ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Functional regulation of the SLC26-family protein prestin by calcium/calmodulin.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- Acbd7 is essential for preserving hair cell-mediated auditory and vestibular function.Experimental & molecular medicine · 2026Article
- From transporter to motor: Evolutionary and structural insights into the emergence of prestin's area-motor activity in mammals.Protein science : a publication of the Protein Society · 2026Article
- Functional Studies of Deafness-Associated Pendrin and Prestin Variants.International journal of molecular sciences · 2024Article
- SLC26 Anion Transporters.Handbook of experimental pharmacology · 2024Review
- Folding of prestin's anion-binding site and the mechanism of outer hair cell electromotility.eLife · 2023Article
- Single particle cryo-EM structure of the outer hair cell motor protein prestin.Nature communications · 2022Article
- The Roles of Solute Carriers in Auditory Function.Frontiers in genetics · 2022Review
- Deletion of Oncomodulin Gives Rise to Early Progressive Cochlear Dysfunction in C57 and CBA Mice.Frontiers in aging neuroscience · 2021Article
- Structural insights into the gating mechanism of human SLC26A9 mediated by its C-terminal sequence.Cell discovery · 2020Article
- Article
- Prestin kinetics and corresponding frequency dependence augment during early development of the outer hair cell within the mouse organ of Corti.Scientific reports · 2019Article
- Deletion of exons 17 and 18 in prestin's STAS domain results in loss of function.Scientific reports · 2019Article
- Oncomodulin: The Enigmatic Parvalbumin Protein.Frontiers in molecular neuroscience · 2019Article
- The extracellular loop of pendrin and prestin modulates their voltage-sensing property.The Journal of biological chemistry · 2018Article
- The R130S mutation significantly affects the function of prestin, the outer hair cell motor protein.Journal of molecular medicine (Berlin, Germany) · 2016Article
- Quarterly intrinsic disorder digest (January-February-March, 2014).Intrinsically disordered proteins · 2016Article
- Activity-dependent regulation of prestin expression in mouse outer hair cells.Journal of neurophysiology · 2015Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The solute carrier gene family 26 (SLC26) encodes membrane proteins with diverse physiological roles but with the common feature of halide involvement. Here, we present bioinformatic and biochemical evidence that SLC26 proteins have intrinsically disordered regions (IDRs) in their C-terminal domains and that these regions contain calmodulin (CaM) binding sites. The veracity of these predictions and the functional consequences of CaM binding were examined in prestin, SLC26A5, as a model for the SLC26 family and as one of the most investigated and best understood members. We found that CaM binds directly to the IDR in the C-terminal domain of prestin in a calcium-obligate manner. Using both isolated murine outer hair cells (OHCs) and a heterologous expression system, we also found that this calcium-obligate CaM binding shifts the operating point of the protein to more hyperpolarized potentials with consequent alteration of the function of the prestin. Because calcium is the main intracellular second messenger used by the efferent medial olivocochlear (MOC) pathway of the auditory system and CaM is abundant in OHCs, the CaM-prestin interaction may be involved in the MOC-mediated modulation of cochlear amplification. However, this regulatory mechanism is not likely to be restricted to cochlear OHCs, in light of both clear bioinformatic evidence and the fact that calcium and CaM are ubiquitous intracellular second messengers used by virtually all cell types. Hence, the calcium/CaM-dependent regulatory mechanism described herein is likely applicable to most, if not all, SLC26 paralogs.
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