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.
TANC CRISPR/Cas9 KO Plasmid (h): sc-406741
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TANC 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 TANC 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: TANC Antibody (H-8): sc-514679
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TANC CRISPR/Cas9 KO Plasmid (h) | sc-406741 | 20 µg | $397.00 |
Overview
TANC1 encodes TANC, a multidomain scaffold protein enriched at excitatory synapses where it supports postsynaptic density organization and the assembly of signaling complexes. Through its interactions with synaptic receptors and cytoskeletal regulators, TANC contributes to dendritic spine morphogenesis, synaptic stability, and activity-dependent remodeling. These functions place TANC1 within neuronal development and synaptic plasticity pathways that influence circuit formation and homeostatic signaling. Altered regulation of synaptic scaffolding and connectivity has been linked to neurodevelopmental and neuropsychiatric disease mechanisms, making TANC1 a useful locus for studying genotype-to-phenotype relationships in neuronal models.
TANC CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TANC1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TANC1 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 TANC1 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 TANC protein expression.
This CRISPR knockout system enables efficient generation of TANC1-deficient cell models for investigation of TANC signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TANC1 exon(s) critical for TANC 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 TANC1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TANC CRISPR/Cas9 KO Plasmid (h) and TANC CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TANC1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TANC HDR Plasmid (h) and TANC HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TANC1 homology arms to support homology-directed repair at defined TANC1 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.