C1q-C CRISPR/Cas9 KO Plasmid (m): sc-419388
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- C1q-C 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 C1q-C 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 | |
C1q-C CRISPR/Cas9 KO Plasmid (m) | sc-419388 | 20 µg | $397.00 |
Overview
C1qc encodes the C chain of complement component C1q, a recognition molecule that initiates the classical complement pathway through association with C1r and C1s and binding to immune complexes, apoptotic cells, and altered self. In mouse, C1q contributes to innate immune surveillance by promoting opsonization, phagocytic clearance, and modulation of inflammatory signaling, with downstream effects on complement cascade activation and cytokine networks. C1q-C–dependent processes are frequently studied in macrophage and microglial biology, including synapse remodeling and tissue homeostasis, where complement-mediated tagging can influence cellular pruning and clearance mechanisms. Dysregulated C1q activity and complement activation are linked to inflammatory and neuroimmune phenotypes relevant to autoimmunity, infection responses, and neurodegeneration research models.
C1q-C CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the C1qc gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the C1qc 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 C1qc 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 C1q-C protein expression.
This CRISPR knockout system enables efficient generation of C1qc-deficient cell models for investigation of C1q-C signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting C1qc exon(s) critical for C1q-C 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 C1qc genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by C1q-C CRISPR/Cas9 KO Plasmid (m) and C1q-C CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the C1qc locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by C1q-C HDR Plasmid (m) and C1q-C HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by C1qc homology arms to support homology-directed repair at defined C1qc 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.