TNFα-IP 1 Activators
TNFα-IP1 activators engage in a variety of molecular interactions that culminate in the functional enhancement of TNFα-IP1. Compounds such as Phorbol 12-myristate 13-acetate (PMA) and Prostratin exert their effects through the activation of Protein Kinase C (PKC), which is a pivotal kinase in the signaling pathways that lead to the functional activation of NF-κB. The activation of NF-κB is a crucial step in the functional enhancement of TNFα-IP1, as this transcription factor directly influences the activity of TNFα-IP1. Furthermore, the action of Tumor necrosis factor-alpha (TNFα) itself potentiates the functional activation of TNFα-IP1 by initiating a cascade via its receptors that culminates in NF-κB activation.
In contrast to activators that work through PKC, compounds like Anisomycin and Cycloheximide operate through the JNK signaling pathway. Anisomycin activates JNK, leading to the activation of the AP-1 transcription factor, which can enhance the functional activity of TNFα-IP1. Cycloheximide, by inhibiting protein synthesis, can cause stress within the cell that leads to the activation of stress response pathways, including the JNK signaling pathway. JNK activation can result in the enhancement of transcription factors that promote the functional activity of TNFα-IP1.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
PMA | 16561-29-8 | sc-3576 sc-3576A sc-3576B sc-3576C sc-3576D | 1 mg 5 mg 10 mg 25 mg 100 mg | $40.00 $129.00 $210.00 $490.00 $929.00 | 119 | |
Activates Protein Kinase C (PKC) which then enhances the phosphorylation of proteins involved in the NF-κB pathway, leading to the functional activation of NF-κB. TNFα-IP1, being a downstream effector in this pathway, has its function enhanced as a consequence of this activation. | ||||||
Prostratin | 60857-08-1 | sc-203422 sc-203422A | 1 mg 5 mg | $138.00 $530.00 | 24 | |
Activates PKC, similarly to PMA, which results in the activation of NF-κB and subsequent functional activation of TNFα-IP1 as part of the NF-κB signaling response. | ||||||
Anisomycin | 22862-76-6 | sc-3524 sc-3524A | 5 mg 50 mg | $97.00 $254.00 | 36 | |
Acts as a JNK activator, which can lead to the activation of transcription factors such as AP-1. AP-1 activation can enhance the functional activity of TNFα-IP1 as it may be a downstream target for AP-1 mediated transcriptional activation. | ||||||
Thalidomide | 50-35-1 | sc-201445 sc-201445A | 100 mg 500 mg | $109.00 $350.00 | 8 | |
Modulates the TNFα signaling pathway, which can lead to subsequent activation of the NF-κB pathway and the functional enhancement of TNFα-IP1 associated with this signaling. | ||||||
Sulfasalazine | 599-79-1 | sc-204312 sc-204312A sc-204312B sc-204312C | 1 g 2.5 g 5 g 10 g | $60.00 $75.00 $125.00 $205.00 | 8 | |
Inhibits NF-κB activation, which can paradoxically lead to the functional enhancement of TNFα-IP1 through the initiation of compensatory mechanisms to overcome the inhibition of the NF-κB signaling pathway. | ||||||
Cycloheximide | 66-81-9 | sc-3508B sc-3508 sc-3508A | 100 mg 1 g 5 g | $40.00 $82.00 $256.00 | 127 | |
By inhibiting protein synthesis, it leads to the accumulation of JNK pathway components, indirectly promoting the functional activation of TNFα-IP1 via JNK-mediated signaling pathways. | ||||||
Sodium Salicylate | 54-21-7 | sc-3520 sc-3520A sc-3520B sc-3520C | 1 g 25 g 500 g 1 kg | $10.00 $25.00 $80.00 $136.00 | 8 | |
Inhibits NF-κB activation, which can lead to functional activation of TNFα-IP1 through the induction of compensatory signaling mechanisms that aim to maintain NF-κB pathway function. | ||||||
Betulinic Acid | 472-15-1 | sc-200132 sc-200132A | 25 mg 100 mg | $115.00 $337.00 | 3 | |
Activates NF-κB, leading to the functional enhancement of TNFα-IP1 as this protein is functionally active within the NF-κB signaling pathway. | ||||||
Celastrol, Celastrus scandens | 34157-83-0 | sc-202534 | 10 mg | $155.00 | 6 | |
Inhibits NF-κB activation and could thereby enhance the functional activity of TNFα-IP1 through the induction of alternative signaling pathways aiming to restore NF-κB function. | ||||||