Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
GRP 75 CRISPR/Cas9 KO Plasmid (m): sc-420983
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GRP 75 CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 GRP 75 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
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: GRP 75 Antibody (D-9): sc-133137
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GRP 75 CRISPR/Cas9 KO Plasmid (m) | sc-420983 | 20 µg | $397.00 |
Overview
Hspa9 encodes GRP75 (mortalin), a mitochondrial HSP70-family chaperone that supports protein import, folding, and proteostasis within the mitochondrial matrix. GRP75 participates in mitochondrial quality control, regulation of oxidative phosphorylation, and maintenance of iron–sulfur cluster and heme-related processes that influence redox homeostasis. It also contributes to mitochondria–ER communication through chaperone networks that shape calcium handling and stress signaling. Dysregulation of Hspa9/GRP75 has been associated with mitochondrial dysfunction and cellular stress phenotypes relevant to neurodegeneration, cardiometabolic dysfunction, and transformation-associated remodeling of bioenergetic pathways.
GRP 75 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Hspa9 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Hspa9 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 Hspa9 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 GRP 75 protein expression.
This CRISPR knockout system enables efficient generation of Hspa9-deficient cell models for investigation of GRP 75 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Hspa9 exon(s) critical for GRP 75 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 Hspa9 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by GRP 75 CRISPR/Cas9 KO Plasmid (m) and GRP 75 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Hspa9 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by GRP 75 HDR Plasmid (m) and GRP 75 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Hspa9 homology arms to support homology-directed repair at defined Hspa9 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.