VMA21 CRISPR/Cas9 KO Plasmid (h): sc-407112
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- VMA21 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 VMA21 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 | |
VMA21 CRISPR/Cas9 KO Plasmid (h) | sc-407112 | 20 µg | $397.00 |
Overview
VMA21 encodes an endoplasmic reticulum (ER) membrane chaperone required for assembly of the vacuolar H+-ATPase (V-ATPase) V0 sector, a core driver of organelle acidification. By enabling proper V-ATPase biogenesis and trafficking, VMA21 supports lysosomal and endosomal pH control, autophagic flux, receptor recycling, and broader proteostasis pathways linked to ER quality control. Disruption of VMA21 perturbs acidification-dependent processes and cellular homeostasis, providing a mechanistic connection to stress responses and degradative pathway dysfunction. Pathogenic variation in VMA21 has been associated with X-linked myopathy with excessive autophagy, underscoring its relevance to muscle cell maintenance and lysosome-autophagy pathway regulation.
VMA21 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the VMA21 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the VMA21 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 VMA21 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 VMA21 protein expression.
This CRISPR knockout system enables efficient generation of VMA21-deficient cell models for investigation of VMA21 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting VMA21 exon(s) critical for VMA21 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 VMA21 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by VMA21 CRISPR/Cas9 KO Plasmid (h) and VMA21 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the VMA21 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by VMA21 HDR Plasmid (h) and VMA21 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by VMA21 homology arms to support homology-directed repair at defined VMA21 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.