
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BCLAF1 CRISPR/Cas9 KO Plasmid (m) | sc-428381 | 20 µg | $397.00 |
Bclaf1 encodes BCLAF1, a nuclear DNA- and RNA-binding factor implicated in transcriptional regulation, pre-mRNA splicing, and chromatin-associated control of gene expression. BCLAF1 has been linked to DNA damage responses and apoptosis-related programs through interactions with BCL2-family signaling and stress-responsive transcriptional networks. In mouse cells, BCLAF1 contributes to maintenance of genome stability and regulation of cell-cycle and survival pathways that shape developmental and immune-relevant gene expression. Dysregulated BCLAF1 activity has been associated with altered proliferative capacity and aberrant RNA processing phenotypes relevant to cancer biology and neuroimmune signaling contexts.
BCLAF1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Bclaf1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Bclaf1 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 Bclaf1 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 BCLAF1 protein expression.
This CRISPR knockout system enables efficient generation of Bclaf1-deficient cell models for investigation of BCLAF1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
CRISPRs +/- HDRs
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.