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.
CDKN1B/Kip1 p27 Double Nickase Plasmid (m): sc-419608-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CDKN1B/Kip1 p27 Double Nickase Plasmid (m) 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 (m) and CDKN1B/Kip1 p27 Double Nickase Plasmid (m2) 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 (m) | sc-419608-NIC | 20 µg | $410.00 |
Cdkn1b encodes the cyclin-dependent kinase inhibitor p27^Kip1 (CDKN1B), a key negative regulator of cell-cycle progression that restrains CDK2–cyclin E/A activity and helps maintain the G1/S checkpoint. p27 integrates mitogenic cues with growth control through pathways including PI3K–AKT signaling, where phosphorylation-dependent subcellular localization and proteasomal turnover modulate its inhibitory function. In mouse systems, altered Cdkn1b dosage or regulation is widely used to study proliferation–differentiation balance, tissue homeostasis, and cellular senescence programs. Dysregulated p27 expression or stability is frequently associated with aberrant cell-cycle control in cancer biology models and with hyperproliferative phenotypes in developmental and regenerative contexts.
CDKN1B/Kip1 p27 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Cdkn1b locus in mouse 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.