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.
DDAH I CRISPR/Cas9 KO Plasmid (h): sc-402719
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DDAH I 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 DDAH I 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: DDAH I Antibody (D-6): sc-514841
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DDAH I CRISPR/Cas9 KO Plasmid (h) | sc-402719 | 20 µg | $397.00 |
Overview
DDAH1 encodes dimethylarginine dimethylaminohydrolase 1 (DDAH I), a cytosolic enzyme that hydrolyzes asymmetric dimethylarginine (ADMA) and related methylarginines, thereby modulating nitric oxide synthase activity and cellular nitric oxide (NO) bioavailability. Through regulation of the ADMA–NO axis, DDAH I influences endothelial function, redox balance, vascular tone, and inflammatory signaling pathways. Altered DDAH1 expression or activity has been associated with cardiovascular and metabolic phenotypes and is frequently examined in contexts of endothelial dysfunction and oxidative stress. DDAH1 is also studied in tumor biology and tissue remodeling where NO-dependent signaling impacts angiogenesis and cell migration.
DDAH I CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the DDAH1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the DDAH1 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 DDAH1 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 DDAH I protein expression.
This CRISPR knockout system enables efficient generation of DDAH1-deficient cell models for investigation of DDAH I signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting DDAH1 exon(s) critical for DDAH I 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 DDAH1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by DDAH I CRISPR/Cas9 KO Plasmid (h) and DDAH I CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the DDAH1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by DDAH I HDR Plasmid (h) and DDAH I HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by DDAH1 homology arms to support homology-directed repair at defined DDAH1 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.