Exosomal secretion of truncated cytosolic lysyl-tRNA synthetase induces inflammation during cell starvation

Sang Bum Kim, Seongmin Cho, Sunghoon Kim

Research output: Contribution to journalReview articlepeer-review

4 Citations (Scopus)


Previous work by Kim, et al. (2017) unveiled that lysyltRNA synthetase (KRS) is secreted through a mechanism involving syntenin-containing exosomes. They described how KRS, commonly known as part of the translational machinery in the cytoplasm, is secreted into the extracellular space where it induces inflammation. First, KRS secretion is triggered by starvation conditions. The increase in caspase-8 levels during starvation is responsible for proteolysis and generation of the N-terminal truncated form of KRS, and this event is required for KRS dissociation from the multisynthetase complex (MSC). N-terminal cleavage of KRS eventually leads to a conformational change that allows its interaction with the C-terminal PDZ binding motif of syntenin and subsequent exosome biogenesis. The KRS-syntenin complex translocates to multivesicular bodies (MVBs) that originate from endosomes involved with intraluminal vesicle (ILVs). MVBs are transporters for the secretion of cellular contents into the extracellular space. Syntenin localizes intraluminal vesicles within endosomal membranes. The KRS-syntenin complex transfers on to intraluminal vesicles in MVBs. MVBs are translocated to the plasma membrane for ILV secretion mediated by Rab family proteins. Once KRS exosomes are secreted, their membranes are eventually ruptured by proteases and KRS is released from the exosomes where it can act as an inflammatory cytokine in the extracellular space. Secreted KRS triggers macrophage/neutrophil migration and induces inflammation.

Original languageEnglish
Pages (from-to)119-121
Number of pages3
JournalCell Stress
Issue number5
Publication statusPublished - 2018 May

Bibliographical note

Funding Information:
This work was supported by the Global Frontier Project grant (NRF-M3A6A4-2010-0029785) of National Research Foundation funded by the Ministry of Science and ICT (MSIT) of Korea.

Publisher Copyright:
© 2018 Kim et al.

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology (miscellaneous)
  • Cancer Research
  • Molecular Medicine
  • Physiology


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