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E-GEOD-49657 - The inducuction of UPR target genes in response to zinc depletion and serum starvation in HeLa cells

Released on 9 August 2013, last updated on 3 June 2014
Homo sapiens
Samples (4)
Array (1)
Protocols (5)
Zinc is an essential trace element, and impaired zinc homeostasis is implicated in the pathogenesis of various human diseases. However, the mechanisms cells use to respond to zinc deficiency are poorly understood. We previously reported that amyotrophic lateral sclerosis (ALS)-linked pathogenic mutants of SOD1 cause chronic ER stress through specific interactions with Derlin-1, which is a component of the ER-associated degradation machinery. Moreover, we recently demonstrated that this interaction is common to ALS-linked SOD1 mutants, and SOD1WT comprises a masked Derlin-1-binding region. We found that under serum starved and zinc-deficient conditions, SOD1WT adopts a mutant-like conformation that exposes the Derlin-1-binding region, suggesting that SOD1-Derlin-1 interaction may contribute to induce ER stress under these conditions. Using RNA microarrays, we revealed that the zinc depletion and serum starvation induce the expression of the unfolded protein response (UPR) target genes, including HSPA5/BiP, SEL1L, DNAJC3/p58, and ARMET. We conclude that SOD1 has a novel function as a molecular switch that activates the ER stress response under zinc-deficient conditions HeLa cells were treated with 8µM TPEN for 9h or exposured to 36h of serum starvation with or without 30µM zinc.Then the total RNA was isolated from cells using the Isogen reagent (Wako) following the manufacturer's recommendations.
Experiment type
transcription profiling by array 
Hidenori Ichijo, Kengo Homma
Investigation descriptionE-GEOD-49657.idf.txt
Sample and data relationshipE-GEOD-49657.sdrf.txt
Raw data (1)
Processed data (1)
Array designA-AGIL-28.adf.txt