KLF15 CRISPR Activation Plasmid (h): sc-402267-ACT

KLF15 (Krüppel-like factor 15) is a zinc-finger transcription factor that regulates cell type–specific metabolic and differentiation programs by binding GC-rich promoter elements and coordinating transcriptional networks. In human tissues it contributes to control of gluconeogenic and lipid metabolic gene expression, modulates amino acid catabolism, and interfaces with hormone-responsive signaling pathways that shape nutrient sensing and stress adaptation. KLF15 activity influences mitochondrial and oxidative metabolism outputs and can shift cellular states through broad transcriptional reprogramming. Dysregulated KLF15 expression has been associated with metabolic phenotypes and remodeling processes in muscle and cardiovascular-relevant contexts, supporting its use as a mechanistic node in pathway studies.

KLF15 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KLF15 expression without altering the underlying DNA sequence.

KLF15 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KLF15 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.

Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the KLF15 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous KLF15 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KLF15 locus and enabling the study of KLF15-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of KLF15 pathway restoration in tumor cells with silenced or reduced KLF15 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.