Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
cyclin T1 CRISPR/Cas9 KO Plasmid (h): sc-400623
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- cyclin T1 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 cyclin T1 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: cyclin T1 Antibody (E-3): sc-271348
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
cyclin T1 CRISPR/Cas9 KO Plasmid (h) | sc-400623 | 20 µg | $397.00 |
Overview
CCNT1 encodes cyclin T1, a regulatory subunit of the P-TEFb complex that partners with CDK9 to phosphorylate RNA polymerase II and promote transcriptional elongation. Through control of promoter-proximal pausing, cyclin T1 influences expression programs linked to cell-cycle progression, stress responses, and differentiation. CCNT1 activity intersects with transcription-coupled RNA processing and chromatin-associated regulation, shaping global gene expression dynamics. Dysregulation of P-TEFb signaling and cyclin T1–dependent transcriptional control has been implicated in contexts including oncogenic transcriptional programs and host–pathogen interactions relevant to viral transcription.
cyclin T1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CCNT1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CCNT1 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 CCNT1 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 cyclin T1 protein expression.
This CRISPR knockout system enables efficient generation of CCNT1-deficient cell models for investigation of cyclin T1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting CCNT1 exon(s) critical for cyclin T1 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 CCNT1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by cyclin T1 CRISPR/Cas9 KO Plasmid (h) and cyclin T1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CCNT1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by cyclin T1 HDR Plasmid (h) and cyclin T1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CCNT1 homology arms to support homology-directed repair at defined CCNT1 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.