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Fructosamine 3 kinase

FN3K, fructosamine-3-kinase
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. [provided by RefSeq, Feb 2012] (from NCBI)
Top mentioned proteins: FN3KRP, HAD, fibrillin-1, CAN, iMpact
Papers on FN3K
Possible role of fructosamine 3-kinase genotyping for the management of diabetic patients.
Mosca et al., In Clin Chem Lab Med, Aug 2015
The identification of fructosamine 3-kinase (FN3K), an enzyme involved in protein deglycation, a new form of protein repair, is of great interest.
Multiple nonglycemic genomic loci are newly associated with blood level of glycated hemoglobin in East Asians.
Tai et al., Singapore, Singapore. In Diabetes, 2014
Several of these variants (TMEM79, HBS1L/MYB, CYBA, MYO9B, ANK1, and FN3K) showed no association with either blood glucose or type 2 diabetes.
Protein damage, repair and proteolysis.
Gonos et al., Athens, Greece. In Mol Aspects Med, 2014
With regard to protein repair, only few repair mechanisms have been evidenced including the reduction of methionine sulfoxide residues by the methionine sulfoxide reductases, the conversion of isoaspartyl residues to L-aspartate by L-isoaspartate methyl transferase and deglycation by phosphorylation of protein-bound fructosamine by fructosamine-3-kinase.
A new HPLC-based assay for the measurement of fructosamine-3-kinase (FN3K) and FN3K-related protein activity in human erythrocytes.
Henle et al., In Clin Chem Lab Med, 2014
BACKGROUND: An impact on glycation, and possibly on diabetic complications, is attributed to fructosamine-3-kinase (FN3K) and its related protein (FN3K-RP) because they degrade Amadori compounds in vivo.
Genetic variability in enzymes of metabolic pathways conferring protection against non-enzymatic glycation versus diabetes-related morbidity and mortality.
Kaňková et al., In Clin Chem Lab Med, 2014
BACKGROUND: We hypothesized that genetic variability in genes encoding enzymes metabolizing glycolytic intermediates produced in excess under hyperglycemic conditions [i.e., transketolase (TKT), transaldolase, TKT-like protein 1, fructosamine 3-kinase (FN3K), glyoxalase 1 and glucose-6-phosphate dehydrogenase] could influence progression of diabetic nephropathy (DN) and diabetes-related morbidity and mortality.
Fructosamine 3-kinase and glyoxalase I polymorphisms and their association with soluble RAGE and adhesion molecules in diabetes.
Kalousová et al., Praha, Czech Republic. In Physiol Res, 2013
Several enzymes such as fructosamine 3-kinase (FN3K) and glyoxalase I (GLO I) are crucial in preventing glycation processes.
Differential response to α-oxoaldehydes in tamoxifen resistant MCF-7 breast cancer cells.
Kalinski et al., Magdeburg, Germany. In Plos One, 2013
However, mRNA accumulation of the aldehyde- and AGE-defence enzymes glyoxalase-1 and -2 (GLO1, GLO2) as well as fructosamine-3-kinase (FN3K) was not significantly altered.
Enzymatic repair of Amadori products.
Veiga-da-Cunha et al., Brussels, Belgium. In Amino Acids, 2012
Fructosamine-3-kinase (FN3K), an enzyme found in mammals and birds, phosphorylates fructosamines on the third carbon of their sugar moiety, making them unstable and causing them to detach from proteins.
Race-ethnic differences in the association of genetic loci with HbA1c levels and mortality in U.S. adults: the third National Health and Nutrition Examination Survey (NHANES III).
MAGIC Investigators et al., Boston, United States. In Bmc Med Genet, 2011
We tested the hypotheses that there is race-ethnic variation in 1) HbA1c-associated risk allele frequencies (RAFs) for SNPs near SPTA1, HFE, ANK1, HK1, ATP11A, FN3K, TMPRSS6, G6PC2, GCK, MTNR1B; 2) association of SNPs with HbA1c and 3) association of SNPs with mortality.
The physiological substrates of fructosamine-3-kinase-related-protein (FN3KRP) are intermediates of nonenzymatic reactions between biological amines and ketose sugars (fructation products).
Loomes et al., United States. In Med Hypotheses, 2011
The physiological function of fructosamine-3-kinase (FN3K) is relatively well understood.
Identification of a gene-expression signature for predicting lymph node metastasis in patients with early stage cervical carcinoma.
Wang et al., Guangzhou, China. In Cancer, 2011
RESULTS: A gene-expression signature for predicting PLNM was developed in patients from the training group, including 11 genes: ribosomal protein L35 (RPL35); thymosin β 10 (TMSB10); tyrosine 3-mono-oxytenase/tryptophan 5-mono-oxygenase activation protein, ζ polypeptide (YWHAZ); biotinidase (BTD); lactate dehydrogenase A (LDHA); glucuronidase β (GUSB); superoxide dismutase 2 (SOD2); nuclear receptor subfamily 3, group C, member 2 (NR3C2); fructosamine 3 kinase (FN3K); x-ray repair cross-complementing 4 (XRCC4); and wingless-type mouse mammary tumor virus integration site family member 2 (WNT2).
Purification and identification of activating enzymes of CS-0777, a selective sphingosine 1-phosphate receptor 1 modulator, in erythrocytes.
Nara et al., Tokyo, Japan. In J Biol Chem, 2011
We purified CS-0777 kinase activity from human RBCs by more than 10,000-fold using ammonium sulfate precipitation and successive chromatography steps, and we identified fructosamine 3-kinase (FN3K) and fructosamine 3-kinase-related protein (FN3K-RP) by mass spectrometry.
Genetic variability of the fructosamine 3-kinase gene in diabetic patients.
Mosca et al., Milano, Italy. In Clin Chem Lab Med, 2011
two new mutations and additional variants within the FN3K gene in diabetic patients
Low red blood cell levels of deglycating enzymes in colorectal cancer patients.
Misciagna et al., Bari, Italy. In World J Gastroenterol, 2011
These findings suggest that deglycating enzymes Glyoxalase I and fructosamine-3-kinase may be involved in the malignant transformation of colon mucosa.
A polymorphism within the fructosamine-3-kinase gene is associated with HbA1c Levels and the onset of type 2 diabetes mellitus.
Wittmann et al., Pécs, Hungary. In Exp Clin Endocrinol Diabetes, 2010
G900C polymorphism associates with the level of HbA (1c) and the onset of type 2 diabetes mellitus, but not with either of the diabetic microvascular complications.
Effects of fructosamine-3-kinase deficiency on function and survival of mouse pancreatic islets after prolonged culture in high glucose or ribose concentrations.
Jonas et al., Brussels, Belgium. In Am J Physiol Endocrinol Metab, 2010
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-6-phosphates are deglycated by phosphorylation to fructosamine-3,6-bisphosphates catalyzed by fructosamine-3-kinase (FN3K) and/or fructosamine-3-kinase-related-protein (FN3KRP).
Szwergold, United States. In Med Hypotheses, 2006
In this paper we propose a resolution of both these quandaries by proposing that fructosamine-6-phosphates are deglycated by phosphorylation to fructosamine-3,6-bisphosphates catalyzed by FN3KRP and/or possibly FN3K.
Enzymatic deglycation--a new paradigm or an epiphenomenon?
Beisswenger et al., United States. In Biochem Soc Trans, 2003
Following the discovery of FN3K (fructosamine 3-kinase), and more recently of FN3KRP (FN3K-related protein), research in our laboratory has been focused on testing the enzymatic deglycation hypothesis and investigating the roles of FN3K and FN3KRP.
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