BPGM Double Nickase Plasmid (h): sc-405810-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BPGM 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
- BPGM Double Nickase Plasmid (h) and BPGM Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting BPGM. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: BPGM Antibody (C-4): sc-373819
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BPGM Double Nickase Plasmid (h) | sc-405810-NIC | 20 µg | $410.00 | |||
BPGM Double Nickase Plasmid (h2) | sc-405810-NIC-2 | 20 µg | $410.00 |
Bisphosphoglycerate mutase (BPGM) is an erythroid-enriched enzyme that regulates the Rapoport–Luebering shunt by synthesizing and degrading 2,3-bisphosphoglycerate (2,3-BPG), a key allosteric effector of hemoglobin oxygen affinity. By controlling 2,3-BPG levels, BPGM links glycolytic flux to oxygen delivery and red blood cell metabolic homeostasis, influencing energy balance and redox-sensitive processes in mature erythrocytes. Altered BPGM activity perturbs 2,3-BPG abundance and can shift oxygen dissociation dynamics, making BPGM a relevant target in studies of erythrocyte physiology and hypoxia adaptation. Genetic or metabolic dysregulation of this pathway is investigated in the context of inherited red cell disorders and anemia-associated phenotypes where oxygen transport and glycolytic remodeling are impacted.
BPGM Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the BPGM locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within BPGM. 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 BPGM 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 BPGM-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.