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.
KLF12 CRISPR Activation Plasmid (h): sc-403992-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KLF12 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- KLF12 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 KLF12 CRISPR Activation Plasmid (h) and KLF12 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the KLF12 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: KLF12 Antibody (NQ-C45): sc-134373
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KLF12 CRISPR Activation Plasmid (h) | sc-403992-ACT | 20 µg | $397.00 |
KLF12 (Krüppel-like factor 12) is a C2H2 zinc-finger transcription factor that binds GC-rich promoter elements to regulate gene expression programs controlling proliferation, differentiation, and epithelial–mesenchymal plasticity. As a nuclear regulator, KLF12 interfaces with transcriptional networks that shape cell-cycle progression and lineage specification, with downstream effects on cytoskeletal organization and cell motility. Altered KLF12 activity or expression has been linked to dysregulated transcriptional control in cancer-related processes, including invasion and metastatic behavior, and has also been explored in developmental and endocrine-relevant gene regulatory contexts. Modulating KLF12 levels provides a tractable approach for dissecting transcription factor–driven regulatory circuits and context-specific enhancer–promoter control.
KLF12 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KLF12 expression without altering the underlying DNA sequence.
KLF12 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KLF12 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 KLF12 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous KLF12 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KLF12 locus and enabling the study of KLF12-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of KLF12 pathway restoration in tumor cells with silenced or reduced KLF12 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.