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.
SRPK1 Double Nickase Plasmid (h): sc-402855-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SRPK1 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
- SRPK1 Double Nickase Plasmid (h) and SRPK1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SRPK1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: SRPK1 Antibody (EE-13): sc-100443
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SRPK1 Double Nickase Plasmid (h) | sc-402855-NIC | 20 µg | $410.00 | |||
SRPK1 Double Nickase Plasmid (h2) | sc-402855-NIC-2 | 20 µg | $410.00 |
SRPK1 encodes serine/arginine-rich protein-specific kinase 1, a conserved regulator of pre-mRNA splicing that phosphorylates SR splicing factors to control their localization and activity. Through modulation of splice-site choice and exon inclusion, SRPK1 influences gene expression programs linked to cell-cycle progression, stress responses, and signaling outputs that depend on alternative splicing. SRPK1 activity interfaces with phosphorylation-dependent RNA processing pathways and can reshape transcript isoform landscapes affecting apoptosis, proliferation, and cytoskeletal dynamics. Dysregulation of SRPK1-mediated splicing control has been associated with disease-relevant phenotypes in cancer biology, neurodegeneration, and angiogenesis-related mechanisms, supporting its use as a target for mechanistic studies of splicing-dependent regulation.
SRPK1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SRPK1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SRPK1. 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 SRPK1 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 SRPK1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.