TMEM63B CRISPR/Cas9 KO Plasmid (h): sc-412530
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TMEM63B 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 TMEM63B 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 | |
TMEM63B CRISPR/Cas9 KO Plasmid (h) | sc-412530 | 20 µg | $397.00 |
Overview
TMEM63B encodes transmembrane protein 63B, a multi-pass membrane protein implicated in mechanosensitive and osmoregulatory signaling through ion-permeable channel activity. It contributes to cellular homeostasis by linking membrane tension and volume changes to downstream Ca²⁺-dependent processes, influencing neuronal excitability, cytoskeletal dynamics, and stress-response pathways. TMEM63B expression is enriched in the nervous system and has been associated with neurodevelopmental and neuropsychiatric phenotypes, making it relevant for studies of synaptic function and sensory transduction. Altered TMEM63B activity has also been explored in the context of cell migration and membrane trafficking, supporting broader roles in tissue-specific signaling networks.
TMEM63B CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TMEM63B gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TMEM63B 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 TMEM63B 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 TMEM63B protein expression.
This CRISPR knockout system enables efficient generation of TMEM63B-deficient cell models for investigation of TMEM63B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TMEM63B exon(s) critical for TMEM63B 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 TMEM63B genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TMEM63B CRISPR/Cas9 KO Plasmid (h) and TMEM63B CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TMEM63B locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TMEM63B HDR Plasmid (h) and TMEM63B HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TMEM63B homology arms to support homology-directed repair at defined TMEM63B 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.