TIF1γ CRISPR/Cas9 KO Plasmid (h): sc-403230
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TIF1γ 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 TIF1γ 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: TIF1γ Antibody (XX-19): sc-101179
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TIF1γ CRISPR/Cas9 KO Plasmid (h) | sc-403230 | 20 µg | $397.00 |
Overview
TRIM33 encodes TIF1γ, a tripartite motif (TRIM) family transcriptional regulator and E3 ubiquitin ligase that integrates chromatin-dependent gene control with signal transduction. TIF1γ modulates TGF-β/SMAD signaling by regulating SMAD4 availability and influences lineage-specific transcriptional programs through interactions with corepressors and epigenetic machinery. It also contributes to genome stability and DNA damage responses, linking transcriptional control to cellular stress pathways. Dysregulated TRIM33 activity has been associated with altered differentiation and oncogenic signaling contexts, making it relevant for mechanistic studies in cancer biology and developmental regulation.
TIF1γ CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TRIM33 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TRIM33 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 TRIM33 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 TIF1γ protein expression.
This CRISPR knockout system enables efficient generation of TRIM33-deficient cell models for investigation of TIF1γ signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TRIM33 exon(s) critical for TIF1γ 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 TRIM33 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TIF1γ CRISPR/Cas9 KO Plasmid (h) and TIF1γ CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TRIM33 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TIF1γ HDR Plasmid (h) and TIF1γ HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TRIM33 homology arms to support homology-directed repair at defined TRIM33 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.