Date published: 2026-7-6

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C3aR Double Nickase Plasmid (h): sc-401448-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • C3aR Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
  • Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
  • One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
  • C3aR Double Nickase Plasmid (h) and C3aR Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting C3AR1. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: C3aR Antibody (D-12): sc-133172
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    C3aR Double Nickase Plasmid (h)

    sc-401448-NIC
    20 µg
    $410.00

    C3aR Double Nickase Plasmid (h2)

    sc-401448-NIC-2
    20 µg
    $410.00

    C3AR1 encodes the complement component 3a receptor (C3aR), a G protein–coupled receptor that binds the anaphylatoxin C3a to couple complement activation with cellular responses. C3aR signaling engages Gαi/Gαq pathways to modulate intracellular calcium flux, MAPK/ERK cascades, and chemotactic programs that shape leukocyte trafficking and inflammatory mediator release. In myeloid and tissue-resident immune cells, C3aR integrates innate immune cues with cytokine networks and can influence barrier function and neuroimmune communication. Dysregulated C3AR1 activity has been implicated in inflammatory and autoimmune phenotypes, infection-associated immunopathology, and tumor microenvironment remodeling, supporting its use in mechanistic studies of complement-driven disease biology.

    C3aR Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the C3AR1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within C3AR1. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt C3AR1 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.

    To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of C3AR1-disrupted clones.

    For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.