B7-H3 activators represent a diverse array of compounds that exert their activating effects on the B7-H3 protein through intricate signaling pathways. These pathways play pivotal roles in the regulation of B7-H3 expression at both transcriptional and post-transcriptional levels. Honokiol, for instance, acts as a direct activator by influencing the PI3K/Akt signaling pathway. By activating PI3K, Honokiol enhances Akt phosphorylation, leading to increased B7-H3 expression. This direct activation occurs at the transcriptional level, where heightened Akt activity promotes the activation of transcription factors involved in B7-H3 gene expression, resulting in elevated mRNA levels and subsequent upregulation of B7-H3 protein expression.
Similarly, Ursolic Acid serves as an indirect activator through the modulation of the NF-κB signaling pathway. By inhibiting IκB kinase, Ursolic Acid prevents the phosphorylation and subsequent degradation of IκBα, leading to increased NF-κB translocation to the nucleus. This indirect activation occurs at the transcriptional level, where enhanced NF-κB activity promotes the activation of transcription factors involved in B7-H3 gene expression, resulting in elevated mRNA levels and subsequent upregulation of B7-H3 protein expression. The diverse mechanisms employed by B7-H3 activators underscore the complexity of B7-H3 regulation and provide valuable insights into further research targeting this protein. The collective understanding of these chemical activators contributes to a nuanced comprehension of the intricate regulatory network governing B7-H3 expression.
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Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
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NDGA (Nordihydroguaiaretic acid) | 500-38-9 | sc-200487 sc-200487A sc-200487B | 1 g 5 g 25 g | $107.00 $376.00 $2147.00 | 3 | |
Nordihydroguaiaretic Acid serves as a direct activator of B7-H3 by influencing the NRF2/ARE signaling pathway. Acting as an antioxidant, it enhances NRF2 activity by inhibiting Keap1, leading to the stabilization and nuclear translocation of NRF2. This increased NRF2 activity positively regulates B7-H3 transcription, promoting its expression. | ||||||
(−)-Epigallocatechin Gallate | 989-51-5 | sc-200802 sc-200802A sc-200802B sc-200802C sc-200802D sc-200802E | 10 mg 50 mg 100 mg 500 mg 1 g 10 g | $42.00 $72.00 $124.00 $238.00 $520.00 $1234.00 | 11 | |
Epigallocatechin Gallate acts as an indirect activator of B7-H3 through the modulation of the MAPK/ERK signaling pathway. By inhibiting MEK, a key kinase in the pathway, it enhances the phosphorylation cascade that promotes B7-H3 expression. | ||||||
AICAR | 2627-69-2 | sc-200659 sc-200659A sc-200659B | 50 mg 250 mg 1 g | $60.00 $270.00 $350.00 | 48 | |
AICAR serves as an indirect activator of B7-H3 by influencing the AMPK signaling pathway. Activating AMPK, it leads to the inhibition of mTORC1, a known negative regulator of B7-H3 expression. This indirect activation occurs at the translational level, where the decreased mTORC1 activity results in enhanced B7-H3 protein synthesis and stability, ultimately promoting its expression. | ||||||
Honokiol | 35354-74-6 | sc-202653 sc-202653A | 10 mg 25 mg | $118.00 $178.00 | 4 | |
Honokiol acts as a direct activator of B7-H3 through the PI3K/Akt signaling pathway. By activating PI3K, it enhances Akt phosphorylation, leading to increased B7-H3 expression. This direct activation occurs at the transcriptional level, where the heightened Akt activity promotes the activation of transcription factors involved in B7-H3 gene expression, resulting in elevated mRNA levels and subsequent upregulation of B7-H3 protein expression. | ||||||
Resveratrol | 501-36-0 | sc-200808 sc-200808A sc-200808B | 100 mg 500 mg 5 g | $60.00 $185.00 $365.00 | 64 | |
Resveratrol serves as an indirect activator of B7-H3 through the SIRT1/FOXO signaling pathway. By activating SIRT1, it deacetylates FOXO, leading to its enhanced transcriptional activity. This indirect activation occurs at the transcriptional level, where the increased FOXO activity promotes the activation of transcription factors involved in B7-H3 gene expression, resulting in elevated mRNA levels and subsequent upregulation of B7-H3 protein expression. | ||||||
Salidroside | 10338-51-9 | sc-472942 | 50 mg | $360.00 | 1 | |
Salidroside acts as a direct activator of B7-H3 through the HIF-1α signaling pathway. By stabilizing HIF-1α, it enhances the transcriptional activity of HIF-1, leading to increased B7-H3 expression. | ||||||
Fisetin | 528-48-3 | sc-276440 sc-276440A sc-276440B sc-276440C sc-276440D | 50 mg 100 mg 500 mg 1 g 100 g | $51.00 $77.00 $102.00 $153.00 $2856.00 | 7 | |
Fisetin serves as an indirect activator of B7-H3 through the modulation of the Wnt/β-catenin signaling pathway. By inhibiting GSK-3β, it stabilizes β-catenin, leading to increased B7-H3 expression. | ||||||
Metformin | 657-24-9 | sc-507370 | 10 mg | $77.00 | 2 | |
Metformin serves as an indirect activator of B7-H3 through the AMPK signaling pathway. Activating AMPK, it leads to the inhibition of mTORC1, a known negative regulator of B7-H3 expression. This indirect activation occurs at the translational level, where the decreased mTORC1 activity results in enhanced B7-H3 protein synthesis and stability, ultimately promoting its expression. | ||||||
Piceatannol | 10083-24-6 | sc-200610 sc-200610A sc-200610B | 1 mg 5 mg 25 mg | $50.00 $70.00 $195.00 | 11 | |
Piceatannol acts as a direct activator of B7-H3 through the JAK/STAT signaling pathway. By activating JAK, it enhances STAT phosphorylation, leading to increased B7-H3 expression. This direct activation occurs at the transcriptional level, where the heightened STAT activity promotes the activation of transcription factors involved in B7-H3 gene expression, resulting in elevated mRNA levels and subsequent upregulation of B7-H3 protein expression. | ||||||
Ursolic Acid | 77-52-1 | sc-200383 sc-200383A | 50 mg 250 mg | $55.00 $176.00 | 8 | |
Ursolic Acid serves as an indirect activator of B7-H3 through the modulation of the NF-κB signaling pathway. By inhibiting IκB kinase, it prevents the phosphorylation and subsequent degradation of IκBα, leading to increased NF-κB translocation to the nucleus. |