TMEM53 CRISPR/Cas9 KO Plasmid (h): sc-413194
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TMEM53 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 TMEM53 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 | |
TMEM53 CRISPR/Cas9 KO Plasmid (h) | sc-413194 | 20 µg | $397.00 |
Overview
TMEM53 (transmembrane protein 53) encodes a small membrane-associated protein implicated in the regulation of nuclear envelope–linked signaling and cellular homeostasis. Emerging studies connect TMEM53 to pathways governing BMP/SMAD signaling and transcriptional control, suggesting roles in coordinating intracellular signal transduction with nuclear responses. Altered TMEM53 function has been associated with perturbations in skeletal and craniofacial development and related bone phenotypes, making it of interest for mechanistic studies in osteogenic differentiation and developmental biology. Its expression and putative membrane localization also support investigation into organelle crosstalk, protein trafficking, and context-dependent pathway modulation.
TMEM53 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TMEM53 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TMEM53 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 TMEM53 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 TMEM53 protein expression.
This CRISPR knockout system enables efficient generation of TMEM53-deficient cell models for investigation of TMEM53 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TMEM53 exon(s) critical for TMEM53 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 TMEM53 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TMEM53 CRISPR/Cas9 KO Plasmid (h) and TMEM53 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TMEM53 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TMEM53 HDR Plasmid (h) and TMEM53 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TMEM53 homology arms to support homology-directed repair at defined TMEM53 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.