TIG2 CRISPR/Cas9 KO Plasmid (h): sc-403443
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TIG2 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 TIG2 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: TIG2 Antibody (E-7): sc-373797
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TIG2 CRISPR/Cas9 KO Plasmid (h) | sc-403443 | 20 µg | $397.00 |
Overview
RARRES2 encodes tazarotene-induced gene 2 (TIG2), also known as chemerin, a secreted adipokine and chemoattractant that signals primarily through CMKLR1 and related receptors to coordinate leukocyte trafficking and tissue immune surveillance. TIG2 influences inflammatory cascades, adipocyte differentiation, and metabolic homeostasis, linking adipose biology to innate immune signaling and endothelial function. Dysregulated RARRES2/TIG2 expression has been associated with chronic inflammation and metabolic disorders and has been investigated in contexts including obesity, insulin resistance, and cardiovascular pathophysiology. In cancer biology, chemerin signaling is studied for its roles in shaping the tumor microenvironment and modulating immune cell recruitment.
TIG2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the RARRES2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the RARRES2 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 RARRES2 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 TIG2 protein expression.
This CRISPR knockout system enables efficient generation of RARRES2-deficient cell models for investigation of TIG2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting RARRES2 exon(s) critical for TIG2 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 RARRES2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TIG2 CRISPR/Cas9 KO Plasmid (h) and TIG2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the RARRES2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TIG2 HDR Plasmid (h) and TIG2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by RARRES2 homology arms to support homology-directed repair at defined RARRES2 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.