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.
MaxiKβ CRISPR/Cas9 KO Plasmid (h): sc-403096
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MaxiKβ 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 MaxiKβ 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: MaxiKβ Antibody (A-5): sc-377023
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MaxiKβ CRISPR/Cas9 KO Plasmid (h) | sc-403096 | 20 µg | $397.00 |
Overview
KCNMB1 encodes the β1 regulatory subunit of large-conductance, Ca²⁺- and voltage-activated potassium (BK/MaxiK) channels, commonly referred to as MaxiKβ. By increasing BK channel Ca²⁺ sensitivity and altering gating kinetics, MaxiKβ shapes membrane excitability, intracellular Ca²⁺ dynamics, and smooth muscle tone. This modulatory activity integrates into pathways controlling vascular reactivity, airway contractility, and renal electrolyte handling, with downstream effects on NO/cGMP-linked signaling and Ca²⁺-dependent processes. Altered KCNMB1 function or expression has been associated with dysregulated blood pressure control, smooth muscle hypercontractility phenotypes, and broader excitability-related disorders.
MaxiKβ CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the KCNMB1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the KCNMB1 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 KCNMB1 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 MaxiKβ protein expression.
This CRISPR knockout system enables efficient generation of KCNMB1-deficient cell models for investigation of MaxiKβ signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting KCNMB1 exon(s) critical for MaxiKβ 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 KCNMB1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by MaxiKβ CRISPR/Cas9 KO Plasmid (h) and MaxiKβ CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the KCNMB1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by MaxiKβ HDR Plasmid (h) and MaxiKβ HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by KCNMB1 homology arms to support homology-directed repair at defined KCNMB1 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.