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Brain o-glcnacylation: from molecular mechanisms to clinical phenotype
Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
2023 (Engelska)Ingår i: Advances in neurobiology, ISSN 2190-5215, Vol. 29, s. 255-280Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

O-GlcNAc is the attachment of β-N-acetylglucosamine to the hydroxyl group of serine and threonine in nuclear and cytoplasmic proteins. It is generally not further elongated but exists as a monosaccharide that can be rapidly added or removed. Thousands of proteins involved in gene transcription, protein translation and degradation as well as the regulation of signal transduction contain O-GlcNAc. Brain is one of the tissues where O-GlcNAc is the most highly expressed and deletion of neuronal O-GlcNAc leads to death early in development. O-GlcNAc is also important for normal adult brain function, where dynamic processes like learning and memory at least in part depend on the modification of specific proteins by O-GlcNAc. Conversely, too much or too little O-GlcNAc in the brain contributes to several disorders including obesity, intellectual disability and Alzheimer's disease. In this chapter, we describe the expression and regulation of O-GlcNAc in the nervous system.

Ort, förlag, år, upplaga, sidor
Springer Nature, 2023. Vol. 29, s. 255-280
Nyckelord [en]
Alzheimer’s disease, Food intake, Learning and memory, Neurodegeneration, Nutrient sensing, O-GlcNAc, O-linked N-acetylglucosamine, Obesity, Post-translational modifications, Signaling
Nationell ämneskategori
Biokemi och molekylärbiologi
Identifikatorer
URN: urn:nbn:se:umu:diva-200660DOI: 10.1007/978-3-031-12390-0_9PubMedID: 36255678Scopus ID: 2-s2.0-85140171507OAI: oai:DiVA.org:umu-200660DiVA, id: diva2:1709080
Tillgänglig från: 2022-11-07 Skapad: 2022-11-07 Senast uppdaterad: 2022-11-07Bibliografiskt granskad

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Uygar, BatuhanLagerlöf, Olof

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