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Signal sequences are short amino acid sequences that guide newly synthesized proteins to their proper location within the cell. Classical signal sequences are fifteen to sixty amino acids long and present at the N-terminus of a polypeptide chain. Each signal sequence has a conserved segment of basic residues towards their N terminus, a hydrophobic core, and a C-terminus rich in polar residues. The C-terminus also contains a signal cleavage site and features a -3 -1 sequence motif. The -3-1...
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Flow-sorting and Exome Sequencing of the Reed-Sternberg Cells of Classical Hodgkin Lymphoma
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Sort Your Self Out!

Carolina Uggenti1, Yanick J Crow2

  • 1Laboratory of Neurogenetics and Neuroinflammation, INSERM UMR1163, Institut Imagine, Paris, France.

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|February 10, 2018
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Summary
This summary is machine-generated.

Distinguishing viral from self-nucleic acids is key for immunity. Studies on MDA5 and ADAR1 show how this balance is disrupted, blurring self and non-self distinctions.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Effective antiviral immunity requires precise discrimination between foreign (viral) and self-derived nucleic acids.
  • Dysregulation in nucleic acid sensing can lead to autoimmune diseases.

Purpose of the Study:

  • To investigate the roles of MDA5 gain-of-function and ADAR1 loss-of-function in immune responses.
  • To explore how these genetic alterations impact the self/non-self discrimination critical for immunity and autoinflammation.

Main Methods:

  • Analysis of MDA5 gain-of-function mutations.
  • Assessment of ADAR1 deficiency models.
  • Examination of immune responses to nucleic acids in genetic models.

Main Results:

  • Gain of function in MDA5 leads to aberrant sensing of nucleic acids.
  • Loss of ADAR1 activity results in impaired discrimination of self-nucleic acids.
  • Both conditions contribute to a compromised self/non-self boundary.

Conclusions:

  • MDA5 and ADAR1 are critical regulators of nucleic acid sensing and immune homeostasis.
  • Disruptions in these pathways blur the lines between self and non-self, potentially driving autoinflammation.