PropertyValue
?:abstract
  • Several human pathologies including neurological, cardiac, infectious, cancerous, and metabolic diseases have been associated with altered mitochondria morphodynamics. Here, we identify a small organic molecule, which we named Mito-C. Mito-C is targeted to mitochondria and rapidly provokes mitochondrial network fragmentation. Biochemical analyses reveal that Mito-C is a member of a new class of heterocyclic compounds that target the NEET protein family, previously reported to regulate mitochondrial iron and ROS homeostasis. One of the NEET proteins, NAF-1, is identified as an important regulator of mitochondria morphodynamics that facilitates recruitment of DRP1 to the ER-mitochondria interface. Consistent with the observation that certain viruses modulate mitochondrial morphogenesis as a necessary part of their replication cycle, Mito-C counteracts dengue virus-induced mitochondrial network hyperfusion and represses viral replication. The newly identified chemical class including Mito-C is of therapeutic relevance for pathologies where altered mitochondria dynamics is part of disease etiology and NEET proteins are highlighted as important therapeutic targets in anti-viral research.
is ?:annotates of
?:creator
?:doi
  • 10.15252/embr.201949019
?:doi
?:journal
  • EMBO_reports
?:license
  • unk
?:pmid
?:pmid
  • 33180995
?:publication_isRelatedTo_Disease
is ?:relation_isRelatedTo_publication of
?:source
  • Medline
?:title
  • Chemical targeting of NEET proteins reveals their function in mitochondrial morphodynamics.
?:type
?:year
  • 2020-11-12

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