Date published: 2026-7-10

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SREBP-1 Double Nickase Plasmid (m): sc-423152-NIC

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • SREBP-1 Double Nickase Plasmid (m) 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
  • SREBP-1 Double Nickase Plasmid (m) and SREBP-1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Srebf1. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: SREBP-1 Antibody (A-4): sc-365513
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    SREBP-1 Double Nickase Plasmid (m)

    sc-423152-NIC
    20 µg
    $410.00

    Mouse Srebf1 encodes sterol regulatory element-binding protein 1 (SREBP-1), a membrane-tethered transcription factor that is proteolytically activated to drive lipogenic gene programs. SREBP-1 coordinates fatty acid and triglyceride synthesis by regulating enzymes such as ACACA, FASN, and SCD1, integrating nutrient, insulin, and mTOR signaling with endoplasmic reticulum lipid sensing. Through control of membrane biogenesis and energy storage, SREBP-1 influences adipogenesis, hepatic lipid accumulation, and macrophage lipid handling. Dysregulated Srebf1/SREBP-1 activity is frequently studied in models of metabolic syndrome, insulin resistance, nonalcoholic fatty liver disease, and lipid-dependent aspects of oncogenic growth.

    SREBP-1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Srebf1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Srebf1. 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 Srebf1 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 Srebf1-disrupted clones.

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