UTF1 CRISPR/Cas9 KO Plasmid (m): sc-423632
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- UTF1 CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 UTF1 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 | |
UTF1 CRISPR/Cas9 KO Plasmid (m) | sc-423632 | 20 µg | $397.00 |
Overview
Mouse Utf1 encodes UTF1, a chromatin-associated transcriptional regulator enriched in pluripotent embryonic stem cells and early embryonic lineages. UTF1 contributes to maintenance of the undifferentiated state by modulating transcriptional programs linked to self-renewal and lineage commitment, including interactions with epigenetic mechanisms that shape promoter accessibility and RNA output. Its expression is tightly coupled to pluripotency networks and is commonly used as a molecular indicator of stem cell identity and reprogramming efficiency. Dysregulated Utf1/UTF1 activity is therefore relevant to models of developmental defects and oncogenic dedifferentiation where pluripotency-like gene expression states can emerge.
UTF1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Utf1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Utf1 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 Utf1 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 UTF1 protein expression.
This CRISPR knockout system enables efficient generation of Utf1-deficient cell models for investigation of UTF1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Utf1 exon(s) critical for UTF1 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 Utf1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by UTF1 CRISPR/Cas9 KO Plasmid (m) and UTF1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Utf1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by UTF1 HDR Plasmid (m) and UTF1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Utf1 homology arms to support homology-directed repair at defined Utf1 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.