RB1CC1 Double Nickase Plasmid (h): sc-416259-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RB1CC1 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
- RB1CC1 Double Nickase Plasmid (h) and RB1CC1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RB1CC1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RB1CC1 Double Nickase Plasmid (h) | sc-416259-NIC | 20 µg | $410.00 | |||
RB1CC1 Double Nickase Plasmid (h2) | sc-416259-NIC-2 | 20 µg | $410.00 |
RB1CC1 (also known as FIP200) encodes a large scaffold protein that coordinates autophagy initiation through the ULK1–ATG13–RB1CC1 complex and couples nutrient sensing to phagophore formation. Beyond autophagy, RB1CC1 contributes to regulation of focal adhesion dynamics and cytoskeletal organization, shaping cell migration and survival signaling. Disruption of RB1CC1-dependent autophagy has been linked to cellular stress sensitivity and altered proteostasis, processes frequently investigated in neurodegeneration and cancer biology. As a multifunctional hub, RB1CC1 is widely studied for its roles in metabolic adaptation, organelle quality control, and signaling network rewiring.
RB1CC1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RB1CC1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RB1CC1. 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 RB1CC1 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 RB1CC1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.