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.
LITAF Double Nickase Plasmid (h): sc-404337-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LITAF 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
- LITAF Double Nickase Plasmid (h) and LITAF Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LITAF. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LITAF Antibody (C-5): sc-166719
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LITAF Double Nickase Plasmid (h) | sc-404337-NIC | 20 µg | $410.00 |
LITAF (lipopolysaccharide-induced TNF factor) is a small, endosome-associated transcriptional regulator implicated in innate immune signaling and inflammatory gene expression, including modulation of TNF pathway outputs. It participates in membrane trafficking and endolysosomal processes through its C-terminal SIMPLE/LITAF domain, influencing ubiquitin-dependent sorting and turnover of signaling components. LITAF activity has been linked to cellular responses to microbial stimuli and stress, with downstream effects on cytokine networks and NF-κB-associated transcriptional programs. Dysregulation or mutation of LITAF has been associated with neurodegenerative and inflammatory phenotypes, including reports connecting altered LITAF function to peripheral neuropathy and aberrant cytokine regulation.
LITAF Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LITAF locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LITAF. 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 LITAF 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 LITAF-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.