NELF-B CRISPR/Cas9 KO Plasmid (h): sc-405667
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NELF-B 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 NELF-B 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 | |
NELF-B CRISPR/Cas9 KO Plasmid (h) | sc-405667 | 20 µg | $397.00 |
Overview
NELFB encodes NELF-B, a core subunit of the negative elongation factor (NELF) complex that cooperates with DSIF to regulate promoter-proximal pausing of RNA polymerase II and coordinate productive transcription elongation. Through this checkpoint, NELF-B influences rapid stimulus-responsive gene expression programs, co-transcriptional RNA processing, and chromatin-linked control of transcriptional kinetics. NELF-B–dependent pausing is integrated with signaling and stress-response pathways that fine-tune transcriptional output and cell-state transitions. Dysregulation of elongation control and pausing-associated networks has been implicated in oncogenic transcriptional programs and other diseases characterized by altered gene regulation, making NELFB a useful node for mechanistic studies of transcriptional control.
NELF-B CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the NELFB gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the NELFB 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 NELFB 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 NELF-B protein expression.
This CRISPR knockout system enables efficient generation of NELFB-deficient cell models for investigation of NELF-B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting NELFB exon(s) critical for NELF-B 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 NELFB genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by NELF-B CRISPR/Cas9 KO Plasmid (h) and NELF-B CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the NELFB locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by NELF-B HDR Plasmid (h) and NELF-B HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by NELFB homology arms to support homology-directed repair at defined NELFB 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.