TUTase CRISPR/Cas9 KO Plasmid (h): sc-406803
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TUTase 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 TUTase 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 | |
TUTase CRISPR/Cas9 KO Plasmid (h) | sc-406803 | 20 µg | $397.00 |
Overview
Human TUT1 encodes terminal uridylyltransferase 1 (TUTase), a non-canonical RNA polymerase that catalyzes 3′ uridylation of diverse RNA substrates. By shaping RNA 3′ end structure, TUTase contributes to RNA maturation and turnover, influencing spliceosomal snRNA metabolism and broader post-transcriptional gene regulation. TUT1-dependent uridylation interfaces with RNA quality control pathways that govern the stability of small RNAs and select mRNA populations. Dysregulated RNA tailing and decay programs involving TUT1 have been linked to altered gene expression states observed in cancer and other disorders with perturbed RNA processing.
TUTase CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TUT1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TUT1 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 TUT1 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 TUTase protein expression.
This CRISPR knockout system enables efficient generation of TUT1-deficient cell models for investigation of TUTase signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TUT1 exon(s) critical for TUTase 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 TUT1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TUTase CRISPR/Cas9 KO Plasmid (h) and TUTase CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TUT1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TUTase HDR Plasmid (h) and TUTase HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TUT1 homology arms to support homology-directed repair at defined TUT1 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.