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A high concentration of glucose can result in non-enzymatic oxidation of proteins by reaction of glucose and lysine residues (glycation). Additionally we are shipping Fructosamine 3 Kinase Antibodies (40) and Fructosamine 3 Kinase Kits (7) and many more products for this protein.
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Human FN3K Protein expressed in Escherichia coli (E. coli) - ABIN1098503
Conner, Beisswenger, Szwergold: Some clues as to the regulation, expression, function, and distribution of fructosamine-3-kinase and fructosamine-3-kinase-related protein. in Annals of the New York Academy of Sciences 2005
Show all 2 references for ABIN1098503
We conclude that, despite its ability to reduce the glycation of intracellular islet proteins, FN3K is neither required for the maintenance of beta-cell survival and function under control conditions.
fructosamine 3-kinase and fructosamine 3-kinase-related protein (show FN3KRP Proteins) have roles in repairing damage caused by ribose 5-phosphate
These data indicate that FN3K serves as a protein repair enzyme and also in the metabolism of endogenously produced free fructose-epsilon-lysine.
FN3K could act in concert with other molecular mechanisms and may impact on gene expression and activity of other enzymes involved in deglycation process
Report association of rs1056534 and rs3848403 of fructosamine 3-kinase gene with sRAGE in patients with diabetes.
The marginal association of rs1056534 of FN3K is located in exon 6 with diabetic nephropathy progression.
two new mutations and additional variants within the FN3K gene in diabetic patients
These findings suggest that deglycating enzymes Glyoxalase I (show GLO1 Proteins) and fructosamine-3-kinase may be involved in the malignant transformation of colon mucosa.
G900C polymorphism associates with the level of HbA (show SCN2A Proteins) (1c) and the onset of type 2 diabetes mellitus, but not with either of the diabetic microvascular complications.
involved in the removal of fructosamine residues from hemoglobin in erythrocytes.
The aim of this work was to identify the fructosamine residues on hemoglobin (show HBB Proteins) that are removed as a result of the action of FN3K in intact erythrocytes.
These data suggest that FN3K and FN3KRP (show FN3KRP Proteins) act as protein repair enzymes and are expressed constitutively in human cells independently of some of the variables altered in the diabetic state.
No significant correlation between FN3K activity and the levels of HbA1c, total glycated haemoglobin (GHb) and haemoglobin fructoselysine residues, either in the normoglycaemic or diabetic group.
A high concentration of glucose can result in non-enzymatic oxidation of proteins by reaction of glucose and lysine residues (glycation). Proteins modified in this way, fructosamines, are less active or functional. This gene encodes an enzyme which catalyzes the phosphorylation of fructosamines which may result in deglycation.
, fructosamine 3-kinase