MAP-7 Double Nickase Plasmid (h): sc-411239-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MAP-7 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
- MAP-7 Double Nickase Plasmid (h) and MAP-7 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MAP7. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MAP-7 Double Nickase Plasmid (h) | sc-411239-NIC | 20 µg | $410.00 | |||
MAP-7 Double Nickase Plasmid (h2) | sc-411239-NIC-2 | 20 µg | $410.00 |
MAP7 encodes microtubule-associated protein 7 (MAP-7), a microtubule-stabilizing factor that supports microtubule polymerization and organization and promotes kinesin-1–dependent cargo transport. By modulating microtubule dynamics, MAP-7 contributes to intracellular trafficking, cell polarity, and cytoskeletal remodeling processes that influence neurite outgrowth and mitotic spindle behavior. Altered MAP7 expression or microtubule-binding activity can perturb cytoskeleton-driven signaling and transport networks, making it relevant to studies of neurobiology and proliferative cell states. As a cytoskeletal regulator, MAP-7 is frequently examined in contexts where microtubule stability intersects with stress responses, differentiation programs, and cellular architecture changes associated with disease phenotypes.
MAP-7 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MAP7 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MAP7. 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 MAP7 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 MAP7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.