FN3KRP contain inhibitor compounds such as Alloxan and Streptozotocin can alter the cellular redox environment and DNA integrity, respectively, which can indirectly influence the function of FN3KRP, possibly by affecting the enzyme's expression or stability. Aminoguanidine and Pyridoxamine act by interfering with the formation of AGEs, thus potentially reducing the accumulation of substrates that FN3KRP might act upon. This reduction in substrate availability can translate to decreased FN3KRP activity.
On a broader scale, agents like Rosiglitazone and Metformin that modify glucose metabolism and energy regulation pathways can lead to changes in intracellular glycation levels. These changes, in turn, can have downstream effects on FN3KRP's role in repairing glycated proteins. Other molecules, including anti-inflammatory and antioxidant compounds such as Acetylsalicylic acid, Rutin, Quercetin, Ascorbic acid, Taurine, and EGCG, can influence systemic levels of glycation and oxidative stress. By modulating these states, they can alter the extent of protein glycation and thereby potentially affect the functional demand on FN3KRP.
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