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.
Integrin α4/ITGA4/CD49d Double Nickase Plasmid (h): sc-401336-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Integrin α4/ITGA4/CD49d 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
- Integrin α4/ITGA4/CD49d Double Nickase Plasmid (h) and Integrin α4/ITGA4/CD49d Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ITGA4. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Integrin α4/ITGA4/CD49d Antibody (C-2): sc-365569
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Integrin α4/ITGA4/CD49d Double Nickase Plasmid (h) | sc-401336-NIC | 20 µg | $410.00 | |||
Integrin α4/ITGA4/CD49d Double Nickase Plasmid (h2) | sc-401336-NIC-2 | 20 µg | $410.00 |
ITGA4 encodes integrin α4 (CD49d), an adhesion receptor that pairs with β1 or β7 to form α4β1 and α4β7 heterodimers that regulate leukocyte trafficking, firm adhesion, and transendothelial migration. Through binding ligands such as VCAM1 and fibronectin, integrin α4 coordinates outside-in signaling that interfaces with cytoskeletal remodeling and survival pathways, including focal adhesion, PI3K–AKT, and MAPK signaling. ITGA4 activity contributes to immune cell positioning within tissues and influences inflammatory microenvironments by modulating cell–cell and cell–matrix interactions. Dysregulated integrin α4–dependent adhesion and migration has been implicated in chronic inflammatory conditions and hematologic malignancy biology, supporting its use as a research node for immune and tumor–stroma interaction studies.
Integrin α4/ITGA4/CD49d Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ITGA4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ITGA4. 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 ITGA4 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 ITGA4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.