Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
BPGM CRISPR/Cas9 KO Plasmid (h): sc-405810
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BPGM CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the BPGM genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
- 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 CRISPR/Cas9 KO Plasmid (h) | sc-405810 | 20 µg | $397.00 |
Overview
Bisphosphoglycerate mutase (BPGM) is an erythroid-enriched enzyme that regulates levels of 2,3-bisphosphoglycerate (2,3-BPG), a key allosteric effector of hemoglobin oxygen affinity. By interconverting 1,3-bisphosphoglycerate and 2,3-BPG, BPGM links glycolytic flux to oxygen delivery physiology and red blood cell metabolic homeostasis. Altered BPGM activity can shift 2,3-BPG concentrations and modulate tissue oxygenation, making it relevant to studies of erythrocyte metabolism, hypoxia adaptation, and hematologic phenotypes. Because 2,3-BPG impacts hemoglobin function without changing hemoglobin abundance, BPGM is frequently used to dissect metabolic control points that influence oxygen-binding dynamics.
BPGM CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the BPGM gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the BPGM together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the BPGM open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish BPGM protein expression.
This CRISPR knockout system enables efficient generation of BPGM-deficient cell models for investigation of BPGM signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting BPGM exon(s) critical for BPGM function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple BPGM genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by BPGM CRISPR/Cas9 KO Plasmid (h) and BPGM CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the BPGM locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by BPGM HDR Plasmid (h) and BPGM HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by BPGM homology arms to support homology-directed repair at defined BPGM target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.