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Effects of REDD1 KO in transcriptomic response to wounding and glucocorticoid treatment in HaCaT human keratinocytes

ABSTRACT: Effects of REDD1 KO in transcriptomic response to wounding and glucocorticoid treatment in HaCaT human keratinocytes

PROVIDER: PRJNA736990 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14790300_1.fastq.gz	Fastqsanger.gz
	SRR14790300_2.fastq.gz	Fastqsanger.gz
	SRR14790301_1.fastq.gz	Fastqsanger.gz
	SRR14790301_2.fastq.gz	Fastqsanger.gz
	SRR14790302_1.fastq.gz	Fastqsanger.gz

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Effects of REDD1 KO in transcriptomic response to wounding and glucocorticoid treatment in HaCaT human keratinocytes

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Project description:The p53 protein is encoded by TP53 gene and plays the key role in significant number of cellular processes including proliferation, apoptosis and regulation of many stress response pathways. P53 acts like a direct transcription activator of numerous genes regulating cell cycle arrest, DNA repair, growth inhibition and many others (Mollereau and Ma, 2014). The canonical biological function of p53 is maintaining genome integrity via elimination of damaged or exposed to genotoxic stress cells. Immortalized HaCaT cells are widely used for keratinocyte research, since they maintain stable keratinocyte phenotype, have nearly unlimited proliferative potential, do not require specific growth and differentiation factors (Colombo et al., 2017). Also, HaCaT cells produce typical differentiation markers such as cytokeratins K14 and K10, involucrin (Colombo et al., 2017) and respond to keratinocyte differentiation stimuli. Taking together, HaCaT cells have similar to normal human keratinocytes (NHK) properties, however, as many of spontaneously immortalized cell lines HaCaT cells bear two mutant p53 alleles - R282Q and H179Y (Lehman et al., 1993). Mutp53 in HaCaT has an increased affinity to other p53 family members (p63, p73), which significantly expands p53 properties. Moreover, mutp53 indirectly affects specific target genes via protein-protein interactions with other transcription factors (NF-Y, E2F1, NF-KB) or by tethering p63 to new promotor locations. For more detailed investigation of mutp53 impact on various processes in HaCaT cells we performed a shRNA mediated knockdown of mutp53. For generation of stable TP53 knockdown we employed plasmid vector pLKO-p53-shRNA-941 (Addgene # #25637) followed by puromycin selection of transduced cells. Here we present proteomic dataset obtained from wild type HaCaT cells and p53 knock down HaCaT keratinocytes.

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