Target intelligence / Profile preview

Xyloside xylosyltransferase 1 (XXYLT1)

Target
XXYLT1
Molecular classification
Enzyme, Glycosyltransferase (specifically, glycosyltransferase family 8), Type II membrane protein
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Overview

Xyloside xylosyltransferase 1 (XXYLT1) is a type II membrane glycosyltransferase of the glycosyltransferase family 8, primarily residing in the endoplasmic reticulum. It transfers a xylose residue from UDP-xylose to a pre-existing xylose on the glucose-xylose (Xyl-Glc) disaccharide of epidermal growth factor (EGF)-like repeats, notably on the Notch receptor extracellular domain. This post-translational modification is part of the canonical glycosylation of Notch receptors and modulates their signaling function. Mutations or dysregulation of XXYLT1 can influence Notch-dependent cellular processes, with emerging evidence supporting a role in some cancers, particularly where Notch signaling is implicated. The detailed mechanism of catalysis involves direct nucleophilic attack from the acceptor xylose, consistent with an S~N~i-like retaining glycosyltransferase mechanism[1].

Other names
C3orf21PSEC0251FLJ35155UDP-xylose:alpha-xyloside alpha-1,3-xylosyltransferasexyloside xylosyltransferase 1
02

Mechanism of action

Catalytic transfer of xylose in an α1–3 linkage to an existing xylose on EGF-like repeats using a retaining glycosyltransferase mechanism; mechanistically, likely uses an S~N~i-like internal return reaction retaining the configuration at the anomeric carbon[1].

03

Biological functions

Glycosylation of Notch receptor: transfers xylose from UDP-xylose to xylose-glucose disaccharide-modified EGF repeats in Notch and similar proteinsModulation of Notch signaling pathway (key in development and cell signaling)
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Disease associations

Cancer (Notch dysregulation linked to cancer, e.g., lung squamous cell carcinoma)Developmental disorders (altered Notch signaling impacts development)
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Safety considerations

Potential concerns relate to modulation of Notch signaling, as dysregulation can lead to tumorigenesis or developmental defects[1].

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