TRAP230 CRISPR/Cas9 KO Plasmid (h2): sc-404820-KO-2
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRAP230 CRISPR/Cas9 Knockout (KO) Plasmid (h2) 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 TRAP230 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: TRAP230 Antibody (E-2): sc-515695
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRAP230 CRISPR/Cas9 KO Plasmid (h2) | sc-404820-KO-2 | 20 µg | $397.00 |
Overview
MED12 encodes TRAP230, a core component of the Mediator complex that couples sequence-specific transcription factors to RNA polymerase II and coordinates transcription initiation and elongation. Through Mediator-dependent regulation, TRAP230 influences developmental gene programs and signaling pathways including Wnt/β-catenin, TGF-β, and nuclear receptor–mediated transcription. Disruption of MED12 perturbs chromatin-associated transcriptional control, altering cell identity and proliferation-associated transcriptional networks. Genetic alterations in MED12 have been linked to multiple disease-relevant contexts, making it a useful target for studying transcriptional dysregulation mechanisms in human cells.
TRAP230 CRISPR/Cas9 KO Plasmid (h2) is a pool of plasmids designed for targeted disruption of the MED12 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the MED12 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 MED12 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 TRAP230 protein expression.
This CRISPR knockout system enables efficient generation of MED12-deficient cell models for investigation of TRAP230 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting MED12 exon(s) critical for TRAP230 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 MED12 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TRAP230 CRISPR/Cas9 KO Plasmid (h) and TRAP230 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the MED12 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TRAP230 HDR Plasmid (h) and TRAP230 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by MED12 homology arms to support homology-directed repair at defined MED12 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.