Редактирование: FUT8 (раздел)

==Publications==

{{medline-entry
|title=Alteration in N-glycomics during mouse aging: a role for [[FUT8]].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/21951615
|abstract=We recently reported that N-glycosylation changes during human aging. To further investigate the molecular basis determining these alterations, the aging process in mice was studied. N-glycan profiling of mouse serum glycoproteins in different age groups of healthy C57BL/6 mice showed substantial age-related changes in three major N-glycan structures: under-galactosylated biantennary (NGA2F), biantennary (NA2), and core α-1,6-fucosylated -β-galactosylated biantennary structures (NA2F). Mice defective in klotho gene expression (kl/kl), which have a shortened lifespan, displayed a similar but accelerated trend. Interestingly, the opposite trend was observed in slow-aging Snell Dwarf mice (dw/dw) and in mice fed a calorically restricted diet. We also discovered that increased expression and activity of α-1,6-fucosyltransferase ([[FUT8]]) in the liver are strongly linked to the age-related changes in glycosylation and that this increased [[FUT8]] and fucosylation influence IGF-1 signaling. These data demonstrate that the glycosylation machinery in liver cells is significantly affected during aging and that age-related increased [[FUT8]] activity could influence the aging process by altering the sensitivity of the IGF-1R signaling pathway.
|mesh-terms=* Aging
* Animals
* Blood Proteins
* Caloric Restriction
* Fucose
* Fucosyltransferases
* Gene Expression
* Glucuronidase
* Glycomics
* Glycoproteins
* Glycosylation
* Insulin-Like Growth Factor I
* Liver
* Male
* Mice
* Mice, Inbred C57BL
* Mice, Transgenic
* Polysaccharides
* Receptor, IGF Type 1
* Signal Transduction

|full-text-url=https://sci-hub.do/10.1111/j.1474-9726.2011.00749.x
}}