Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
KLF17 CRISPR Activation Plasmid (h): sc-414317-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KLF17 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- KLF17 CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by KLF17 CRISPR Activation Plasmid (h) and KLF17 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the KLF17 transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: KLF17 Antibody (B-6): sc-398132
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KLF17 CRISPR Activation Plasmid (h) | sc-414317-ACT | 20 µg | $397.00 | |||
KLF17 CRISPR Activation Plasmid (h2) | sc-414317-ACT-2 | 20 µg | $397.00 |
KLF17 (Krüppel-like factor 17) is a zinc-finger transcription factor that regulates epithelial differentiation programs and transcriptional networks controlling cell adhesion, polarity, and motility. By modulating gene expression through GC-rich promoter binding, KLF17 interfaces with pathways linked to epithelial–mesenchymal plasticity, cytoskeletal remodeling, and context-dependent MAPK/PI3K signaling outputs. Dysregulated KLF17 expression has been associated with altered invasive phenotypes and metastatic competency in multiple tumor models, making it a relevant node for mechanistic studies of progression and cellular state transitions. In human cells, KLF17 activity is commonly interrogated in relation to transcriptional repression/activation circuitry and the regulation of downstream EMT-associated targets.
KLF17 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KLF17 expression without altering the underlying DNA sequence.
KLF17 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KLF17 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 KLF17 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous KLF17 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KLF17 locus and enabling the study of KLF17-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of KLF17 pathway restoration in tumor cells with silenced or reduced KLF17 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.