TIN2 CRISPR/Cas9 KO Plasmid (h): sc-404636
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TIN2 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 TIN2 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: TIN2 Antibody (59B388): sc-52960
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TIN2 CRISPR/Cas9 KO Plasmid (h) | sc-404636 | 20 µg | $397.00 |
Overview
TINF2 encodes TIN2, a core component of the shelterin complex that safeguards telomere ends by organizing TRF1/TRF2 interactions and coordinating telomerase access with end-protection mechanisms. Through these scaffolding functions, TIN2 supports telomere length homeostasis, prevents inappropriate DNA damage signaling at chromosome termini, and helps regulate replication-associated stress at telomeric repeats. Disruption of TINF2 perturbs telomere capping and can activate ATM/ATR-dependent DNA damage responses, linking shelterin dysfunction to genome instability. Pathogenic variants in TINF2 are associated with telomere biology disorders characterized by accelerated telomere shortening and tissue-specific failure phenotypes, making it a key target for mechanistic studies of telomere maintenance.
TIN2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TINF2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TINF2 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 TINF2 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 TIN2 protein expression.
This CRISPR knockout system enables efficient generation of TINF2-deficient cell models for investigation of TIN2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TINF2 exon(s) critical for TIN2 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 TINF2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TIN2 CRISPR/Cas9 KO Plasmid (h) and TIN2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TINF2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TIN2 HDR Plasmid (h) and TIN2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TINF2 homology arms to support homology-directed repair at defined TINF2 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.