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Related Concept Videos

Autophagy01:27

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Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
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siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
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TRIM-directed selective autophagy regulates immune activation.

Tomonori Kimura1, Ashish Jain2, Seong Won Choi1

  • 1a Department of Molecular Genetics and Microbiology , University of New Mexico Health Sciences Center , Albuquerque , NM , USA.

Autophagy
|March 18, 2016
PubMed
Summary

Tripartite motif (TRIM) proteins like MEFV/TRIM20 and TRIM21 act as novel autophagy receptors. They selectively degrade inflammatory signaling regulators, offering new therapeutic targets for inflammatory diseases.

Keywords:
BEC1IRF3ULK1autophagy receptorsfamilial Mediterranean feverinflammasomeinterferoninterleukin-1βtripartite motif class of proteins (TRIMs)

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Area of Science:

  • Cell Biology
  • Immunology
  • Molecular Biology

Background:

  • Selective autophagy relies on specific receptor-mediated target recognition.
  • The known repertoire of autophagy receptors is limited, hindering a full understanding of cellular regulation.
  • Inflammatory signaling pathways are crucial in disease but require precise control.

Purpose of the Study:

  • To identify novel autophagy receptors involved in regulating inflammatory signaling.
  • To elucidate the mechanism by which tripartite motif (TRIM) proteins mediate selective autophagy.
  • To investigate the role of MEFV/TRIM20 and TRIM21 in inflammasome and interferon responses.

Main Methods:

  • Utilized biochemical assays to identify protein-protein interactions.
  • Employed cell-based models to study autophagic degradation pathways.
  • Investigated the function of MEFV and TRIM21 in inflammatory signaling using genetic and molecular approaches.

Main Results:

  • Demonstrated that MEFV/TRIM20 and TRIM21 function as autophagic receptors.
  • MEFV/TRIM20 recognizes inflammasome components (NLRP3, CASP1, NLRP1), while TRIM21 recognizes activated IRF3.
  • Both proteins recruit and organize core autophagy machinery, with MEFV mutations impacting this function.

Conclusions:

  • TRIM proteins act as a general class of "autophagic receptor-regulators" mediating "precision autophagy".
  • MEFV/TRIM20 suppresses inflammasome activation and pyroptosis, while TRIM21 dampens type I interferon responses.
  • These findings reveal a novel mechanism for controlling inflammation and offer potential therapeutic strategies.