PLEKHG4B CRISPR/Cas9 KO Plasmid (h): sc-407381
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PLEKHG4B 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 PLEKHG4B 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 | |
PLEKHG4B CRISPR/Cas9 KO Plasmid (h) | sc-407381 | 20 µg | $397.00 |
Overview
PLEKHG4B encodes a Rho guanine nucleotide exchange factor–like protein containing pleckstrin homology and RhoGEF-related domains that are implicated in coupling phosphoinositide signaling to small GTPase regulation. Through modulation of Rho family GTPase activity, PLEKHG4B is linked to control of actin cytoskeletal dynamics, membrane trafficking, and cell morphology programs that influence adhesion and motility. Expression and network associations place PLEKHG4B within broader signaling contexts that intersect with neuronal and immune-relevant pathways where cytoskeletal remodeling is rate-limiting. Dysregulation of Rho GTPase signaling and cytoskeleton-dependent processes is recurrently associated with neurodevelopmental and neurodegenerative phenotypes as well as invasive behavior in cancer models, motivating functional interrogation of PLEKHG4B in mechanistic studies.
PLEKHG4B CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the PLEKHG4B gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the PLEKHG4B 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 PLEKHG4B 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 PLEKHG4B protein expression.
This CRISPR knockout system enables efficient generation of PLEKHG4B-deficient cell models for investigation of PLEKHG4B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting PLEKHG4B exon(s) critical for PLEKHG4B 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 PLEKHG4B genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by PLEKHG4B CRISPR/Cas9 KO Plasmid (h) and PLEKHG4B CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the PLEKHG4B locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by PLEKHG4B HDR Plasmid (h) and PLEKHG4B HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by PLEKHG4B homology arms to support homology-directed repair at defined PLEKHG4B 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.