TMED4 CRISPR/Cas9 KO Plasmid (h): sc-406737
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TMED4 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 TMED4 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 | |
TMED4 CRISPR/Cas9 KO Plasmid (h) | sc-406737 | 20 µg | $397.00 |
Overview
TMED4 (also known as p25) is a member of the p24 family of type I transmembrane proteins that function as cargo receptors in the early secretory pathway. It participates in COPI- and COPII-dependent vesicular trafficking between the endoplasmic reticulum and Golgi apparatus, supporting protein sorting, quality control, and maintenance of secretory pathway homeostasis. By influencing ER–Golgi transport dynamics, TMED4 can affect processing and surface delivery of signaling receptors and secreted factors, linking it to broader regulation of cellular communication. Dysregulation of secretory trafficking components, including TMED4-associated pathways, has been investigated in contexts such as oncogenic growth programs and stress-adaptation phenotypes relevant to human disease biology.
TMED4 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TMED4 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TMED4 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 TMED4 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 TMED4 protein expression.
This CRISPR knockout system enables efficient generation of TMED4-deficient cell models for investigation of TMED4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TMED4 exon(s) critical for TMED4 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 TMED4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TMED4 CRISPR/Cas9 KO Plasmid (h) and TMED4 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TMED4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TMED4 HDR Plasmid (h) and TMED4 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TMED4 homology arms to support homology-directed repair at defined TMED4 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.