Disease relevance of FN3KRP

• One can imagine that, at some point in the future, measurement of FN3K/FN3KRP activity may be of diagnostic value in assessing an individual's susceptibility to diabetic complications [1].

High impact information on FN3KRP

• These data suggest that FN3K and FN3KRP act as protein repair enzymes and are expressed constitutively in human cells independently of some of the variables altered in the diabetic state [2].
• (3) Treatment of fibroblasts with high glucose, IL-1beta, and activation of NFkappaB does not affect the expression of either FN3K or FN3KRP [3].
• Our results indicate that (1) both FN3K and FN3KRP promoters are TATA-less and CAAT-less and contain several homologous CpG islands and Sp1 binding sites [3].
• Fructosamine 3-kinase-related protein and deglycation in human erythrocytes [4].

Biological context of FN3KRP

• Two such important questions are 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 [1].

Anatomical context of FN3KRP

• Cultured fibroblasts treated with conditions mimicking the hormonal and biochemical profile of the diabetic state showed no changes in FN3K and FN3KRP expression relative to untreated cells [2].

References