Histone cluster 1 H1D Double Nickase Plasmid (h): sc-408739-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Histone cluster 1 H1D 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
- Histone cluster 1 H1D Double Nickase Plasmid (h) and Histone cluster 1 H1D Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HIST1H1D. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Histone cluster 1 H1D Double Nickase Plasmid (h) | sc-408739-NIC | 20 µg | $410.00 |
HIST1H1D encodes histone cluster 1 H1D, a linker histone that binds nucleosomal DNA at entry/exit sites to promote higher-order chromatin compaction and regulate genome accessibility. By modulating nucleosome spacing and chromatin fiber organization, H1D influences transcriptional programs, DNA replication timing, and the efficiency of DNA damage signaling and repair. Altered histone H1 abundance or distribution is associated with epigenetic dysregulation, genomic instability, and aberrant differentiation states observed across diverse cancer and developmental biology models. As part of the histone cluster, HIST1H1D is also relevant for studying replication-coupled chromatin assembly and cell cycle–linked chromatin remodeling.
Histone cluster 1 H1D Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HIST1H1D locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HIST1H1D. 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 HIST1H1D 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 HIST1H1D-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.