Literature summary for 2.7.1.171 extracted from

Skrha, J.; Muravska, A.; Flekac, M.; Horova, E.; Novak, J.; Novotny, A.; Prazny, M.; Skrha, J.; Kvasnicka, J.; Landova, L.; Jachymova, M.; Zima, T.; Kalousova, M.
Fructosamine 3-kinase and glyoxalase I polymorphisms and their association with soluble RAGE and adhesion molecules in diabetes (2014), Physiol. Res., 63 Suppl 2, S283-S291.

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Cloned(Commentary)

Cloned (Comment)	Organism
gene FN3K, located on chromosome 17q25, genotyping	Homo sapiens

Protein Variants

Protein Variants	Comment	Organism
additional information	while GG and CG genotypes of rs1056534 with mutated G allele are associated with significant decrease of sRAGE, in rs3848403 polymorphism TT genotype with mutated T allele is related with significant sRAGE increase	Homo sapiens

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	Q9H479	gene FN3K	-

Synonyms

Synonyms	Comment	Organism
FN3K	-	Homo sapiens
fructosamine 3-kinase	-	Homo sapiens

General Information

General Information	Comment	Organism
malfunction	significant relationship of FN3K (rs1056534) and (rs3848403) polymorphisms with with endothelial dysfunction and concentration of soluble receptor for advanced glycation end-products (sRAGE) in patients with diabetes, clinical parameters, overview	Homo sapiens
physiological function	advanced glycation end-products are key players in pathogenesis of long-term vascular diabetes complications, several enzymes such as fructosamine 3-kinase (FN3K) and glyoxalase I (GLO I) are crucial in preventing glycation processes	Homo sapiens

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Release 2023.1 (January 2023)