SCLIP CRISPR/Cas9 KO Plasmid (h): sc-406430
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SCLIP 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 SCLIP 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 | |
SCLIP CRISPR/Cas9 KO Plasmid (h) | sc-406430 | 20 µg | $397.00 |
Overview
STMN3 (SCLIP) is a neuron-enriched stathmin family protein that binds tubulin and modulates microtubule dynamics, supporting axonal growth, neurite branching, and synaptic organization. By regulating microtubule polymerization and stability, SCLIP contributes to cytoskeletal remodeling processes that influence intracellular transport and neuronal polarity. Altered STMN3 expression or function has been associated with disrupted neuronal connectivity and has been studied in the context of neurodevelopmental and neurodegenerative mechanisms where microtubule homeostasis is perturbed. As a cytoskeletal regulator, SCLIP is relevant for investigating pathways linking microtubule dynamics to neuronal differentiation, plasticity, and stress responses.
SCLIP CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the STMN3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the STMN3 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 STMN3 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 SCLIP protein expression.
This CRISPR knockout system enables efficient generation of STMN3-deficient cell models for investigation of SCLIP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting STMN3 exon(s) critical for SCLIP 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 STMN3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SCLIP CRISPR/Cas9 KO Plasmid (h) and SCLIP CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the STMN3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SCLIP HDR Plasmid (h) and SCLIP HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by STMN3 homology arms to support homology-directed repair at defined STMN3 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.