ArticleVirulence2012
To UPR… and beyond! A new role for a BiP/GRP78 protein in the control of antimicrobial peptide expression in C. elegans epidermis.
Article in Virulence, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Immunity-linked genes are stimulated by a membrane stress pathway linked to Golgi function and the ARF-1 GTPase.Science advances · 2023Article
- Planarians (Platyhelminthes)-An Emerging Model Organism for Investigating Innate Immune Mechanisms.Frontiers in cellular and infection microbiology · 2021Review
- N,N'-dinitrosopiperazine--mediated heat-shock protein 70-2 expression is involved in metastasis of nasopharyngeal carcinoma.PloS one · 2013Article
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
The fungal pathogen Drechmeria coniospora infects C. elegans and elicits an innate immune response mediated, in part, by the induction of antimicrobial peptides in the epidermis. The signaling pathways controlling this phenomenon remain to be fully characterized. In this issue of Virulence, Couillault and colleagues use both proteomics and genetics to discover an unexpected role for the unfolded protein response (UPR) target chaperone BiP/GRP78/hsp-3 in the control of fungal infection-induced antimicrobial peptide expression in C. elegans. Although the expression of hsp-3 is regulated by the UPR, Couillault and colleagues describe a novel signaling role for this BiP/GRP78 homolog.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.