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Mitofusin 2 builds a bridge between ER and mitochondria.

Author(s): Carsten Merkwirth, Thomas Langer

Publication date: 2008-12-26

Journal: Cell

Keywords: Animals, Axonal Transport, Cell Line, Endoplasmic Reticulum, metabolism, GTP Phosphohydrolases, Mice, Mitochondria, Purkinje Cells

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Abstract

Mutations in mitofusin 2 (MFN2), a dynamin-like GTPase required for mitochondrial fusion, cause the peripheral neuropathy Charcot-Marie-Tooth type 2A. In a recent report in Nature, de Brito and Scorrano (2008) demonstrate a new function of MFN2-tethering the endoplasmic reticulum and mitochondria to control the efficiency of mitochondrial uptake of Ca2+ ions.

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PubMed ID:: 19109886

DOI:: 10.1016/j.cell.2008.12.005

ScienceOpen disciplines: Chemistry

Keywords: Animals,Axonal Transport,Cell Line,Endoplasmic Reticulum,metabolism,GTP Phosphohydrolases,Mice,Mitochondria,Purkinje Cells

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ScienceOpen disciplines: Chemistry

Keywords: Animals, Axonal Transport, Cell Line, Endoplasmic Reticulum, metabolism, GTP Phosphohydrolases, Mice, Mitochondria, Purkinje Cells

Mitofusin 2 builds a bridge between ER and mitochondria.

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