Topics {✒️}
supplementary material nihms1808242-supplement-supplementary_material semi-quantitative light-microscopic scoring genome-wide crispr/cas9 knock table s1 nihms1808242-supplement-table_s1 table s4 nihms1808242-supplement-table_s4 table s2 nihms1808242-supplement-table_s2 table s5 nihms1808242-supplement-table_s5 copper ionophore-induced death copper-induced cell death copper induced cell-death elesclomol-induced cell death copper-induced death mechanisms dual-purpose isocyanides produced copper-mediated cell death hms-tcmp proteomic facility molecularly-defined effector mechanisms 30μm z-vad-fmk copper-dependent death occurs [4fe-4s] cluster assembly disulfiram modulated ros-mapk pmc beta search 50μm d-boc-fmk 40μm z-vad-fmk copper-binding small molecules free intracellular copper short-term exposure leads glioblastoma-patient-derived cells caspase-independent cell death lipoic acid-specific antibody elesclomol-insensitive cell lines potential anti-copper agent copper-induced death primary intracellular targets scl31a1 wild-type cells viability 72h post-supplementation small molecule chaperones tca-cycle active cells regulated cell death cellular respiration similar analyzed 72h post-treatment elesclomol-resistant a549 cells supplementary materials included cell death pathway [google scholar] 10 subsequent cell cytotoxicity ultimately cell death potentiate cell death triggered cell death paraptotic cell death host cell death
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