RPRD1B CRISPR/Cas9 KO Plasmid (h): sc-412911
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RPRD1B 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 RPRD1B 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 | |
RPRD1B CRISPR/Cas9 KO Plasmid (h) | sc-412911 | 20 µg | $397.00 |
Overview
RPRD1B encodes a CTD-interacting regulator of RNA polymerase II that helps coordinate transcription initiation, elongation, and termination through modulation of polymerase CTD phosphorylation states. By linking transcriptional control to mRNA processing, RPRD1B contributes to global gene expression programs, including cell-cycle and stress-responsive transcriptional networks. Dysregulated RPRD1B expression or function has been associated with altered transcriptional homeostasis observed in cancer-related contexts, where shifts in RNA polymerase II dynamics can impact proliferation and genome stability. As a nuclear transcriptional regulator, it is also relevant for mechanistic studies of transcription-coupled RNA processing and chromatin-associated regulation.
RPRD1B CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the RPRD1B gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the RPRD1B 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 RPRD1B 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 RPRD1B protein expression.
This CRISPR knockout system enables efficient generation of RPRD1B-deficient cell models for investigation of RPRD1B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting RPRD1B exon(s) critical for RPRD1B 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 RPRD1B genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by RPRD1B CRISPR/Cas9 KO Plasmid (h) and RPRD1B CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the RPRD1B locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by RPRD1B HDR Plasmid (h) and RPRD1B HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by RPRD1B homology arms to support homology-directed repair at defined RPRD1B 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.