SLC23A3 is a renal hypoxanthine transporter
Makoto Hosoyamada1, Naoko H Tomioka1, Tamaki Watanabe2
1Laboratory of Human Physiology and Pathology, Faculty of Pharma-Science, Teikyo University, Tokyo, Japan.
Nucleosides, Nucleotides & Nucleic Acids
|January 31, 2022
Summary
The human kidney contains SLC23A3, a transporter protein that facilitates hypoxanthine uptake. This transporter is sodium-dependent and is inhibited by adenine, not xanthine.
Area of Science:
- Nephrology
- Molecular Biology
- Biochemistry
Background:
- Renal cells exhibit both sodium-dependent and sodium-independent hypoxanthine uptake.
- The intestinal transporter Slc23a4, while inhibited by xanthine, is not found in the kidney.
Purpose of the Study:
- To clone the human kidney gene SLC23A3, a paralog of Slc23a4.
- To investigate the hypoxanthine transport activity of SLC23A3.
Main Methods:
- Cloning of SLC23A3 from human kidney cDNA.
- Expression of SLC23A3 in Xenopus oocytes.
- Measurement of [3H]-hypoxanthine uptake in oocytes.
Main Results:
- Sodium-dependent hypoxanthine uptake was observed in oocytes expressing SLC23A3.
- Adenine inhibited uptake, while xanthine did not affect this process.
- This confirms SLC23A3's role as a hypoxanthine transporter.
Conclusions:
- SLC23A3 functions as a hypoxanthine transporter in the human kidney.
- The transporter's activity is sodium-dependent and modulated by adenine.
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