SDHD CRISPR/Cas9 KO Plasmid (h2): sc-403276-KO-2
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SDHD CRISPR/Cas9 Knockout (KO) Plasmid (h2) 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 SDHD 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 | |
SDHD CRISPR/Cas9 KO Plasmid (h2) | sc-403276-KO-2 | 20 µg | $397.00 |
Overview
Succinate dehydrogenase complex subunit D (SDHD) is an essential membrane-anchoring component of mitochondrial complex II, coupling succinate oxidation in the tricarboxylic acid (TCA) cycle to electron transfer into the ubiquinone pool of the oxidative phosphorylation (OXPHOS) pathway. By supporting succinate-to-fumarate conversion and respiratory chain flux, SDHD helps maintain mitochondrial redox balance, ATP production, and reactive oxygen species homeostasis. Perturbation of SDHD function alters metabolic signaling, including succinate-dependent regulation of hypoxia-responsive pathways and broader mitochondrial stress responses. SDHD dysregulation is implicated in inherited and sporadic tumor predisposition syndromes affecting neuroendocrine and paraganglial lineages, making it a useful target for mechanistic studies of mitochondrial metabolism and disease-relevant signaling.
SDHD CRISPR/Cas9 KO Plasmid (h2) is a pool of plasmids designed for targeted disruption of the SDHD gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SDHD 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 SDHD 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 SDHD protein expression.
This CRISPR knockout system enables efficient generation of SDHD-deficient cell models for investigation of SDHD signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting SDHD exon(s) critical for SDHD 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 SDHD genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SDHD CRISPR/Cas9 KO Plasmid (h) and SDHD CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SDHD locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SDHD HDR Plasmid (h) and SDHD HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SDHD homology arms to support homology-directed repair at defined SDHD 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.