MACF1 Double Nickase Plasmid (h): sc-402923-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MACF1 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
- MACF1 Double Nickase Plasmid (h) and MACF1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MACF1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MACF1 Double Nickase Plasmid (h) | sc-402923-NIC | 20 µg | $410.00 | |||
MACF1 Double Nickase Plasmid (h2) | sc-402923-NIC-2 | 20 µg | $410.00 |
MACF1 (microtubule actin crosslinking factor 1) encodes a large spectraplakin that physically links microtubules and F-actin to coordinate cytoskeletal architecture, intracellular trafficking, and polarized cell migration. Through its interactions with plus-end tracking proteins and actin regulatory complexes, MACF1 supports microtubule capture at the cortex and contributes to processes such as focal adhesion turnover, neurite outgrowth, and epithelial organization. MACF1 has also been implicated in Wnt/β-catenin–related signaling dynamics via scaffolding functions that influence pathway component localization. Dysregulation or mutation of MACF1 is associated with altered cell motility and developmental phenotypes and has been reported in genomic studies of neurodevelopmental disorders and cancer-related cytoskeletal remodeling.
MACF1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MACF1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MACF1. 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 MACF1 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 MACF1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.