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.
CRTAP CRISPR/Cas9 KO Plasmid (h): sc-405828
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CRTAP 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 CRTAP 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: CRTAP Antibody (E-1): sc-393136
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CRTAP CRISPR/Cas9 KO Plasmid (h) | sc-405828 | 20 µg | $397.00 |
Overview
CRTAP (cartilage associated protein) encodes an endoplasmic reticulum–resident component of the prolyl 3-hydroxylation complex that also includes P3H1/LEPRE1 and cyclophilin B (PPIB). This complex coordinates post-translational modification, folding, and quality control of fibrillar collagens, supporting extracellular matrix assembly and connective tissue integrity. CRTAP function links collagen biosynthesis to ER protein homeostasis pathways, including chaperone-assisted folding and proteostasis surveillance. Loss of CRTAP activity is associated with recessive osteogenesis imperfecta and related skeletal dysplasias characterized by defective collagen maturation and matrix organization.
CRTAP CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CRTAP gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CRTAP 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 CRTAP 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 CRTAP protein expression.
This CRISPR knockout system enables efficient generation of CRTAP-deficient cell models for investigation of CRTAP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting CRTAP exon(s) critical for CRTAP 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 CRTAP genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CRTAP CRISPR/Cas9 KO Plasmid (h) and CRTAP CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CRTAP locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CRTAP HDR Plasmid (h) and CRTAP HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CRTAP homology arms to support homology-directed repair at defined CRTAP 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.