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| TrxR is an enzyme that reduces Trx, allowing it to perform its reducing functions. It has been shown to have a role in cancer cell metabolism and survival. TrxR is overexpressed in various types of cancer, including breast, lung, colon, and prostate cancer. - Part of the thioredoxin system, which regulates reactive oxygen species (ROS). - TrxR is a major antioxidant systems that maintains the intracellular redox homeostasis. - Inhibition causes an increase in ROS. - TrxR is often upregulated in cancer cells to help manage increased oxidative stress, it is seen as a potential therapeutic target. Inhibiting TrxR may result in increased ROS in cancer cells, pushing them toward apoptosis. - TrxR is a selenoprotein—meaning it incorporates the trace element selenium in the form of the amino acid selenocysteine. TrxR inhibitors: -Piperlongumine -Withania somnifera (Ashwagandha) -Parthenolide -EGCG -Curcumin -Myricetin -Gambogic Acid |
| 2962- | PL, | Synthesis of Piperlongumine Analogues and Discovery of Nuclear Factor Erythroid 2‑Related Factor 2 (Nrf2) Activators as Potential Neuroprotective Agents |
| - | in-vitro, | Nor, | PC12 |
| 4485- | Se, | Selenium stimulates the antitumour immunity: Insights to future research |
| - | Review, | NA, | NA |
| 4717- | Se, | A systematic review of Selenium as a complementary treatment in cancer patients |
| - | Review, | Var, | NA |
| 3663- | SFN, | Efficacy of Sulforaphane in Neurodegenerative Diseases |
| - | Review, | AD, | NA | - | Review, | Park, | NA |
| 3658- | SFN, | Pre-Clinical Neuroprotective Evidences and Plausible Mechanisms of Sulforaphane in Alzheimer’s Disease |
| - | Review, | AD, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:825 State#:% Dir#:2
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