



Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MyoD Double Nickase Plasmid (h) | sc-400092-NIC | 20 µg | $410.00 | |||
MyoD Double Nickase Plasmid (h2) | sc-400092-NIC-2 | 20 µg | $410.00 |
MYOD1 encodes MyoD, a basic helix–loop–helix transcription factor that functions as a master regulator of skeletal myogenesis by binding E-box motifs and coordinating chromatin remodeling with lineage-specific gene expression. MyoD integrates cues from myogenic regulatory factor networks and intersects with Notch, Wnt/β-catenin, TGF-β, and MAPK signaling to balance progenitor proliferation and differentiation. Through cooperative and antagonistic interactions with factors such as MYOG, MEF2, and ID proteins, it drives myoblast commitment, cell-cycle exit, and muscle structural gene programs. Dysregulation of MYOD1 activity is relevant to impaired muscle regeneration and neuromuscular disease biology, and MYOD1 alterations are studied in the context of myogenic tumors and lineage plasticity.
MyoD Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MYOD1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MYOD1. 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 MYOD1 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 MYOD1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.