NLRX1/NOD5 deficiency does not affect MAVS signalling (original) (raw)

Cell Death & Differentiation volume 18, page 1387 (2011)Cite this article

Subjects

Dear Editor,

NLRX1/NOD5 belongs to the NOD clade of the NOD-like receptor (NLR) family. NLRs have emerged as key intracellular sensors for pathogen-derived molecules and endogenous danger signals to activate innate immune responses and inflammation. However, the function of most of these receptors still remains unclear.1 Beside the NACHT and LRR domains present in most NLRs, NLRX1/NOD5 possesses a _N_-terminal mitochondrial targeting sequence.2, 3 The function of NLRX1/NOD5 is still controversial; one study proposed that NLRX1/NOD5 inhibits the RIG-like receptor (RLR) antiviral pathways by binding the adaptor protein MAVS/IPS-1/Cardif/VISA,2 whereas another report implicated NLRX1/NOD5 in the generation of reactive oxygen species (ROS) and the amplification of NF-_κ_B and JNK activation triggered by different stimuli such TNF-α, poly (I:C) and Shigella infection.3 Interestingly, a recent study proposed that NLRX1/NOD5 is imported to the mitochondrial matrix, making NLRX1/NOD5 interaction with the outer mitochondrial membrane protein MAVS difficult to explain.4

References

  1. Schroder K, Tschopp J . Cell 2010; 140: 821–832.
    Article CAS Google Scholar
  2. Moore CB et al. Nature 2008; 451: 573–577.
  3. Tattoli I et al. EMBO Rep 2008; 9: 293–300.
  4. Arnoult D et al. J Cell Sci 2009; 122 (Part 17): 3161–3168.
  5. Sun Q et al. Immunity 2006; 24: 633–642.
  6. Kumar H et al. J Immunol 2010; 186: 994–1000.
  7. Cui J et al. Cell 2010; 141: 483–496.
  8. Abdul-Sater AA et al. J Biol Chem 2010; 285: 41637–41645.

Download references

Acknowledgements

We thank Professor Jürg Tschopp for the inspiring mentorship and great support over the years. This work was supported by grants from the Swiss National Science Foundation (FNRS 3100A0-128658/1), the Association ‘Institute for Arthritis Research’, the Foundation Louis-Jeantet, and the University of Lausanne.

Author information

Author notes

  1. J Tschopp: Deceased.

Authors and Affiliations

  1. Department of Biochemistry, University of Lausanne, Epalinges, CH-1066, Switzerland
    M Rebsamen, J Vazquez, A Tardivel, G Guarda & J Tschopp
  2. Department of Microbiology and Molecular Medicine, Faculty of Medicine, University of Geneva, Geneva 4 CH-1211, Switzerland,
    J Curran

Authors

  1. M Rebsamen
  2. J Vazquez
  3. A Tardivel
  4. G Guarda
  5. J Curran
  6. J Tschopp

Corresponding author

Correspondence toM Rebsamen.

Ethics declarations

Competing interests

The authors declare no conflict of interest.

Additional information

Supplementary Information accompanies the paper on Cell Death and Differentiation website

Supplementary information

Rights and permissions

About this article

Cite this article

Rebsamen, M., Vazquez, J., Tardivel, A. et al. NLRX1/NOD5 deficiency does not affect MAVS signalling.Cell Death Differ 18, 1387 (2011). https://doi.org/10.1038/cdd.2011.64

Download citation

This article is cited by