Cardiolipin-deficient cells have decreased levels of the iron–sulfur biogenesis protein frataxin
Yiran Li, Wenjia Lou, Alexander Grevel, Lena Böttinger, Zhuqing Liang, Jiajia Ji, Vinay A. Patil, Jenney Liu, Cunqi Ye, Maik Hüttemann, Thomas Becker, Miriam L. Greenberg
Abstract
Δ cells exhibited decreased processing of the Yfh1 precursor upon import, which likely contributes to the iron homeostasis defects. Implications for understanding the pathogenesis of BTHS are discussed.
Topics & Concepts
CardiolipinFrataxinMitochondrionAconitaseIron-binding proteinsBiologyBiochemistryCell biologyTransferrin receptorBiogenesisFerroportinMitochondrial biogenesisIron–sulfur clusterChemistryTransferrinMetabolismEnzymePhospholipidGeneMembraneIron homeostasisMitochondrial Function and PathologyGenetic Neurodegenerative DiseasesMetalloenzymes and iron-sulfur proteins