RT1-Bα inhibitors are a class of chemical compounds that target the RT1-Bα protein, a major histocompatibility complex (MHC) class II molecule found in rats. RT1-Bα is an essential component of the MHC class II system, which plays a critical role in presenting extracellular antigens to CD4+ T cells. The protein is involved in antigen processing, where it binds peptides derived from external pathogens and displays them on the surface of antigen-presenting cells, such as dendritic cells and macrophages, for recognition by T cells. By inhibiting RT1-Bα, these compounds interfere with the ability of antigen-presenting cells to display antigens, which can significantly alter immune signaling and cell-mediated immune responses.
The mechanism of action for RT1-Bα inhibitors involves preventing the binding of antigenic peptides to the MHC class II molecule or blocking the formation of the peptide-MHC complex. This can result from direct binding to the RT1-Bα protein, altering its conformation or stability, or interfering with the machinery responsible for loading peptides onto RT1-Bα. By inhibiting this process, RT1-Bα inhibitors disrupt the communication between antigen-presenting cells and T cells, effectively halting the initiation of immune responses that rely on MHC class II-mediated antigen presentation. These inhibitors are useful in studying the intricacies of immune system regulation and provide insights into how MHC class II molecules, particularly RT1-Bα, contribute to immune recognition and the maintenance of immune homeostasis in rats. They offer valuable tools for exploring the molecular dynamics of antigen presentation and immune signaling.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Dexamethasone | 50-02-2 | sc-29059 sc-29059B sc-29059A | 100 mg 1 g 5 g | $76.00 $82.00 $367.00 | 36 | |
This glucocorticoid could downregulate RT1-Bα expression by repressing transcription factors specific to immune response genes. | ||||||
Tunicamycin | 11089-65-9 | sc-3506A sc-3506 | 5 mg 10 mg | $169.00 $299.00 | 66 | |
May disrupt proper folding and stability of RT1-Bα by blocking N-linked glycosylation, leading to its decreased expression. | ||||||
Ascomycin | 104987-12-4 | sc-207303B sc-207303 sc-207303A | 1 mg 5 mg 25 mg | $36.00 $173.00 $316.00 | ||
Could suppress calcineurin, resulting in reduced nuclear translocation of NFAT and subsequent downregulation of RT1-Bα transcription. | ||||||
Rapamycin | 53123-88-9 | sc-3504 sc-3504A sc-3504B | 1 mg 5 mg 25 mg | $62.00 $155.00 $320.00 | 233 | |
By inhibiting mTOR, rapamycin could decrease the synthesis of RT1-Bα through global reduction of protein translation. | ||||||
Cyclosporin A | 59865-13-3 | sc-3503 sc-3503-CW sc-3503A sc-3503B sc-3503C sc-3503D | 100 mg 100 mg 500 mg 10 g 25 g 100 g | $62.00 $90.00 $299.00 $475.00 $1015.00 $2099.00 | 69 | |
Could suppress T-cell activation pathways by inhibiting calcineurin, leading to decreased expression of RT1-Bα. | ||||||
Hydroxyurea | 127-07-1 | sc-29061 sc-29061A | 5 g 25 g | $76.00 $255.00 | 18 | |
Might decrease DNA synthesis by inhibiting ribonucleotide reductase, leading to reduced transcription of RT1-Bα. | ||||||
Methotrexate | 59-05-2 | sc-3507 sc-3507A | 100 mg 500 mg | $92.00 $209.00 | 33 | |
Could lead to folate depletion and subsequent reduction in DNA synthesis, which may result in decreased levels of RT1-Bα. | ||||||
Azathioprine | 446-86-6 | sc-210853D sc-210853 sc-210853A sc-210853B sc-210853C | 500 mg 1 g 2 g 5 g 10 g | $199.00 $173.00 $342.00 $495.00 $690.00 | 1 | |
As a purine synthesis inhibitor, it may lead to reduced nucleotide pools and consequent decrease of RT1-Bα expression. | ||||||
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 | |
By disrupting Golgi apparatus function, it may interfere with the processing and subsequent surface expression of RT1-Bα. | ||||||
Flavopiridol | 146426-40-6 | sc-202157 sc-202157A | 5 mg 25 mg | $78.00 $254.00 | 41 | |
Could inhibit cell cycle progression by targeting cyclin-dependent kinases, which may lead to reduced transcription of RT1-Bα. | ||||||