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.
Menin CRISPR/Cas9 KO Plasmid (h): sc-402759
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Menin 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 Menin 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: Menin Antibody (B-9): sc-374371
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Menin CRISPR/Cas9 KO Plasmid (h) | sc-402759 | 20 µg | $397.00 |
Overview
MEN1 encodes menin, a predominantly nuclear scaffold protein that coordinates transcriptional regulation and chromatin state through interactions with histone modifiers and sequence-specific transcription factors. Menin is closely linked to epigenetic control of gene expression programs governing cell-cycle progression, differentiation, and genome stability, including pathways associated with MLL/COMPASS complexes and other chromatin-associated regulators. Disruption of MEN1 perturbs endocrine lineage homeostasis and transcriptional networks implicated in tumor suppressor biology. As a context-dependent regulator, menin is widely studied for its effects on hormone-producing tissues, DNA damage responses, and transcriptional fidelity.
Menin CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the MEN1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the MEN1 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 MEN1 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 Menin protein expression.
This CRISPR knockout system enables efficient generation of MEN1-deficient cell models for investigation of Menin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting MEN1 exon(s) critical for Menin 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 MEN1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Menin CRISPR/Cas9 KO Plasmid (h) and Menin CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the MEN1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Menin HDR Plasmid (h) and Menin HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by MEN1 homology arms to support homology-directed repair at defined MEN1 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.