The NLR protein, NLRX1, and its partner, TUFM, reduce type I interferon, and enhance autophagy

Yu Lei, Haitao Wen, Jenny P.Y. Ting

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

The NLR (nucleotide-binding domain leucine-rich repeat containing) proteins serve as regulators of inflammatory signaling pathways. NLRX1, a mitochondria-localized NLR protein, has been previously shown to negatively regulate inflammatory cytokine production activated via the MAVSDDX58 (RIG-I) pathway. The literature also indicates that DDX58 has a negative impact upon autophagy. Consistent with the inhibitory role of NLRX1 on DDX58, our recent study indicates a role of NLRX1 in augmenting virus-induced autophagy. This effect is through its interaction with another mitochondrial protein TUFM (Tu translation elongation factor, mitochondrial, also known as EF-TuMT, COXPD4, and P43). TUFM also reduces DDX58-activated cytokines but augments autophagy. Additionally it interacts with ATG12-ATG5-ATG16L1 to form a molecular complex that modulates autophagy. The work shows that both NLRX1 and TUFM work in concert to reduce cytokine response and augment autophagy.

Original languageEnglish (US)
Pages (from-to)432-433
Number of pages2
JournalAutophagy
Volume9
Issue number3
DOIs
StatePublished - Mar 2013

Fingerprint

Interferon Type I
Autophagy
Cytokines
Peptide Elongation Factor Tu
Mitochondrial Proteins
Mitochondria
NLR Proteins
Viruses

Keywords

  • Atg12
  • Atg16L1
  • Atg5
  • Autophagy
  • Interferon
  • NLRX1
  • RIG-I
  • RLR
  • TUFM

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

Cite this

The NLR protein, NLRX1, and its partner, TUFM, reduce type I interferon, and enhance autophagy. / Lei, Yu; Wen, Haitao; Ting, Jenny P.Y.

In: Autophagy, Vol. 9, No. 3, 03.2013, p. 432-433.

Research output: Contribution to journalArticle

Lei, Yu ; Wen, Haitao ; Ting, Jenny P.Y. / The NLR protein, NLRX1, and its partner, TUFM, reduce type I interferon, and enhance autophagy. In: Autophagy. 2013 ; Vol. 9, No. 3. pp. 432-433.
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