Weidberg


Research Interest
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Mitochondria are organelles that serve as a hub for cellular signaling and the biogenesis of indispensable metabolites. We aim to understand how mitochondrial homeostasis is maintained under challenging physiological and disease conditions. We focus on stress caused by perturbations in mitochondrial protein import which is associated with multiple human disorders as well as with aging and neurodegenerative diseases.

Publications
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  1. Shpilka, T., Du, Y.G., Yang Q., Melber A., Naresh N.U., Lavelle J., Liu P., Weidberg H., Li R., Yu J., Zhu L.J., Strittmatter L., Haynes C.M. UPRmt scales mitochondrial network expansion with protein synthesis via mitochondrial import in Caenorhabditis elegans. Nature Communication 12, 479 (2021).
  2. Weidberg H, Amon, A. (2018) MitoCPR—A surveillance pathway that protects mitochondria in response to protein import stress. Science eaan4146 360.
  3. Weidberg H, Moretto F, Spedale G, Amon A, J. van Werven F. (2016) Nutrient control of yeast gametogenesis is mediated by TORC1, PKA and energy availability. PLoS Genet. 12(6).
  4. Weidberg H, Shpilka T, Shvets E, Abada Adi, Shimron F, Elazar Z. (2011) LC3 and GATE-16 N-termini mediate membrane fusion processes required for autophagosome biogenesis. Dev Cell, 20, 444-54.
  5. Weidberg H, Shvets E, Shpilka T, Shimron F, Shinder V, Elazar Z. (2010) LC3 and GATE-16/GABARAP subfamilies are both essential yet act differently in autophagosome biogenesis. EMBO J, 29, 1792-802.
Further publications can be found here.