Date published: 2026-7-10

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ARID1B Double Nickase Plasmid (h): sc-402365-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • ARID1B 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
  • ARID1B Double Nickase Plasmid (h) and ARID1B Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ARID1B. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ARID1B Antibody (KMN1): sc-32762
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    ARID1B Double Nickase Plasmid (h)

    sc-402365-NIC
    20 µg
    $410.00

    ARID1B encodes a DNA-binding subunit of the SWI/SNF (BAF) ATP-dependent chromatin remodeling complex that regulates nucleosome positioning and enhancer–promoter accessibility to shape transcriptional programs. Through its roles in chromatin organization, ARID1B influences lineage specification, cell-cycle control, and differentiation-associated gene expression, interfacing with pathways that govern developmental and stress-responsive transcription. Perturbation of ARID1B function alters epigenetic regulation and transcriptional fidelity, making it a key factor in studies of genome regulation. Dysregulation of SWI/SNF components, including ARID1B, is frequently investigated in contexts of developmental disorders and cancer-associated chromatin remodeling defects.

    ARID1B Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ARID1B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ARID1B. 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 ARID1B 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 ARID1B-disrupted clones.

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