Abstract
Background: Krueppel-like transcription factor 11 (KLF11, TIEG2) is a member of the Sp1/KLF transcription factor family which plays an important role in mammalian gene regulation via binding to GC-rich promoter elements comprising CGCCC (GC) or CACCC box core sequences. Previously we demonstrated that human KLF11 (hKLF11) inhibits human proinsulin promoter activity in rodent beta-cell lines (INS-1, beta-TC3). At insulin gene upstream sequences hKLF11 binds to a GC box but not to a proximal CACCC box. Surprisingly, deletion and mutation of the GC box did not alter hKLF11-mediated inhibition of proinsulin promoter activity. Here we present results from ongoing experiments which were designed to clarify the underlying molecular mechanisms of hKLF11 proinsulin promoter regulation and the functional role of the CACCC box.
Published Version
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