BLM CRISPR/Cas9 KO Plasmid (m): sc-419336
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BLM CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 BLM 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: BLM Antibody (B-4): sc-365753
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BLM CRISPR/Cas9 KO Plasmid (m) | sc-419336 | 20 µg | $397.00 |
Overview
Blm encodes the mouse BLM RecQ family DNA helicase, a central factor in genome maintenance that limits aberrant homologous recombination and helps resolve stalled replication forks. BLM functions with topoisomerase IIIα, RMI1/2, and other repair proteins to process recombination intermediates, promote accurate DNA double-strand break repair, and support S-phase progression. Through roles in replication stress responses, telomere stability, and checkpoint signaling, BLM influences mutation accumulation and chromosomal rearrangements. Dysregulated BLM activity is linked to elevated genomic instability phenotypes that are broadly relevant to studies of cancer biology, DNA damage signaling, and aging-associated genome maintenance.
BLM CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Blm gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Blm 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 Blm 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 BLM protein expression.
This CRISPR knockout system enables efficient generation of Blm-deficient cell models for investigation of BLM signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Blm exon(s) critical for BLM 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 Blm genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by BLM CRISPR/Cas9 KO Plasmid (m) and BLM CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Blm locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by BLM HDR Plasmid (m) and BLM HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Blm homology arms to support homology-directed repair at defined Blm 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.