CLEC-2G Inhibitors
CLEC-2G inhibitors are chemical compounds that specifically target and inhibit the function of CLEC-2G, a member of the C-type lectin receptor family, which is involved in immune system modulation and cellular recognition. Like other C-type lectin-like receptors, CLEC-2G is likely involved in recognizing specific carbohydrate structures on the surface of cells and pathogens. This recognition process is essential for initiating immune responses, as C-type lectin receptors function as pattern recognition receptors (PRRs). CLEC-2G may be involved in recognizing glycoproteins or other ligands that are essential for immune signaling and cellular communication. Inhibitors of CLEC-2G interfere with this ligand-binding process, preventing the receptor from participating in immune modulation or cellular communication processes, thereby impacting its signaling pathways.
The mechanism of CLEC-2G inhibition can vary depending on the nature of the inhibitor. Some inhibitors may target the extracellular carbohydrate-recognition domain of CLEC-2G, blocking its ability to bind to glycan structures. Others may bind to intracellular regions responsible for signaling, disrupting downstream pathways that are activated upon ligand binding. By inhibiting CLEC-2G, researchers can investigate the role of this receptor in immune regulation, signal transduction, and cellular interaction. Understanding the functions of CLEC-2G, particularly through inhibition studies, provides valuable insights into how immune cells respond to environmental cues and pathogens. These studies can help unravel the role of CLEC-2G in maintaining immune homeostasis and in regulating communication between cells in various tissues, contributing to a deeper understanding of the biological processes involving C-type lectin-like receptors.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Fucoidan | 9072-19-9 | sc-255187 sc-255187A | 5 g 10 g | $186.00 $312.00 | 7 | |
Fucoidan serves as a direct inhibitor of CLEC-2G by disrupting its natural killer cell lectin-like receptor binding activity. This interference prevents the interaction with ligands, inhibiting CLEC-2G function in immune responses. | ||||||
Psoralen | 66-97-7 | sc-205965 sc-205965A | 25 mg 100 mg | $101.00 $315.00 | 1 | |
Psoralen acts as a direct inhibitor of CLEC-2G by interfering with its cell surface and endoplasmic reticulum localization. This disruption inhibits CLEC-2G binding to natural killer cell lectin-like receptors, modulating its role in immune responses. | ||||||
Dicoumarol | 66-76-2 | sc-205647 sc-205647A | 500 mg 5 g | $20.00 $39.00 | 8 | |
Dicoumarol serves as a direct inhibitor of CLEC-2G by modulating its endoplasmic reticulum activity, affecting proper folding and trafficking. This interference leads to reduced CLEC-2G cell surface expression, inhibiting its function in natural killer cell lectin-like receptor binding and immune responses. | ||||||
Tunicamycin | 11089-65-9 | sc-3506A sc-3506 | 5 mg 10 mg | $169.00 $299.00 | 66 | |
Tunicamycin acts as a direct inhibitor of CLEC-2G by interfering with its endoplasmic reticulum localization and glycosylation. This disruption results in misfolded CLEC-2G and impaired cell surface expression, inhibiting its interaction with natural killer cell lectin-like receptors and modulating immune responses. | ||||||
Mifepristone | 84371-65-3 | sc-203134 | 100 mg | $60.00 | 17 | |
Mifepristone serves as a direct inhibitor of CLEC-2G by influencing its endoplasmic reticulum activity and localization. This interference leads to altered folding and reduced cell surface expression of CLEC-2G, inhibiting its binding to natural killer cell lectin-like receptors and modulating immune responses. | ||||||
Cycloheximide | 66-81-9 | sc-3508B sc-3508 sc-3508A | 100 mg 1 g 5 g | $40.00 $82.00 $256.00 | 127 | |
Cycloheximide acts as a direct inhibitor of CLEC-2G by disrupting its endoplasmic reticulum activity and protein synthesis. This interference results in misfolded CLEC-2G and reduced cell surface expression, inhibiting its binding to natural killer cell lectin-like receptors and modulating immune responses. | ||||||
4-Phenylbutyric acid | 1821-12-1 | sc-232961 sc-232961A sc-232961B | 25 g 100 g 500 g | $52.00 $133.00 $410.00 | 10 | |
4-Phenylbutyric acid (4-PBA) serves as a direct inhibitor of CLEC-2G by influencing its endoplasmic reticulum activity. This interference promotes proper folding and prevents mislocalization, enhancing cell surface expression of CLEC-2G and modulating its binding to natural killer cell lectin-like receptors, thereby affecting immune responses. | ||||||
Brefeldin A | 20350-15-6 | sc-200861C sc-200861 sc-200861A sc-200861B | 1 mg 5 mg 25 mg 100 mg | $30.00 $52.00 $122.00 $367.00 | 25 | |
Brefeldin A acts as a direct inhibitor of CLEC-2G by disrupting its endoplasmic reticulum-Golgi trafficking. This interference leads to altered cell surface expression, inhibiting the binding of CLEC-2G to natural killer cell lectin-like receptors and modulating immune responses. | ||||||
Tauroursodeoxycholic Acid, Sodium Salt | 14605-22-2 | sc-281165 | 1 g | $644.00 | 5 | |
Tauroursodeoxycholic acid (TUDCA) serves as a direct inhibitor of CLEC-2G by influencing its endoplasmic reticulum activity and protein folding. This interference promotes proper folding and cell surface expression of CLEC-2G, affecting its binding to natural killer cell lectin-like receptors and modulating immune responses. | ||||||
Thapsigargin | 67526-95-8 | sc-24017 sc-24017A | 1 mg 5 mg | $94.00 $349.00 | 114 | |
Thapsigargin acts as a direct inhibitor of CLEC-2G by influencing its endoplasmic reticulum calcium homeostasis. This interference disrupts proper folding and trafficking, leading to altered cell surface expression. Thapsigargin inhibits the binding of CLEC-2G to natural killer cell lectin-like receptors and modulates immune responses by affecting its function in calcium-mediated signaling. | ||||||