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.
IRAK-2 Double Nickase Plasmid (h): sc-404304-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IRAK-2 Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- IRAK-2 Double Nickase Plasmid (h) and IRAK-2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IRAK2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: IRAK-2 Antibody (D-8): sc-515885
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IRAK-2 Double Nickase Plasmid (h) | sc-404304-NIC | 20 µg | $410.00 | |||
IRAK-2 Double Nickase Plasmid (h2) | sc-404304-NIC-2 | 20 µg | $410.00 |
Human IRAK2 encodes interleukin-1 receptor–associated kinase 2 (IRAK-2), a serine/threonine kinase–family member that functions as a core signaling intermediate downstream of Toll-like receptors and the IL-1 receptor. IRAK-2 participates in MyD88-dependent signaling complexes, contributing to activation of NF-κB and MAPK pathways and shaping transcriptional programs that regulate inflammatory cytokines and innate immune responses. Through its role in TIR-domain receptor signaling, IRAK-2 influences immune cell activation, pathogen-response signaling, and crosstalk with stress and apoptosis-related pathways. Dysregulated IRAK2-associated signaling has been linked to aberrant inflammatory states and altered immune signaling observed across multiple disease contexts, supporting its use as a mechanistic target in pathway-focused studies.
IRAK-2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IRAK2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IRAK2. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt IRAK2 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of IRAK2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.