MOS CRISPR/Cas9 KO Plasmid (h): sc-406911
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MOS 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 MOS 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 | |
MOS CRISPR/Cas9 KO Plasmid (h) | sc-406911 | 20 µg | $397.00 |
Overview
Human MOS encodes Mos, a serine/threonine protein kinase best known for its role in meiotic cell-cycle control through activation of the MAPK/ERK cascade. Mos functions upstream of MEK1/2 and ERK1/2, helping coordinate cytostatic factor activity, spindle dynamics, and progression through M phase in germ cell contexts, and it has been used as a model regulator of MAPK signaling feedback. Dysregulated MOS expression or kinase activity has been linked to altered proliferative signaling and transformation-like phenotypes in experimental systems, supporting its relevance for studying MAPK pathway wiring and cell-cycle checkpoints. These properties make MOS a useful target for interrogating kinase-driven signaling networks and their downstream transcriptional and cytoskeletal outputs.
MOS CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the MOS gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the MOS 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 MOS 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 MOS protein expression.
This CRISPR knockout system enables efficient generation of MOS-deficient cell models for investigation of MOS signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting MOS exon(s) critical for MOS 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 MOS genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by MOS CRISPR/Cas9 KO Plasmid (h) and MOS CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the MOS locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by MOS HDR Plasmid (h) and MOS HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by MOS homology arms to support homology-directed repair at defined MOS 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.