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.
Cdc37 CRISPR/Cas9 KO Plasmid (m): sc-419584
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Cdc37 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 Cdc37 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: Cdc37 Antibody (E-4): sc-13129
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Cdc37 CRISPR/Cas9 KO Plasmid (m) | sc-419584 | 20 µg | $397.00 |
Overview
Cdc37 (cell division cycle 37) encodes a conserved HSP90 co-chaperone that stabilizes and promotes the maturation of a broad set of protein kinases, including many regulators of MAPK and PI3K–AKT signaling. By coordinating kinase folding, complex assembly, and proteostasis, CDC37 influences cell-cycle progression, stress responses, and signaling network robustness. Perturbation of CDC37 function can reshape phospho-signaling landscapes and alter dependence on chaperone pathways, making it relevant to studies of kinase-driven cellular phenotypes and proteostasis imbalance. Mouse Cdc37 is therefore widely used to interrogate chaperone–kinase circuitry in development, tissue homeostasis, and disease-relevant signaling models.
Cdc37 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Cdc37 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Cdc37 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 Cdc37 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 Cdc37 protein expression.
This CRISPR knockout system enables efficient generation of Cdc37-deficient cell models for investigation of Cdc37 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Cdc37 exon(s) critical for Cdc37 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 Cdc37 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Cdc37 CRISPR/Cas9 KO Plasmid (m) and Cdc37 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Cdc37 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Cdc37 HDR Plasmid (m) and Cdc37 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Cdc37 homology arms to support homology-directed repair at defined Cdc37 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.