MAP-1S CRISPR/Cas9 KO Plasmid (h): sc-406495
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MAP-1S 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 MAP-1S 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: MAP-1S Antibody (4H2): sc-517081
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MAP-1S CRISPR/Cas9 KO Plasmid (h) | sc-406495 | 20 µg | $397.00 |
Overview
MAP1S encodes microtubule-associated protein 1S (MAP-1S), a cytoskeletal adaptor that links microtubules to autophagy machinery and influences intracellular trafficking, organelle dynamics, and cellular stress responses. MAP-1S has been implicated in regulation of autophagosome formation and cargo handling, connecting microtubule stability with proteostasis and mitochondrial quality control. Through these processes, MAP1S contributes to homeostatic responses to oxidative stress and metabolic perturbation, pathways frequently altered in cancer and neurodegeneration. Altered MAP1S expression or function has been associated with dysregulated autophagy and genome stability phenotypes relevant to tumor biology and other stress-linked pathologies.
MAP-1S CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the MAP1S gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the MAP1S 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 MAP1S 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 MAP-1S protein expression.
This CRISPR knockout system enables efficient generation of MAP1S-deficient cell models for investigation of MAP-1S signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting MAP1S exon(s) critical for MAP-1S 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 MAP1S genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by MAP-1S CRISPR/Cas9 KO Plasmid (h) and MAP-1S CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the MAP1S locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by MAP-1S HDR Plasmid (h) and MAP-1S HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by MAP1S homology arms to support homology-directed repair at defined MAP1S 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.