Literature DB >> 18606143

Unfolded protein response genes regulated by CED-1 are required for Caenorhabditis elegans innate immunity.

Kylie A Haskins1, Jonathan F Russell, Nathan Gaddis, Holly K Dressman, Alejandro Aballay.   

Abstract

The endoplasmic reticulum stress response, also known as the unfolded protein response (UPR), has been implicated in the normal physiology of immune defense and in several disorders, including diabetes, cancer, and neurodegenerative disease. Here, we show that the apoptotic receptor CED-1 and a network of PQN/ABU proteins involved in a noncanonical UPR response are required for proper defense to pathogen infection in Caenorhabditis elegans. A full-genome microarray analysis indicates that CED-1 functions to activate the expression of pqn/abu genes. We also show that ced-1 and pqn/abu genes are required for the survival of C. elegans exposed to live Salmonella enterica, and that overexpression of pqn/abu genes confers protection against pathogen-mediated killing. The results indicate that unfolded protein response genes, regulated in a CED-1-dependent manner, are involved in the C. elegans immune response to live bacteria.

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Year:  2008        PMID: 18606143      PMCID: PMC2517226          DOI: 10.1016/j.devcel.2008.05.006

Source DB:  PubMed          Journal:  Dev Cell        ISSN: 1534-5807            Impact factor:   12.270


  55 in total

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Journal:  Nat Cell Biol       Date:  2000-03       Impact factor: 28.824

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Authors:  D J Hoeppner; M O Hengartner; R Schnabel
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Review 3.  Evolution of host innate defence: insights from Caenorhabditis elegans and primitive invertebrates.

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4.  Endoplasmic Reticulum Homeostasis and Stress Responses in Caenorhabditis elegans.

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Review 8.  The molecular basis of organ formation: insights from the C. elegans foregut.

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10.  Nucleolar proteins suppress Caenorhabditis elegans innate immunity by inhibiting p53/CEP-1.

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