MSR CRISPR/Cas9 KO Plasmid (h): sc-409650
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MSR 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 MSR 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MSR CRISPR/Cas9 KO Plasmid (h) | sc-409650 | 20 µg | $397.00 |
Overview
Human MTRR encodes methionine synthase reductase (MSR), an FAD/NADPH-dependent oxidoreductase that restores catalytic activity of methionine synthase by reductive reactivation of its cobalamin cofactor. Through this role, MSR supports one-carbon metabolism, linking the folate and methionine cycles to S-adenosylmethionine-dependent methylation reactions and homocysteine remethylation. Disruption of MTRR perturbs redox-dependent enzyme maintenance and can alter cellular methylation capacity, nucleotide biosynthesis, and metabolic stress responses. Genetic variation or impaired MSR function has been associated with disturbed homocysteine handling and folate-related metabolic phenotypes relevant to studies of developmental biology and cardiometabolic risk.
MSR CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the MTRR gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the MTRR 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 MTRR 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 MSR protein expression.
This CRISPR knockout system enables efficient generation of MTRR-deficient cell models for investigation of MSR signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting MTRR exon(s) critical for MSR 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 MTRR genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by MSR CRISPR/Cas9 KO Plasmid (h) and MSR CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the MTRR locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by MSR HDR Plasmid (h) and MSR HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by MTRR homology arms to support homology-directed repair at defined MTRR 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.