CDKN1B/Kip1 p27 Double Nickase Plasmid (h): sc-400074-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CDKN1B/Kip1 p27 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
- CDKN1B/Kip1 p27 Double Nickase Plasmid (h) and CDKN1B/Kip1 p27 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CDKN1B. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CDKN1B/Kip1 p27 Antibody (F-8): sc-1641
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CDKN1B/Kip1 p27 Double Nickase Plasmid (h) | sc-400074-NIC | 20 µg | $410.00 | |||
CDKN1B/Kip1 p27 Double Nickase Plasmid (h2) | sc-400074-NIC-2 | 20 µg | $410.00 |
CDKN1B encodes p27Kip1, a cyclin-dependent kinase inhibitor that restrains CDK2- and CDK4/6-driven progression through the G1/S checkpoint by modulating cyclin E/A–CDK2 and cyclin D–CDK4/6 complexes. p27 integrates mitogenic signaling and growth-inhibitory cues to control cell-cycle arrest, cellular quiescence, and differentiation, with regulation governed by phosphorylation-dependent subcellular localization and proteasomal turnover via SCF ubiquitin ligases. Altered CDKN1B expression or stability is frequently linked to dysregulated proliferation and aberrant checkpoint control, making it relevant to studies of oncogenic signaling, lineage commitment, and stress responses in human cells.
CDKN1B/Kip1 p27 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDKN1B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDKN1B. 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 CDKN1B 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 CDKN1B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.