Nicotinic Acetylcholine Receptor beta 2/CHRNB2 CRISPR/Cas9 KO Plasmid (h): sc-401641

Overview

CHRNB2 encodes the β2 subunit of neuronal nicotinic acetylcholine receptors (nAChRs), ligand-gated cation channels that assemble as heteromeric pentamers with α subunits to regulate membrane excitability. Upon acetylcholine or nicotine binding, β2-containing nAChRs mediate Na⁺ and Ca²⁺ influx, coupling cholinergic signaling to calcium-dependent pathways that influence neurotransmitter release, synaptic plasticity, and circuit development. CHRNB2 activity intersects with processes governing reward, attention, and arousal through modulation of dopaminergic and other neuromodulatory networks. Genetic and functional alterations in CHRNB2 have been linked to neuropsychiatric phenotypes and seizure susceptibility, supporting its relevance for mechanistic studies in neuronal models.

Nicotinic Acetylcholine Receptor beta 2/CHRNB2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CHRNB2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CHRNB2 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 CHRNB2 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 Nicotinic Acetylcholine Receptor beta 2/CHRNB2 protein expression.

This CRISPR knockout system enables efficient generation of CHRNB2-deficient cell models for investigation of Nicotinic Acetylcholine Receptor beta 2/CHRNB2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

Key Features

• sgRNAs targeting CHRNB2 exon(s) critical for Nicotinic Acetylcholine Receptor beta 2/CHRNB2 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 CHRNB2 genomic sites to improve knockout efficiency
• Compatible with delivery by transfection

Design Variants

CRISPRs +/- HDRs

• gRNAs encoded by Nicotinic Acetylcholine Receptor beta 2/CHRNB2 CRISPR/Cas9 KO Plasmid (h) and Nicotinic Acetylcholine Receptor beta 2/CHRNB2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CHRNB2 locus. One or both targeting designs may be available. See Related Products for availability.
• HDR donor constructs encoded by Nicotinic Acetylcholine Receptor beta 2/CHRNB2 HDR Plasmid (h) and Nicotinic Acetylcholine Receptor beta 2/CHRNB2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CHRNB2 homology arms to support homology-directed repair at defined CHRNB2 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.