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.
PGAM1 CRISPR/Cas9 KO Plasmid (h): sc-404283
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PGAM1 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 PGAM1 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: PGAM1 Antibody (6): sc-130334
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PGAM1 CRISPR/Cas9 KO Plasmid (h) | sc-404283 | 20 µg | $397.00 |
Overview
Phosphoglycerate mutase 1 (PGAM1) is a cytosolic glycolytic enzyme that catalyzes the interconversion of 3-phosphoglycerate and 2-phosphoglycerate, regulating glycolytic flux and the balance of downstream biosynthetic intermediates. Through its position at a key branch point in central carbon metabolism, PGAM1 supports ATP generation and provides precursors for anabolic pathways linked to nucleotide and amino acid synthesis. Altered PGAM1 activity has been associated with metabolic rewiring and proliferative phenotypes, making it relevant to studies of tumor metabolism and cellular growth control. PGAM1 is also used as a node for investigating connections between glycolysis, redox homeostasis, and stress-adaptive signaling.
PGAM1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the PGAM1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the PGAM1 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 PGAM1 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 PGAM1 protein expression.
This CRISPR knockout system enables efficient generation of PGAM1-deficient cell models for investigation of PGAM1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting PGAM1 exon(s) critical for PGAM1 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 PGAM1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by PGAM1 CRISPR/Cas9 KO Plasmid (h) and PGAM1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the PGAM1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by PGAM1 HDR Plasmid (h) and PGAM1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by PGAM1 homology arms to support homology-directed repair at defined PGAM1 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.