Date published: 2026-7-11

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ChREBP Double Nickase Plasmid (h): sc-401803-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • ChREBP 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
  • ChREBP Double Nickase Plasmid (h) and ChREBP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MLXIPL. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ChREBP Antibody (G-12): sc-515922
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    ChREBP Double Nickase Plasmid (h)

    sc-401803-NIC
    20 µg
    $410.00

    ChREBP Double Nickase Plasmid (h2)

    sc-401803-NIC-2
    20 µg
    $410.00

    MLXIPL encodes carbohydrate response element–binding protein (ChREBP), a glucose-responsive transcription factor that couples carbohydrate availability to lipogenic and glycolytic gene expression. Upon metabolic signaling, ChREBP cooperates with cofactors such as MLX to regulate promoters containing carbohydrate response elements, integrating nutrient sensing with transcriptional control of hepatic and adipose metabolism. This regulatory axis contributes to pathways governing de novo lipogenesis, triglyceride synthesis, and glucose homeostasis, linking ChREBP activity to metabolic remodeling under conditions of nutrient excess. Dysregulated MLXIPL/ChREBP signaling has been associated with insulin resistance, fatty liver phenotypes, and broader cardiometabolic disease mechanisms, making it a relevant node for studying metabolic gene networks.

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

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