ArticleThe FEBS journal2025
A creatine efflux transporter in oligodendrocytes.
Article in The FEBS journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Creatine kinase regulates energy metabolism and growth of trophoblasts.bioRxiv : the preprint server for biology · 2026Article
- Deconvolution of haematological cancer methylation patterns reveals a predominantly non-disease related proliferation signal and uncovers true disease associated methylation changes.British journal of cancer · 2026Article
- Enhancing transporter activity in heterologous expression systems with SAHA: a 2500-times more potent and odorless alternative to butyrate.FEBS open bio · 2025Article
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Authors and funding
4 authors.
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Abstract
Creatine is essential for ATP regeneration in energy-demanding cells. Creatine deficiency results in severe neurodevelopmental impairments. In the brain, creatine is synthesized locally by oligodendrocytes to supply neighboring neurons. Neuronal uptake is mediated by SLC6A8. However, it is still unknown how creatine is released from the producing cells. Here, we investigated the function of the transporter SLC22A15, which exhibits strikingly high amino acid sequence conservation. The release of substrates from 293 cells via heterologously expressed human and rat SLC22A15 was analyzed by mass spectrometry. A number of zwitterions were identified as substrates, with similar efflux transport efficiencies. However, in absolute numbers, the efflux of creatine far outweighed all other substrates. In contrast to the permanent creatine efflux mediated by SLC16A12 and SLC16A9, SLC22A15 was, by default, completely inactive, thereby preventing continuous creatine loss from producing cells. External substrates such as guanidinoacetic acid, GABA, or MPP
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