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Solute carrier family 22 member 10 (SLC22A10)
- Target
- SLC22A10
- Molecular classification
- Transporter (specifically, organic anion transporter of the SLC22 family), Membrane protein
01
Overview
Solute carrier family 22 member 10 (SLC22A10), also known as organic anion transporter 5 (OAT5), is a protein-encoding gene in the SLC22 family that, in humans, is a unitary pseudogene rendered non-functional by a fixed frameshift mutation, resulting in a non-functional protein that does not reach the plasma membrane and lacks organic anion transport activity. In great apes and some other primates, functional orthologs act as hepatic transporters for steroid glucuronides, but the human gene is evolutionarily inactivated. SLC22A10 was previously and erroneously described as a kidney-expressed organic anion transporter and a potential urinary biomarker for kidney damage, but modern genetic and proteomic evidence confirm absence of function in humans, making it irrelevant as a therapeutic target or biomarker.
- Other names
- Organic anion transporter 5 (OAT5)hOAT5HOAT5Solute carrier family 22 (organic anion/cation transporter) member 10Solute carrier family 22, member 10S22AA Protein
02
Mechanism of action
In humans: Not applicable; no functional protein on the plasma membrane. In non-human primates: Transmembrane steroid glucuronide transporter.
03
Biological functions
In humans: None—no confirmed biological function (unitary pseudogene)In great apes and some non-human primates: Organic anion (especially steroid glucuronide) transport
04
Disease associations
In humans: None known as the gene is non-functionalUrinary excretion tentatively explored as a potential biomarker for kidney damage (historically assumed)In non-human primates: May contribute to hepatic steroid glucuronide transport
05
Safety considerations
None reported, as SLC22A10 is a pseudogene in humans and not a pharmacological target
06
Interacting drugs
In humans: None (no functional transport activity)
1 more in the full profile.
07
Biomarkers
Human SLC22A10 was previously postulated to be an early urinary kidney damage biomarker, but this is undermined by its status as a pseudogene with no validated protein function in humans
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