KRTAP14 CRISPR/Cas9 KO Plasmid (m): sc-423901
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KRTAP14 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 KRTAP14 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 | |
KRTAP14 CRISPR/Cas9 KO Plasmid (m) | sc-423901 | 20 µg | $397.00 |
Overview
Krtap14 encodes keratin-associated protein 14, a small cysteine-rich structural component of the hair shaft matrix in mouse that contributes to the mechanical strength and crosslinking of keratin intermediate filaments. KRTAP14 participates in terminal differentiation programs of hair follicle keratinocytes and is integrated into processes governing hair fiber assembly, cuticle/cortex organization, and disulfide bond–mediated stabilization. Altered expression or structural variation in keratin-associated proteins is linked to changes in hair texture and fragility phenotypes, making Krtap14 relevant for studying hair shaft integrity and follicular biology. Its expression is often considered alongside keratinization networks and epidermal differentiation complex–associated pathways that shape appendage formation.
KRTAP14 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Krtap14 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Krtap14 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 Krtap14 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 KRTAP14 protein expression.
This CRISPR knockout system enables efficient generation of Krtap14-deficient cell models for investigation of KRTAP14 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Krtap14 exon(s) critical for KRTAP14 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 Krtap14 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by KRTAP14 CRISPR/Cas9 KO Plasmid (m) and KRTAP14 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Krtap14 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by KRTAP14 HDR Plasmid (m) and KRTAP14 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Krtap14 homology arms to support homology-directed repair at defined Krtap14 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.