High impact information on Klf5

• Among the putative Wnt-1 target genes, we have identified a mouse homolog of the gene encoding human transcription factor basic transcription element binding protein 2 (mBTEB2) [1].
• Finally, results of co-transfection studies showed that overexpression of IKLF/KLF5 reversed GKLF-dependent repression thus supporting a model of reciprocal activation-repression of SMC gene expression by different members of the KLF gene family [2].
• Krüppel-like factor5 (Klf5) is a zinc-finger transcription factor normally expressed in the skin [3].
• Here, we show that overexpression of Klf5 in the basal layer of the epidermis during embryogenesis affects epidermal development and disrupts epithelial-mesenchymal interactions necessary for skin adnexae formation as well as craniofacial morphogenesis [3].
• Extending our previous observation that KLF5 activates cyclin D1 transcription to promote G1/S transition, our current results further support a crucial function for KLF5 in mediating cellular transformation caused by oncogenic H-Ras [4].

Biological context of Klf5

• We previously showed that the zinc finger-containing transcription factor Krüppel-like factor 5 (KLF5) is important in mediating transformation by oncogenic H-Ras through induction of cyclin D1 expression and acceleration of the G1/S transition of the cell cycle [4].
• By chromatin immunoprecipitation, we demonstrate that Klf5 binds directly to the 5' regulatory region of EGFR [5].

Anatomical context of Klf5

• The same sustained activity of Klf5 is already seen in the gastrointestinal tract of the 10.5 day embryo, and is later confined to the base of the intestinal crypts [6].
• Unlike Klf4, Klf5 mRNA is detected in the E15.5 meninges and in the E.16.5 epithelium of trachea and bronchi [6].
• Here we present evidence of a role for KLF5 in accelerating mitotic entry in H-Ras-transformed NIH3T3 fibroblasts [4].
• Kruppel-like factor 5 is an important mediator for lipopolysaccharide-induced proinflammatory response in intestinal epithelial cells [7].

Associations of Klf5 with chemical compounds

• Arsenite induced the expression of HO1, HIF1alpha, KLF5, PPARgamma and C/EBPalpha [8].

Regulatory relationships of Klf5

• ILK expression restored migratory capacity in keratinocytes with suppression of Klf5, whereas ILK small interfering RNA blocked the increased migration resulting from Klf5 overexpression [9].

Other interactions of Klf5

• Here, we examined the developmental expression of the mouse Klf5 gene and compared it to the established pattern of the Klf4 gene [6].
• Conversely, over-expression of KLF5 in NIH3T3 cells leads to an increase in the promoter activity of the genes encoding cyclin B1 and Cdc2 [4].

References