Tβ-4 Y-linked Double Nickase Plasmid (h): sc-418116-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Tβ-4 Y-linked 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
- Tβ-4 Y-linked Double Nickase Plasmid (h) and Tβ-4 Y-linked Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TMSB4Y. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Tβ-4 Y-linked Double Nickase Plasmid (h) | sc-418116-NIC | 20 µg | $410.00 | |||
Tβ-4 Y-linked Double Nickase Plasmid (h2) | sc-418116-NIC-2 | 20 µg | $410.00 |
TMSB4Y encodes thymosin beta-4 Y-linked, a small actin-sequestering peptide that regulates G-actin availability and influences cytoskeletal remodeling, cell shape changes, and motility. Through modulation of actin dynamics, Tβ-4 Y-linked can impact processes linked to cell migration, adhesion, and stress responses, intersecting with pathways that depend on rapid actin turnover. As a Y chromosome–linked paralog within the thymosin beta family, it is relevant to studies of sex-biased gene regulation and male-specific biology, including contexts where altered cytoskeletal behavior contributes to disease-associated phenotypes.
Tβ-4 Y-linked Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TMSB4Y locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TMSB4Y. 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 TMSB4Y 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 TMSB4Y-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.