TMEM126A CRISPR/Cas9 KO Plasmid (h): sc-406768
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TMEM126A 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 TMEM126A 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TMEM126A CRISPR/Cas9 KO Plasmid (h) | sc-406768 | 20 µg | $397.00 |
Overview
TMEM126A encodes a mitochondria-associated transmembrane protein implicated in respiratory chain biology and maintenance of oxidative phosphorylation capacity. Studies link TMEM126A to mitochondrial complex I–related processes, influencing cellular redox balance, ATP production, and sensitivity to metabolic stress. Altered TMEM126A function has been associated with mitochondrial dysfunction phenotypes, including neuro-ophthalmic presentations such as autosomal recessive optic atrophy, making it relevant for investigating bioenergetic vulnerability in human cells. TMEM126A is therefore a useful target for probing mitochondrial quality control, stress-adaptive signaling, and downstream consequences on cell survival and differentiation programs.
TMEM126A CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TMEM126A gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TMEM126A 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 TMEM126A 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 TMEM126A protein expression.
This CRISPR knockout system enables efficient generation of TMEM126A-deficient cell models for investigation of TMEM126A signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TMEM126A exon(s) critical for TMEM126A 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 TMEM126A genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TMEM126A CRISPR/Cas9 KO Plasmid (h) and TMEM126A CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TMEM126A locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TMEM126A HDR Plasmid (h) and TMEM126A HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TMEM126A homology arms to support homology-directed repair at defined TMEM126A 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.