High impact information on Klf9

• This transactivation was dependent on a GC-rich tract required for basal activity of the endoglin promoter driven by the related GC box binding protein, Sp1 [1].
• The GC box was predominantly bound by the DNA binding transcription factor BTEB (basic transcription element binding protein), expression of which was acetaldehyde and UV inducible [2].
• Cloning and characterization of a GC-box binding protein, G10BP-1, responsible for repression of the rat fibronectin gene [3].
• Basic transcription element-binding protein (BTEB) is a thyroid hormone-regulated gene in the developing central nervous system. Evidence for a role in neurite outgrowth [4].
• Suppression of the basic transcription element-binding protein in brain neuronal cultures inhibits thyroid hormone-induced neurite branching [5].

Biological context of Klf9

• Basic transcription element binding protein (BTEB) is a member of the Krüppel family of zinc finger transcription factors [6].
• The corresponding genes include carnitine palmitoyltransferase I, stromal cell-derived factor 1, a protein associated with MYC mRNA, basic transcription element binding protein, and expressed sequence tags (ESTs) of unknown function [7].

Anatomical context of Klf9

• We identified three genes that were up-regulated by T3, basic transcription element-binding protein, nuclear pore glycoprotein and bone morphogenetic protein-4 and one that was down-regulated, the neuronal apoptosis-inducing gene [8].

Other interactions of Klf9

• The G10BP-1 gene encoding a GC box binding protein, is a target of Myc and Jun/Fos [9].

Analytical, diagnostic and therapeutic context of Klf9

• Southwestern blotting analyses and gel shift assays with basic transcription element-binding protein antiserum suggested that the GC box was bound by basic transcription element-binding protein, a recently described DNA-binding protein [10].

References