
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DUSP22 CRISPR/Cas9 KO Plasmid (h) | sc-405867 | 20 µg | $397.00 |
DUSP22 encodes a dual-specificity phosphatase that dephosphorylates serine/threonine and tyrosine residues to modulate kinase-driven signaling networks. It is implicated in regulation of MAPK pathway outputs and phospho-dependent control of immune receptor signaling, influencing transcriptional programs, cell activation states, and apoptosis. By tuning phosphorylation dynamics, DUSP22 contributes to cellular homeostasis in hematopoietic and other tissues where stimulus-responsive signaling is critical. Altered DUSP22 expression or pathway context has been linked to dysregulated immune signaling and oncogenic processes, supporting its use as a mechanistic node in studies of signaling-driven disease biology.
DUSP22 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the DUSP22 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the DUSP22 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 DUSP22 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 DUSP22 protein expression.
This CRISPR knockout system enables efficient generation of DUSP22-deficient cell models for investigation of DUSP22 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.