alpha 2 Sodium Potassium ATPase/ATP1A2 CRISPR/Cas9 KO Plasmid (h): sc-401939

Overview

ATP1A2 encodes the α2 catalytic subunit of the Na⁺/K⁺-ATPase, a plasma membrane P-type ATPase that maintains intracellular Na⁺ and K⁺ gradients by coupling ATP hydrolysis to ion transport. This electrochemical gradient supports membrane potential, osmotic balance, secondary active transport, and Ca²⁺ homeostasis via Na⁺/Ca²⁺ exchange, thereby influencing excitability and signaling in electrically active tissues. ATP1A2 activity intersects with pathways governing neuronal and glial ion buffering, synaptic transmission, and cellular stress responses to ionic imbalance. Genetic and functional perturbation of ATP1A2 is linked to neurological phenotypes, including familial hemiplegic migraine and related seizure/ataxia presentations, making it a relevant target for mechanistic studies of excitability disorders.

alpha 2 Sodium Potassium ATPase/ATP1A2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the ATP1A2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ATP1A2 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 ATP1A2 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 alpha 2 Sodium Potassium ATPase/ATP1A2 protein expression.

This CRISPR knockout system enables efficient generation of ATP1A2-deficient cell models for investigation of alpha 2 Sodium Potassium ATPase/ATP1A2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

Key Features

• sgRNAs targeting ATP1A2 exon(s) critical for alpha 2 Sodium Potassium ATPase/ATP1A2 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 ATP1A2 genomic sites to improve knockout efficiency
• Compatible with delivery by transfection

Design Variants

CRISPRs +/- HDRs

• gRNAs encoded by alpha 2 Sodium Potassium ATPase/ATP1A2 CRISPR/Cas9 KO Plasmid (h) and alpha 2 Sodium Potassium ATPase/ATP1A2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the ATP1A2 locus. One or both targeting designs may be available. See Related Products for availability.
• HDR donor constructs encoded by alpha 2 Sodium Potassium ATPase/ATP1A2 HDR Plasmid (h) and alpha 2 Sodium Potassium ATPase/ATP1A2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by ATP1A2 homology arms to support homology-directed repair at defined ATP1A2 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.