High impact information on KLF15

• KKLF was found to be abundantly expressed in the liver, kidneys, heart, and skeletal muscle, and immunohistochemistry revealed the nuclear localization of KKLF protein in interstitial cells in heart and skeletal muscle, stellate cells, and fibroblasts in the liver [1].
• On the other hand, KKLF coexpression with MAZ appeared to block the activating effect of MAZ [1].
• We recently reported that the Krüppel-like zinc finger transcription factor KLF15 can induce adipocyte maturation and GLUT4 expression [2].
• We previously isolated KLF15 as a transcription factor that regulates the expression of the ClC-K1 chloride channel [3].
• RESULTS: In EMSA and DNAseI footprinting assays, a KLF15-GST fusion protein containing the C-terminal zinc-finger domains (123 amino acids) showed zinc-dependent and sequence-specific binding to a 9 bp consensus sequence containing a core CG/TCCCC [4].

Biological context of KLF15

• Based on the known expression pattern of KLF15 in non-photoreceptor cells, we hypothesize an in vivo role for KLF15 in repressing photoreceptor-specific gene expression in the inner retina [4].
• Both the bovine rhodopsin and IRBP promoters contained multiple KLF15 binding sites that included the previously identified CRS-1 and G-rich repressor elements [4].

Anatomical context of KLF15

• Quantification of various KLF transcripts revealed that 48 h fasting robustly induced the KLF15 transcripts in the skeletal muscle [5].

Analytical, diagnostic and therapeutic context of KLF15

• Expression studies used RT-PCR and beta-galactosidase (LacZ) histochemistry of retinas from transgenic mice heterozygous for a targeted LacZ replacement of KLF15 [6].

References