C1qL1 Double Nickase Plasmid (r): sc-437294-NIC
- Target species: rat
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- C1qL1 Double Nickase Plasmid (r) 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
- C1qL1 Double Nickase Plasmid (r) and C1qL1 Double Nickase Plasmid (r2) encode distinct paired gRNA designs targeting . One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
C1qL1 Double Nickase Plasmid (r) | sc-437294-NIC | 20 µg | $410.00 | |||
C1qL1 Double Nickase Plasmid (r2) | sc-437294-NIC-2 | 20 µg | $410.00 |
C1qL1 (complement C1q-like protein 1) is a secreted C1q/TNF superfamily member implicated in cell–cell communication and extracellular matrix-associated signaling in the nervous system. It is frequently studied in the context of synapse organization and neuronal circuit maintenance, where C1q-like proteins can influence adhesion-dependent processes and activity-regulated remodeling. Through these roles, C1qL1 is relevant to pathways governing neurodevelopment, synaptic connectivity, and glial–neuronal interactions. Altered regulation of C1q-like signaling has been investigated for potential links to neuropsychiatric and neurodegenerative phenotypes, making C1qL1 a useful target for mechanistic studies in rat neural models.
C1qL1 Double Nickase Plasmid (r) consists of a matched pair of plasmids engineered for high-specificity editing of the locus in rat cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within . 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 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 -disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.