CYTIP CRISPR/Cas9 KO Plasmid (m): sc-432749
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CYTIP 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 CYTIP 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: CYTIP Antibody (H-6): sc-390857
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CYTIP CRISPR/Cas9 KO Plasmid (m) | sc-432749 | 20 µg | $397.00 |
Overview
Cytip (cytohesin 1 interacting protein) encodes CYTIP, an adaptor that regulates cytohesin/ARF GTPase signaling and helps coordinate integrin-dependent adhesion and cytoskeletal remodeling. In immune cells, CYTIP contributes to inside-out signaling that tunes LFA-1/ICAM interactions, influencing leukocyte motility, immune synapse stability, and cell–cell contact dynamics. Through these roles, Cytip is linked to pathways governing lymphocyte activation, migration, and tissue infiltration, making it relevant for mechanistic studies of immune regulation and inflammation-associated phenotypes. Mouse Cytip perturbation is therefore useful for dissecting how adhesion signaling interfaces with downstream polarization and trafficking programs in vivo and in cultured immune models.
CYTIP CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Cytip gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Cytip 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 Cytip 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 CYTIP protein expression.
This CRISPR knockout system enables efficient generation of Cytip-deficient cell models for investigation of CYTIP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Cytip exon(s) critical for CYTIP 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 Cytip genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CYTIP CRISPR/Cas9 KO Plasmid (m) and CYTIP CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Cytip locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CYTIP HDR Plasmid (m) and CYTIP HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Cytip homology arms to support homology-directed repair at defined Cytip 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.