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.
XPC CRISPR Activation Plasmid (h): sc-401499-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- XPC CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- XPC 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 XPC CRISPR Activation Plasmid (h) and XPC CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the XPC 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: XPC Antibody (D-10): sc-74410
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
XPC CRISPR Activation Plasmid (h) | sc-401499-ACT | 20 µg | $397.00 | |||
XPC CRISPR Activation Plasmid (h2) | sc-401499-ACT-2 | 20 µg | $397.00 |
Human XPC encodes a DNA damage recognition factor that initiates global genome nucleotide excision repair (GG-NER) by detecting helix-distorting lesions such as UV-induced photoproducts and bulky chemical adducts. XPC functions with RAD23B and CETN2 to promote lesion verification and recruitment of downstream NER components, supporting genome stability, replication fork integrity, and cell-cycle checkpoint signaling. Disruption of XPC-dependent repair elevates mutational burden and alters cellular responses to genotoxic stress, linking XPC dysfunction to cancer predisposition and photosensitivity phenotypes. As a central node in DNA repair networks, XPC expression is frequently examined in studies of mutagenesis, environmental carcinogenesis, and repair pathway crosstalk.
XPC CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous XPC expression without altering the underlying DNA sequence.
XPC CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the XPC 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 XPC transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous XPC expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native XPC locus and enabling the study of XPC-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of XPC pathway restoration in tumor cells with silenced or reduced XPC expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.