The KLF family of transcription factors has attracted great attention in recent times, due to the versatility of functions that these genes and proteins can perform in organisms. The implication of these transcription factors in important events such as cell growth, differentiation, migration, inflammation and angiogenesis is known. Its implication in the development of pathologies such as cancer is also known. The aim of this article is to show the direct interaction that exists between the transcription factor PPARγ and consensus sequences in KLF6 and its implication in biomedicine, seen from a bioinformatic perspective. For this, a list of co-expressed genes for KLF6 was generated and the promoter sequence close to transcription site start (TSS) was extracted. New consensus sequences were found using the MEME program, and the sequences similar to the new motif found were searched through Tomtom Motif Comparison Tool and JASPAR CORE to assign a possible function to the new motif found. The existence of PPARγ binding sites in the KLF6 promoter was evaluated using the EPD Eukaryotic promoter database. Two PPARγ binding sites were found in the promoter sequence of KLF6, in the regions -1264, -1451 upstream from the transcription start site. This article preliminarily tests the hypothesis that there is a direct interaction between the transcription factor PPARγ and consensus sequences in the KLF6 promoter. This is consistent with a previous finding, in which colon cancer cells were treated with rosiglitazone, a PPARγ agonist, resulting in increased expression of KLF6.
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