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.
Cdc2L5 CRISPR Activation Plasmid (h): sc-403798-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Cdc2L5 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Cdc2L5 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 Cdc2L5 CRISPR Activation Plasmid (h) and Cdc2L5 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the CDK13 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: Cdc2L5 Antibody (ZZ08): sc-81837
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Cdc2L5 CRISPR Activation Plasmid (h) | sc-403798-ACT | 20 µg | $397.00 |
CDK13 encodes the human cyclin-dependent kinase Cdc2L5, a serine/threonine kinase that functions with Cyclin K to coordinate phosphorylation of RNA polymerase II and regulate transcription elongation and co-transcriptional RNA processing. Through these activities, CDK13 contributes to control of gene expression programs linked to cell-cycle progression, DNA damage responses, and differentiation, intersecting with transcriptional and splicing networks. Disruption or dysregulation of CDK13 has been associated with neurodevelopmental phenotypes and cancer-relevant transcriptional dependencies, making it a useful node for studying gene regulatory circuitry. Experimental modulation of Cdc2L5 supports mechanistic work on transcription-coupled RNA metabolism and pathway-level effects on cellular fitness and stress signaling.
Cdc2L5 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CDK13 expression without altering the underlying DNA sequence.
Cdc2L5 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CDK13 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 CDK13 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Cdc2L5 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CDK13 locus and enabling the study of Cdc2L5-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Cdc2L5 pathway restoration in tumor cells with silenced or reduced CDK13 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.