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.
EMAP II CRISPR/Cas9 KO Plasmid (m): sc-420161
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- EMAP II 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 EMAP II 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: EMAP II Antibody (A-4): sc-393228
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
EMAP II CRISPR/Cas9 KO Plasmid (m) | sc-420161 | 20 µg | $397.00 |
Overview
Aimp1 encodes EMAP II (endothelial monocyte-activating polypeptide II), a multifunctional protein best known as a cytokine-like factor derived from the tRNA multisynthetase complex component AIMP1. EMAP II participates in stress and inflammatory signaling, shaping leukocyte chemotaxis, endothelial responses, and broader regulation of innate immune processes. In mouse models, altered Aimp1/EMAP II activity has been linked to pathways controlling apoptosis, angiogenesis-related signaling, and tissue remodeling. Dysregulation of these processes is relevant to studies of chronic inflammation, tumor–immune microenvironment biology, and vascular dysfunction mechanisms.
EMAP II CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Aimp1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Aimp1 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 Aimp1 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 EMAP II protein expression.
This CRISPR knockout system enables efficient generation of Aimp1-deficient cell models for investigation of EMAP II signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Aimp1 exon(s) critical for EMAP II 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 Aimp1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by EMAP II CRISPR/Cas9 KO Plasmid (m) and EMAP II CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Aimp1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by EMAP II HDR Plasmid (m) and EMAP II HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Aimp1 homology arms to support homology-directed repair at defined Aimp1 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.