High impact information on KLF7

• One of the loci is between the candidate genes KLF7 and CREB1, but given possible long-range effects on expression and the unknown importance of untranslated elements such as micro-RNAs, all four loci deserve attention as candidates [1].
• Altogether, our results strongly suggest that MoKA and KLF7 interact functionally to regulate gene expression during cell differentiation and identify the cell cycle regulator p21(WAF1/Cip1) as one of the targeted genes [2].
• KLF7, a member of the Krüppel-like transcription factor family, is believed to regulate neurogenesis and cell cycle progression [2].
• Like CPBP/Zf9, UKLF can function as a transcription activator in co-transfection assays [3].
• The carboxyl-terminal portion of UKLF contains three zinc fingers of the Cys2-His2 type and binds in vitro to the CACCC motif of the beta-globin promoter and to the Sp1 recognition sequence [3].

Biological context of KLF7

• We also examined the effects of the overexpression of KLF7 on adipogenesis in 3T3-L1 cells [4].
• CONCLUSIONS/INTERPRETATION: These results indicate that the gene encoding KLF7 is a novel candidate for conferring genetic susceptibility to type 2 diabetes [4].
• PNAS-133 gene was downregulated by morphine whereas the Krüppel-like factor 7 (KLF7), a zinc finger transcription factor, was upregulated by morphine [5].
• The upregulation of KLF7 by morphine was further studied and found to be at both the transcriptional and the translational levels in a naloxone-reversible manner [5].
• Functional clustering of DNA microarray data revealed that loss of KLF7 affects primarily the activity of genes involved in OSN differentiation, axonal growth, cytoskeletal dynamics, cell adhesion and synaptogenesis [6].

Anatomical context of KLF7

• In human adipocytes overexpressing KLF7, the expression of adiponectin and leptin was decreased compared with that in control cells, whereas expression of IL-6 was increased [7].
• These results suggest that KLF7 may contribute to the pathogenesis of type 2 diabetes through an impairment of insulin biosynthesis and secretion in pancreatic beta-cells and a reduction of insulin sensitivity in peripheral tissues [7].
• We also found that the overexpression of KLF7 resulted in the decrease of hexokinase 2 expression in smooth muscle cells, and of glucose transporter 2 expression in the HepG2 cells [7].
• Identification of genes regulated by transcription factor KLF7 in differentiating olfactory sensory neurons [6].
• Gene targeting in mice has recently demonstrated that transcription factor KLF7 plays a critical role in neurite outgrowth and neuronal survival [6].

Associations of KLF7 with chemical compounds

• The amino-terminal portion of UKLF consists of a hydrophobic region rich in serines and a negatively charged segment with several glutamic acid residues [3].

Regulatory relationships of KLF7

• MoKA is a novel F-box containing protein that interacts with and stimulates the activity of transcription factor KLF7, a regulator of neuronal differentiation [8].
• Cell transfection experiments, on the other hand, demonstrated that the promoters of the genes encoding the OSN-specific OMP and the adhesion molecule L1 are both activated by KLF7 binding to CACCC motifs [6].

Other interactions of KLF7

• Here we report the identification of Luna, the Drosophila progenitor of the mammalian KLF6/KLF7 group [9].
• Multiple pathways regulate intracellular shuttling of MoKA, a co-activator of transcription factor KLF7 [8].
• Micro-opioids inhibited synthesis of common transcription factors AP-1, c-fos, NF-kappaB, and nuclear factor of activated T cells in activated or stimulated immune cells, whereas micro-opioids activated NF-kappaB, GATA-3, and Kruppel-like factor 7 transcription factors in non-stimulated immune cells [10].

References