CUL-4A CRISPR/Cas9 KO Plasmid (h): sc-401967
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CUL-4A CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the CUL-4A genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CUL-4A CRISPR/Cas9 KO Plasmid (h) | sc-401967 | 20 µg | $397.00 |
Overview
CUL4A encodes cullin-4A, a core scaffold of the CRL4 E3 ubiquitin ligase complex that coordinates ubiquitination and proteasomal turnover of proteins governing DNA replication, chromatin dynamics, and cell-cycle progression. By partnering with adaptor proteins such as DDB1 and multiple DCAF substrate receptors, CUL-4A regulates processes including nucleotide excision repair, replication licensing, and responses to UV-induced DNA damage. Disruption of CUL4A-dependent proteostasis can perturb genome stability and checkpoint control, linking altered CRL4 activity to cancer-associated phenotypes and other disorders involving defective DNA repair. As a central node in ubiquitin-mediated signaling, CUL-4A is frequently studied in pathways that couple chromatin regulation to replication stress and transcriptional control.
CUL-4A CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CUL4A gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CUL4A together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the CUL4A open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish CUL-4A protein expression.
This CRISPR knockout system enables efficient generation of CUL4A-deficient cell models for investigation of CUL-4A signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting CUL4A exon(s) critical for CUL-4A function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple CUL4A genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CUL-4A CRISPR/Cas9 KO Plasmid (h) and CUL-4A CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CUL4A locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CUL-4A HDR Plasmid (h) and CUL-4A HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CUL4A homology arms to support homology-directed repair at defined CUL4A target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.