FN3K
Chr 17fructosamine 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]
Clinical Summary— FN3K
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Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
Population Genetics & Constraint
gnomAD v4 — loss-of-function & missense intolerance
Tolerant — LoF & missense variants common in population
LoF Constraint?LOEUF (Loss-of-function Observed/Expected Upper bound Fraction) is the upper bound of the 90% CI for LoF OE — the preferred gnomAD v4 metric. Lower = more intolerant to LoF. LOEUF < 0.35 = highly constrained.
1.36LOEUF
pLI 0.000
Z-score 0.51
OE 0.86 (0.56–1.36)
Highly tolerant — LoF variants common in population
Missense Constraint?Missense Z-score: standard deviations fewer missense variants observed vs. expected. Z > 3.09 (p < 0.001) = gene does not tolerate missense variation. OE missense < 0.6 is also considered constrained.
0.05Z-score
OE missense 0.99 (0.88–1.12)
188 obs / 190.0 exp
Mild missense constraint
Observed / Expected Ratios?Shaded band = 90% confidence interval. Vertical tick = point estimate. Grey threshold line = gnomAD constraint cutoff for that variant class.
LoF OE?Ratio of observed to expected LoF variants. Upper CI bound (LOEUF) ≤ 0.35 = strong LoF constraint signal.0.86 (0.56–1.36)
0≤0.351.4
Missense OE?Ratio of observed to expected missense variants. OE ≤ 0.6 = fewer missense variants than expected by chance.0.99 (0.88–1.12)
0≤0.61.4
Synonymous OE?Control metric — synonymous variants are largely neutral and expected near OE = 1.0. Significant deviation may indicate annotation issues.1.06
0≤1.21.6
LoF obs/exp: 13 / 15.2Missense obs/exp: 188 / 190.0Syn Z: -0.44
ClinVar Variant Classifications
0 submitted variants in ClinVar
Protein Context — Lollipop Plot
FN3K · protein map & ClinVar variants
Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.
OMIM — Genotype-Phenotype Relationships
3 OMIM entries
FRUCTOSAMINE 3-KINASE
MIM #608425 · *
MAGNESIUM-DEPENDENT PHOSPHATASE 1; MDP1
MIM #621484 · *
FRUCTOSAMINE 3-KINASE-RELATED PROTEIN
MIM #611683 · *
External Resources
Links to major genomics databases and tools
Clinical Trials
Active and recruiting trials from ClinicalTrials.gov
No active trials found for this gene.
Search ClinicalTrials.gov →Clinical Literature
Landmark / reviewRecent case evidence
Key Publications
Landmark & review papers · by relevance
Possible role of fructosamine 3-kinase genotyping for the management of diabetic patients.
Avemaria F et al.·Clin Chem Lab Med
2015Cohort
Genetic variability of the fructosamine 3-kinase gene in diabetic patients.
Mosca L et al.·Clin Chem Lab Med
2011Cohort
FN3K alleviates renal ischemia-reperfusion injury by regulating oxidative stress through Nrf2 deglycation.
Zhou Y et al.·Free Radic Biol Med
2026
Detection of oxidized and glycated proteins in clinical samples using mass spectrometry--a user's perspective.
Thornalley PJ et al.·Biochim Biophys Acta
2014Review
Are Polymorphisms Within the Fructosamine-3-Kinase Gene Associated With the Discordance Between HbA1c and Other Measures of Glycemia?
Motshwari DD et al.·Diabetes
2025
Impact of Rare and Common Genetic Variants on Diabetes Diagnosis by Hemoglobin A1c in Multi-Ancestry Cohorts: The Trans-Omics for Precision Medicine Program.
Sarnowski C et al.·Am J Hum Genet
2019Cohort
A polymorphism within the fructosamine-3-kinase gene is associated with HbA1c Levels and the onset of type 2 diabetes mellitus.
Mohás M et al.·Exp Clin Endocrinol Diabetes
2010
Top 10 resultsSearch PubMed ↗
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
The molecular basis of Human FN3K mediated phosphorylation of glycated substrates.
Garg A et al.·Nat Commun
2025Open Access
Multi-omics reveals new links between Fructosamine-3-Kinase (FN3K) and core metabolic pathways.
Shrestha S et al.·NPJ Syst Biol Appl
2024Open Access
Top 5 resultsSearch Europe PMC ↗
Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
Screening fructosamine-3-kinase (FN3K) inhibitors, a deglycating enzyme of oncogenic Nrf2: Human FN3K homology modelling, docking and molecular dynamics simulations
Beeraka NM et al.·PLoS One
2023Functional
The Taming of Nuclear Factor Erythroid-2-Related Factor-2 (Nrf2) Deglycation by Fructosamine-3-Kinase (FN3K)-Inhibitors-A Novel Strategy to Combat Cancers
Beeraka NM et al.·Cancers (Basel)
2021
Ancestral protein reconstruction reveals the mechanism of substrate specificity in FN3K-mediated deglycation
Matlack JK et al.·bioRxiv
2025Functional
Ancestral protein reconstruction reveals the mechanism of substrate specificity in FN3K-mediated deglycation.
Matlack JK et al.·Res Sq
2025Functional
Correction: FN3K expression in COPD: a potential comorbidity factor for cardiovascular disease
·BMJ Open Respir Res
2021
Enzymatic Deglycation of Damaged Skin by Means of Combined Treatment of Fructosamine-3-Kinase and Fructosyl-Amino Acid Oxidase
De Decker I et al.·Int J Mol Sci
2023
Top 6 full-text resultsSearch PubTator3 ↗
External Resources
Links to major genomics databases and tools