Fructosamine 3 Kinase Human Recombinant
Fructosamine 3 Kinase Related Protein Human Recombinant
Fructosamine 3 Kinase (FN3K) is an enzyme encoded by the FN3K gene in humans. It belongs to a conserved family of deglycation enzymes that phosphorylate fructosamines, which are formed by the nonenzymatic reaction of glucose with primary amines followed by Amadori rearrangement . This enzyme plays a crucial role in the metabolism of modified amines and the deglycation of glycated proteins .
Key Biological Properties: FN3K catalyzes the phosphorylation of fructosamines, leading to the formation of fructose 3-phosphate (F3P), which subsequently decomposes to form 3-deoxyglucosone (3DG) . This process is significant in preventing the accumulation of advanced glycation end products (AGEs), which are implicated in various diabetic complications .
Expression Patterns and Tissue Distribution: FN3K is expressed in various tissues, including the sural nerve, adrenal cortex, cerebellum, heart, prefrontal cortex, and auricle . It is also found in the interventricular septum, spinal cord, fetal liver, hematopoietic progenitor cells, and lens epithelium .
Primary Biological Functions: The primary function of FN3K is to catalyze the phosphorylation of fructosamines, which initiates the metabolism of these modified amines and results in the deglycation of glycated proteins . This process is essential in reducing the formation of AGEs and mitigating their harmful effects .
Role in Immune Responses and Pathogen Recognition: While FN3K’s primary role is in deglycation, its activity indirectly supports immune responses by maintaining protein function and preventing the accumulation of dysfunctional glycated proteins .
Mechanisms with Other Molecules and Cells: FN3K interacts with fructosamines by transferring the gamma-phosphate from adenosine triphosphate (ATP) to the 3′ hydroxyl group in the ketosamine substrate . This phosphorylation destabilizes the fructosamine adduct, leading to its spontaneous decomposition .
Binding Partners and Downstream Signaling Cascades: FN3K’s activity results in the production of F3P and 3DG, which are involved in various metabolic pathways . The enzyme’s interaction with ATP and its substrates is crucial for its deglycation function .
Regulatory Mechanisms Controlling Expression and Activity: FN3K activity is regulated by redox-sensitive cysteine residues in its kinase domain . These residues act as redox switches, modulating the enzyme’s activity in response to cellular redox conditions .
Transcriptional Regulation and Post-Translational Modifications: FN3K expression is influenced by various transcriptional factors and post-translational modifications that respond to changes in cellular redox states and metabolic demands .
Biomedical Research: FN3K is a target for research in diabetic complications, as its activity can reduce the formation of harmful AGEs . Understanding FN3K’s role in deglycation can lead to new therapeutic strategies for managing diabetes and its complications .
Diagnostic Tools and Therapeutic Strategies: FN3K inhibitors are being explored as potential therapeutic agents to reduce AGE formation and mitigate diabetic complications . Additionally, FN3K activity assays can serve as diagnostic tools for assessing glycation levels in diabetic patients .
Role Throughout the Life Cycle: FN3K plays a vital role in maintaining protein function and preventing AGE accumulation throughout the life cycle . Its activity is particularly important in aging and disease, where increased glycation can lead to various complications .
From Development to Aging and Disease: FN3K’s deglycation activity is crucial during development to ensure proper protein function and prevent the accumulation of glycated proteins . In aging and disease, FN3K helps mitigate the effects of increased glycation and supports cellular health .