REM CRISPR/Cas9 KO Plasmid (m): sc-422645
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- REM CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 REM 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: REM Antibody (24E4): sc-58472
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
REM CRISPR/Cas9 KO Plasmid (m) | sc-422645 | 20 µg | $397.00 |
Overview
Mouse Rem1 encodes REM, a member of the RGK family of small GTP-binding proteins that modulates membrane excitability by regulating voltage-gated Ca2+ channel trafficking and gating. Through interactions with channel β subunits and cytoskeletal regulators, REM influences Ca2+-dependent signaling, excitation–contraction coupling, and activity-dependent transcriptional programs. Rem1 expression is responsive to cellular stimulation and has been linked to control of cell growth and differentiation in electrically active tissues, supporting research into cardiac electrophysiology, neuronal signaling, and vascular smooth muscle function. Dysregulated RGK signaling is investigated in the context of arrhythmogenic mechanisms, neuroadaptation, and remodeling processes where altered Ca2+ influx impacts downstream pathways.
REM CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Rem1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Rem1 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 Rem1 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 REM protein expression.
This CRISPR knockout system enables efficient generation of Rem1-deficient cell models for investigation of REM signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Rem1 exon(s) critical for REM 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 Rem1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by REM CRISPR/Cas9 KO Plasmid (m) and REM CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Rem1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by REM HDR Plasmid (m) and REM HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Rem1 homology arms to support homology-directed repair at defined Rem1 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.