



Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD36 Double Nickase Plasmid (h) | sc-400233-NIC | 20 µg | $410.00 | |||
CD36 Double Nickase Plasmid (h2) | sc-400233-NIC-2 | 20 µg | $410.00 |
CD36 encodes a multifunctional class B scavenger receptor expressed on macrophages, adipocytes, endothelial cells, and platelets that binds long-chain fatty acids, oxidized phospholipids, and thrombospondin-1. Through regulation of lipid uptake and intracellular trafficking, CD36 interfaces with metabolic signaling, inflammatory programs, and innate immune pattern recognition, including pathways linked to foam cell formation and oxidative stress responses. CD36-dependent ligand sensing shapes macrophage polarization and vascular homeostasis, making it a key node in studies of atherosclerosis biology, insulin resistance, and inflammation-associated tissue remodeling. Altered CD36 expression or activity has also been connected to platelet activation and microvascular dysfunction, supporting its broad relevance across cardiometabolic and immunometabolic research.
CD36 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CD36 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CD36. 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 CD36 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 CD36-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.