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Modelling HSP60 deficiency using an inducible transgenic HSP60 ATPase deficient mutant

GSE254495 Homo sapiens Expression profiling by high throughput sequencing 9 samples Submitted 2024/09/27 Platform GPL28038
Summary
To investigate the immediate effect of HSP60 dysfunction on mitochondrial functions, we induced the expression of a dominant-negative ATPase-deficient HSP60 mutant (HSP60-D423A) in HEK293 cells using tetracycline . Incorporation of HSP60-D423A subunits into HSP60 heptamer rings leads to dysfunction of the chaperonin complex. We titrated tetracycline levels to have a biologically relevant cellular model that can be monitored over time. Expression of the HSP60-D432A protein resulted in significantly reduced cell counts at 72 hours induction compared to uninduced and HSP60-WT co-expressing cells. To study the effects of onset of HSP60 deficiency, we monitored transcriptional changes using RNASeq.
Published in
HSP60 chaperone deficiency disrupts the mitochondrial matrix proteome and dysregulates cholesterol synthesis
Cömert C, Kjær-Sørensen K, Hansen J et al. · Molecular metabolism 2024 · PMID 39147275 · doi:10.1016/j.molmet.2024.102009
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Also filed as BioProject PRJNA1070667 and SRA study SRP486564. Searching any of these in the dataset finder brings you back here.

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