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.
SUN2 CRISPR/Cas9 KO Plasmid (h): sc-404746
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SUN2 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 SUN2 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: SUN2 Antibody (G-5): sc-377459
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SUN2 CRISPR/Cas9 KO Plasmid (h) | sc-404746 | 20 µg | $397.00 |
Overview
SUN2 encodes a SUN domain–containing inner nuclear membrane protein that is a core component of the LINC (linker of nucleoskeleton and cytoskeleton) complex. By binding nuclear lamins and interacting with KASH-domain proteins across the perinuclear space, SUN2 couples the nucleus to the actin cytoskeleton to regulate nuclear positioning, mechanotransduction, and cytoskeletal force transmission. SUN2 contributes to nuclear envelope integrity, chromatin organization, and DNA damage responses that depend on proper nucleo-cytoskeletal connectivity. Dysregulation of LINC complex components, including SUN2, has been linked to phenotypes relevant to laminopathies, cardiomyopathy, muscular disorders, and cancer-associated changes in nuclear architecture.
SUN2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SUN2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SUN2 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 SUN2 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 SUN2 protein expression.
This CRISPR knockout system enables efficient generation of SUN2-deficient cell models for investigation of SUN2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting SUN2 exon(s) critical for SUN2 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 SUN2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SUN2 CRISPR/Cas9 KO Plasmid (h) and SUN2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SUN2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SUN2 HDR Plasmid (h) and SUN2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SUN2 homology arms to support homology-directed repair at defined SUN2 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.