Date published: 2026-7-11

1-800-457-3801

SCBT Portrait Logo
Seach Input

serum reponse factor /SRF Double Nickase Plasmid (h): sc-400470-NIC

0.0(0)
Write a reviewAsk a question

Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • serum reponse factor /SRF 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
  • serum reponse factor /SRF Double Nickase Plasmid (h) and serum reponse factor /SRF Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SRF. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: serum reponse factor /SRF Antibody (A-11): sc-25290
    Gene Editing Promo Banner

    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    serum reponse factor /SRF Double Nickase Plasmid (h)

    sc-400470-NIC
    20 µg
    $410.00

    serum reponse factor /SRF Double Nickase Plasmid (h2)

    sc-400470-NIC-2
    20 µg
    $410.00

    Human SRF (serum response factor) is a MADS-box transcription factor that binds serum response elements to regulate immediate-early gene expression and actin cytoskeleton programs. It functions downstream of MAPK/ERK signaling and RhoA–actin dynamics through cofactors such as ELK1 and myocardin-related transcription factors, coordinating proliferation, migration, and differentiation. SRF-dependent transcription helps maintain cytoskeletal homeostasis and cell-state transitions, linking it to processes including myogenesis, neurodevelopment, and vascular remodeling. Dysregulated SRF activity has been associated with tumor cell invasiveness and altered stress-responsive transcriptional networks relevant to cancer biology and cardiovascular disease mechanisms.

    serum reponse factor /SRF Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SRF locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SRF. 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 SRF 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 SRF-disrupted clones.

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