
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SUCLA2 CRISPR/Cas9 KO Plasmid (m) | sc-423214 | 20 µg | $397.00 |
Sucla2 encodes the mouse SUCLA2 beta subunit of succinyl-CoA synthetase (ADP-forming), a mitochondrial matrix enzyme that catalyzes the reversible conversion of succinyl-CoA to succinate with ATP generation in the tricarboxylic acid (TCA) cycle. Through this reaction, SUCLA2 supports oxidative metabolism, anaplerotic flux, and coordination between the TCA cycle and heme/ketone body–related succinyl-CoA utilization. SUCLA2 function is closely linked to mitochondrial energy homeostasis and nucleotide balance, and perturbation of this pathway is associated with mitochondrial encephalomyopathy phenotypes and mtDNA maintenance defects reported for SUCLA2-related mitochondrial disorders. In mouse models, Sucla2 is therefore relevant for studying metabolic stress responses, neuromuscular vulnerability, and mechanisms connecting TCA cycle enzymes to mitochondrial genome stability.
SUCLA2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Sucla2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Sucla2 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 Sucla2 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 SUCLA2 protein expression.
This CRISPR knockout system enables efficient generation of Sucla2-deficient cell models for investigation of SUCLA2 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.