Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
PHF6 CRISPR/Cas9 KO Plasmid (m): sc-427858
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PHF6 CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 PHF6 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: PHF6 Antibody (H-4): sc-365237
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PHF6 CRISPR/Cas9 KO Plasmid (m) | sc-427858 | 20 µg | $397.00 |
Overview
Mouse Phf6 encodes PHF6, a nuclear PHD-like zinc finger protein that functions as a chromatin-associated regulator of transcription and RNA biogenesis. PHF6 participates in epigenetic control of gene expression through interactions with chromatin remodeling and histone-modifying complexes, influencing lineage-specific transcriptional programs, cell-cycle progression, and differentiation. Disruption of PHF6-dependent regulatory networks has been linked to altered hematopoietic and neurodevelopmental processes, making Phf6 a useful node for studying transcriptional dysregulation. In mouse models, Phf6 perturbation is commonly investigated in the context of genome stability, chromatin organization, and disease-relevant gene expression signatures.
PHF6 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Phf6 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Phf6 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 Phf6 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 PHF6 protein expression.
This CRISPR knockout system enables efficient generation of Phf6-deficient cell models for investigation of PHF6 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Phf6 exon(s) critical for PHF6 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 Phf6 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by PHF6 CRISPR/Cas9 KO Plasmid (m) and PHF6 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Phf6 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by PHF6 HDR Plasmid (m) and PHF6 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Phf6 homology arms to support homology-directed repair at defined Phf6 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.