hnRNP D0 Double Nickase Plasmid (h): sc-401911-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- hnRNP D0 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
- hnRNP D0 Double Nickase Plasmid (h) and hnRNP D0 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HNRNPD. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
hnRNP D0 Double Nickase Plasmid (h) | sc-401911-NIC | 20 µg | $410.00 | |||
hnRNP D0 Double Nickase Plasmid (h2) | sc-401911-NIC-2 | 20 µg | $410.00 |
Human HNRNPD encodes hnRNP D0 (AUF1), an RNA-binding protein that recognizes AU-rich elements in 3′ UTRs to regulate mRNA stability, turnover, and translation. hnRNP D0 participates in post-transcriptional control networks governing inflammatory signaling, cell-cycle progression, stress responses, and differentiation by modulating the decay of cytokine and immediate-early transcripts. It also contributes to RNA processing and ribonucleoprotein complex dynamics, linking RNA metabolism to pathways such as NF-κB–dependent gene expression and stress granule biology. Dysregulated hnRNP D0 activity has been associated with aberrant inflammatory programs and altered expression of growth- and survival-related genes in cancer and neurodegeneration-relevant contexts, supporting its study as a regulator of transcriptome homeostasis.
hnRNP D0 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HNRNPD locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HNRNPD. 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 HNRNPD 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 HNRNPD-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.