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.
MIS CRISPR/Cas9 KO Plasmid (h): sc-400715
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MIS 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 MIS 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: MIS Antibody (B-11): sc-166752
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MIS CRISPR/Cas9 KO Plasmid (h) | sc-400715 | 20 µg | $397.00 |
Overview
Anti-Müllerian hormone (AMH), also known as Müllerian inhibiting substance (MIS), is a TGF-β superfamily glycoprotein that signals primarily through AMHR2 and downstream SMAD1/5/8 to regulate reproductive tract development and gonadal function. In the ovary, AMH produced by granulosa cells modulates follicle recruitment and FSH responsiveness, shaping the balance between follicle growth and quiescence. In the testis, MIS from Sertoli cells drives regression of Müllerian ducts during male sexual differentiation. Dysregulated AMH/MIS signaling and altered expression are studied in disorders of sex development, ovarian physiology, and endocrine-related tumor biology.
MIS CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the AMH gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the AMH 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 AMH 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 MIS protein expression.
This CRISPR knockout system enables efficient generation of AMH-deficient cell models for investigation of MIS signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting AMH exon(s) critical for MIS 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 AMH genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by MIS CRISPR/Cas9 KO Plasmid (h) and MIS CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the AMH locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by MIS HDR Plasmid (h) and MIS HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by AMH homology arms to support homology-directed repair at defined AMH 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.