Merck
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  • Pro-death signaling of cytoprotective heat shock factor 1: upregulation of NOXA leading to apoptosis in heat-sensitive cells.

Pro-death signaling of cytoprotective heat shock factor 1: upregulation of NOXA leading to apoptosis in heat-sensitive cells.

Cell death and differentiation (2020-01-31)
Patryk Janus, Agnieszka Toma-Jonik, Natalia Vydra, Katarzyna Mrowiec, Joanna Korfanty, Marek Chadalski, Piotr Widłak, Karolina Dudek, Anna Paszek, Marek Rusin, Joanna Polańska, Wiesława Widłak
ABSTRACT

Heat shock can induce either cytoprotective mechanisms or cell death. We found that in certain human and mouse cells, including spermatocytes, activated heat shock factor 1 (HSF1) binds to sequences located in the intron(s) of the PMAIP1 (NOXA) gene and upregulates its expression which induces apoptosis. Such a mode of PMAIP1 activation is not dependent on p53. Therefore, HSF1 not only can activate the expression of genes encoding cytoprotective heat shock proteins, which prevents apoptosis, but it can also positively regulate the proapoptotic PMAIP1 gene, which facilitates cell death. This could be the primary cause of hyperthermia-induced elimination of heat-sensitive cells, yet other pro-death mechanisms might also be involved.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
8-Cyclopentyl-1,3-dimethylxanthine, ≥98% (HPLC), powder
Sigma-Aldrich
eSpCas9-GFP Protein, from Streptococcus pyogenes with mutations conferring enhanced specificity, fused with enhanced GFP, recombinant, expressed in E. coli, 3X NLS
Sigma-Aldrich
Anti-Actin Antibody, clone C4, ascites fluid, clone C4, Chemicon®
Sigma-Aldrich
Anti-NOXA antibody produced in rabbit, affinity isolated antibody, buffered aqueous solution