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Target intelligence / Profile preview
Solute carrier family 35 member D1 (SLC35D1)
- Target
- SLC35D1
- Molecular classification
- Transporter, Solute carrier (SLC) family member, Nucleotide sugar transporter
01
Overview
Solute carrier family 35 member D1 (SLC35D1) is a nucleotide sugar transporter located in the endoplasmic reticulum membrane, functioning as an antiporter that exchanges nucleotide sugars such as UDP-glucuronic acid (UDP-GlcA) and UDP-N-acetylgalactosamine (UDP-GalNAc) from the cytosol into the ER lumen, where they are used as substrates for glycosylation reactions. This transporter is critical for biosynthetic pathways including glucuronidation and chondroitin sulfate biosynthesis, which are essential for proper extracellular matrix formation and skeletal development. Mutations in SLC35D1 are associated with severe skeletal dysplasias, particularly Schneckenbecken dysplasia, highlighting its crucial developmental role.
- Other names
- UGTREL7UDP-glucuronic acid/UDP-N-acetylgalactosamine transporterKIAA0260Solute carrier family 35 (UDP-glucuronic acid/UDP-N-acetylgalactosamine dual transporter), member D1Solute carrier family 35 (UDP-GlcA/UDP-GalNAc transporter), member D1
02
Mechanism of action
Antiporter function: transports UDP-sugars into ER lumen in exchange for cognate nucleoside monophosphate or another nucleotide sugar
03
Biological functions
Nucleotide sugar transport (especially UDP-glucuronic acid and UDP-N-acetylgalactosamine)Glycosylation (specifically glycosylation of glycoconjugates in ER and Golgi)GlucuronidationChondroitin sulfate biosynthesisExtracellular matrix formation and normal skeletal development
04
Disease associations
Skeletal dysplasia (notably Schneckenbecken dysplasia)Acromesomelic dysplasia 2AOther disorders involving glycosylation defects
05
Safety considerations
No direct pharmacological safety concerns reported; gene mutations cause severe congenital skeletal disorders indicating essential role in development
06
Interacting drugs
No specific drugs directly targeting SLC35D1 are reported in the cited databases or literature. Its dysfunction is linked to congenital disorders rather than being a current pharmacological target.
07
Biomarkers
Mutations in SLC35D1 gene serve as biomarkers for Schneckenbecken dysplasia and related congenital skeletal disorders
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