MCP-1 Double Nickase Plasmid (h): sc-401046-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MCP-1 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
- MCP-1 Double Nickase Plasmid (h) and MCP-1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CCL2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MCP-1 Antibody (5J): sc-32771
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MCP-1 Double Nickase Plasmid (h) | sc-401046-NIC | 20 µg | $410.00 | |||
MCP-1 Double Nickase Plasmid (h2) | sc-401046-NIC-2 | 20 µg | $410.00 |
Human CCL2 encodes monocyte chemoattractant protein-1 (MCP-1), a secreted CC chemokine that orchestrates recruitment of monocytes/macrophages and other CCR2-expressing leukocytes to sites of tissue stress. MCP-1 signaling regulates leukocyte chemotaxis, endothelial–leukocyte interactions, and macrophage polarization, integrating with NF-κB- and MAPK-linked inflammatory transcriptional programs. Dysregulated CCL2/MCP-1 expression is implicated in chronic inflammatory microenvironments, including atherosclerosis, metabolic inflammation, neuroinflammation, and tumor-associated myeloid cell infiltration. As a nodal chemokine in immune cell trafficking, CCL2 is frequently used to model how inflammatory cues shape tissue remodeling and disease-associated immune phenotypes.
MCP-1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CCL2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CCL2. 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 CCL2 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 CCL2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.