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.
DinB CRISPR Activation Plasmid (h): sc-405052-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DinB CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- DinB 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 DinB CRISPR Activation Plasmid (h) and DinB CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the POLK 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: DinB Antibody (A-9): sc-166667
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DinB CRISPR Activation Plasmid (h) | sc-405052-ACT | 20 µg | $397.00 |
Human POLK encodes DNA polymerase kappa (DinB), a Y-family translesion synthesis polymerase that enables DNA replication across bulky lesions such as UV-induced photoproducts and benzo[a]pyrene adducts. By promoting damage tolerance during S phase, POLK helps maintain replication fork progression and influences mutation spectra when bypass occurs with reduced fidelity. POLK functions within DNA damage response networks that coordinate lesion bypass, polymerase switching, and post-replicative repair, linking it to genome stability and cellular stress adaptation. Dysregulated POLK activity or altered expression has been associated with mutagenesis and genomic instability contexts relevant to cancer biology and exposure-related DNA damage models.
DinB CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous POLK expression without altering the underlying DNA sequence.
DinB CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the POLK 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 POLK transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DinB expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native POLK locus and enabling the study of DinB-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DinB pathway restoration in tumor cells with silenced or reduced POLK expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.