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  TRPM channels mediate zinc homeostasis and cellular growth during Drosophila larval development

Georgiev, P., Okkenhaug, H., Drews, A., Wright, D., Lambert, S., Flick, M., et al. (2010). TRPM channels mediate zinc homeostasis and cellular growth during Drosophila larval development. Cell Metabolism, 12(4), 386-397. doi:10.1016/j.cmet.2010.08.012.

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https://pubmed.ncbi.nlm.nih.gov/20889130/ (Supplementary material)
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Georgiev, P., Author
Okkenhaug, H., Author
Drews, A., Author
Wright, D., Author
Lambert, S., Author
Flick, M.1, 2, Author           
Carta, V., Author
Martel, C., Author
Oberwinkler, J., Author
Raghu, P., Author
Affiliations:
1Department of Molecular Sensory Systems, Center of Advanced European Studies and Research (caesar), Max Planck Society, ou_2173679              
2Emmy Noether Research Group, Experimentelle und Klinische Pharmakologie und Toxikologie, Uniklinikum des Saarlandes, 66421 Homburg, ou_persistent22              

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 Abstract: TRPM channels have emerged as key mediators of diverse physiological functions. However, the ionic permeability relevant to physiological function in vivo remains unclear for most members. We report that the single Drosophila TRPM gene (dTRPM) generates a conductance permeable to divalent cations, especially Zn(2+) and in vivo a loss-of-function mutation in dTRPM disrupts intracellular Zn(2+) homeostasis. TRPM deficiency leads to profound reduction in larval growth resulting from a decrease in cell size and associated defects in mitochondrial structure and function. These phenotypes are cell-autonomous and can be recapitulated in wild-type animals by Zn(2+) depletion. Both the cell size and mitochondrial defect can be rescued by extracellular Zn(2+) supplementation. Thus our results implicate TRPM channels in the regulation of cellular Zn(2+) in vivo. We propose that regulation of Zn(2+) homeostasis through dTRPM channels is required to support molecular processes that mediate class I PI3K-regulated cell growth

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Language(s): eng - English
 Dates: 2010
 Publication Status: Issued
 Pages: -
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 Table of Contents: -
 Rev. Type: Peer
 Identifiers: DOI: 10.1016/j.cmet.2010.08.012
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Title: Cell Metabolism
  Abbreviation : Cell Metab
Source Genre: Journal
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Publ. Info: Cambridge, MA : Cell Press
Pages: - Volume / Issue: 12 (4) Sequence Number: - Start / End Page: 386 - 397 Identifier: ISSN: 1550-4131
CoNE: https://pure.mpg.de/cone/journals/resource/111088195284928