NLRX1 resides in mitochondrial RNA granules and regulates mitochondrial RNA processing and bioenergetic adaptation.

@article{Singh2018NLRX1RI,
  title={NLRX1 resides in mitochondrial RNA granules and regulates mitochondrial RNA processing and bioenergetic adaptation.},
  author={Kritarth Naman Singh and Lakshmi Sripada and A. V. Lipatova and Milton Roy and Paresh A. Prajapati and Dhruv Gohel and Khyati Bhatelia and Peter M. Chumakov and Rajesh Singh},
  journal={Biochimica et biophysica acta. Molecular cell research},
  year={2018},
  volume={1865 9},
  pages={
          1260-1276
        }
}
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TLDR
Recent research advances on the underlying mechanisms and related disorders behind the complex regulatory role of NLRX1 are reviewed, which may provide a promising target to prevent and/or treat the corresponding diseases.
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TLDR
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Sex-Biased Control of Inflammation and Metabolism by a Mitochondrial Nod-Like Receptor
TLDR
It is shown that in an infectious model with the human protozoan parasite, Leishmania guyanensis, NLRX1 attenuated inflammation in females but not in male mice, suggesting that NLRx1 prevents uncontrolled inflammation and metabolism in females and therefore may contribute to the sex differences observed in infectious and inflammatory diseases.
Behind the Scenes: Nod-Like Receptor X1 Controls Inflammation and Metabolism
TLDR
The current findings on NLRX1 are summarized and its role in both infectious and inflammatory context is discussed and a better understanding of the underlying mechanism is crucial for future research and development of novel therapeutic approaches.
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An N-terminal addressing sequence targets NLRX1 to the mitochondrial matrix
TLDR
These results provide the first identification of a protein belonging to the NLR family that is targeted to the mitochondrial matrix, and UQCRC2, a matrix-facing protein of the respiratory chain complex III, is identified as an NLRX1-interacting molecule, thus providing a molecular basis for the role of NLRx1 in ROS generation.
The NLR protein, NLRX1, and its partner, TUFM, reduce type I interferon, and enhance autophagy
TLDR
A role of NLRX1 in augmenting virus-induced autophagy is indicated through its interaction with another mitochondrial protein TUFM (Tu translation elongation factor, mitochondrial, also known as EF-TuMT, COXPD4, and P43), which reduces DDX58-activated cytokines but augments autophagic.
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Mitochondria emerge as a fundamental hub for innate immune signalling because mitochondrial alarmins—such as mitochondrial DNA and formyl peptides—can be released by damaged mitochondria and trigger inflammation.
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