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.
RADX CRISPR/Cas9 KO Plasmid (h): sc-409991
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RADX 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 RADX 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
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: RADX Antibody (A-3): sc-514563
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RADX CRISPR/Cas9 KO Plasmid (h) | sc-409991 | 20 µg | $397.00 |
Overview
CXorf57 encodes RADX, a single-stranded DNA–binding factor that modulates replication fork dynamics and helps maintain genome stability during S phase. RADX antagonizes RAD51 loading at stalled replication forks, shaping homologous recombination and coordinating responses to replication stress. Through these functions it contributes to preservation of replication fork integrity, suppression of aberrant recombination, and control of DNA damage signaling pathways. Dysregulation of RADX-linked fork protection and repair balance is relevant to mechanisms underlying genome instability phenotypes observed in cancer biology and other replication stress–associated disease models.
RADX CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CXorf57 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CXorf57 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 CXorf57 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 RADX protein expression.
This CRISPR knockout system enables efficient generation of CXorf57-deficient cell models for investigation of RADX signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting CXorf57 exon(s) critical for RADX 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 CXorf57 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by RADX CRISPR/Cas9 KO Plasmid (h) and RADX CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CXorf57 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by RADX HDR Plasmid (h) and RADX HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CXorf57 homology arms to support homology-directed repair at defined CXorf57 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.