Pluripotent stem cells (PSCs) are capable of self-renewing, in addition to differentiating into any cell type of the adult organism, a characteristic known as pluripotency. These abilities are due, in part, to the network of protein homeostasis, or proteostasis, of which the Stress Inducible Protein 1 (STI1) protein stands out for its dynamism. STI1 is a co-chaperone that assists in many fundamental molecular processes cell maintenance, such as the formation of the protein complex between HSP70 and HSP90 proteins. Still, the expression of STI1 is essential for the survival of mouse embryos. In spite of this, the exact mechanisms of action of STI1, mainly with regard to its role in the early embryonic development and in the maintenance of pluripotency in PSCs, are not yet fully understood. Thus, the present project proposes to analyze comparatively the transcriptional profile of PSCs with differential expression of STI1, seeking to elucidate molecular mechanisms, signaling pathways and genes of interest directly or indirectly impacted by the variation in the levels of this co-chaperone. The in silico study of data obtained from RNA sequencing and the subsequent validation of selected genes of interest will be fundamental to obtain more information about the activity of STI1 in the transcriptome of PSCs, contributing in a relevant way to the understanding of how proteostasis influences the maintenance of pluripotency.
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