ArticleThe Journal of biological chemistry2010
Properties of the TRPML3 channel pore and its stable expansion by the Varitint-Waddler-causing mutation.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- TRPML3 and TRPML1/3 differentially regulate unconventional MIF secretion through TMED10 and secretory autophagy.Autophagy reports · 2026Article
- The intracellular CaProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Mahogunin Ring Finger 1 regulates pigmentation by controlling the pH of melanosomes in melanocytes and melanoma cells.Cellular and molecular life sciences : CMLS · 2021Article
- Endolysosomal CaCancers · 2018Review
- Cryo-EM structures of the human endolysosomal TRPML3 channel in three distinct states.Nature structural & molecular biology · 2017Article
- Article
- The mucolipin-2 (TRPML2) ion channel: a tissue-specific protein crucial to normal cell function.Pflugers Archiv : European journal of physiology · 2016Review
- How does NAADP release lysosomal Ca2+?Channels (Austin, Tex.) · 2014Article
- Constitutive activity of TRPML2 and TRPML3 channels versus activation by low extracellular sodium and small molecules.The Journal of biological chemistry · 2012Article
- TRPML: transporters of metals in lysosomes essential for cell survival?Cell calcium · 2011Review
- Transient receptor potential mucolipin 1 (TRPML1) and two-pore channels are functionally independent organellar ion channels.The Journal of biological chemistry · 2011Article
- A helix-breaking mutation in the epithelial Ca(2+) channel TRPV5 leads to reduced Ca(2+)-dependent inactivation.Cell calcium · 2010Article
- Constitutive activity of TRP channels methods for measuring the activity and its outcome.Methods in enzymology · 2010Article
- The intracellular Ca²⁺ channels of membrane traffic.Channels (Austin, Tex.)Review
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Authors and funding
5 authors.
Funding
Abstract
TRPML3 is a H(+)-regulated Ca(2+) channel that shuttles between intracellular compartments and the plasma membrane. The A419P mutation causes the varitint-waddler phenotype as a result of gain-of-function (GOF). The mechanism by which A419P leads to GOF is not known. Here, we show that the TRPML3 pore is dynamic when conducting Ca(2+) to change its conductance and permeability, which appears to be mediated by trapping Ca(2+) within the pore. The pore properties can be restored by strong depolarization or by conducting Na(+) through the pore. The A419P mutation results in expanded channel pore with altered permeability that limits modulation of the pore by Ca(2+). This effect is specific for the A419P mutation and is not reproduced by other GOF mutations, including A419G, H283A, and proline mutations in the fifth transmembrane domain. These findings describe a novel mode of a transient receptor potential channel behavior and suggest that pore expansion by the A419P mutation may contribute to the varitint-waddler phenotype.
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