



Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Mcl-1 Double Nickase Plasmid (m) | sc-421589-NIC | 20 µg | $410.00 | |||
Mcl-1 Double Nickase Plasmid (m2) | sc-421589-NIC-2 | 20 µg | $410.00 |
Mouse Mcl1 encodes Mcl-1, an anti-apoptotic BCL-2 family protein that preserves mitochondrial outer membrane integrity by sequestering pro-death BH3-only factors and limiting BAX/BAK-driven permeabilization. Mcl-1 is a short-lived protein tightly regulated by transcriptional programs and ubiquitin–proteasome turnover, linking it to cellular stress responses, growth factor signaling, and metabolic adaptation. By modulating intrinsic apoptosis thresholds, Mcl-1 influences immune cell homeostasis, hematopoietic survival, and tissue development, and altered Mcl1 regulation is frequently studied in contexts of oncogenic signaling, inflammation, and treatment-induced cell death models. Its central role in mitochondrial apoptosis makes Mcl1 a common node for interrogating survival circuitry and pathway crosstalk involving MAPK, PI3K/AKT, and ER stress responses.
Mcl-1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Mcl1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Mcl1. 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 Mcl1 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 Mcl1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.