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Peptidoglycan recognition proteins: pleiotropic sensors and effectors of antimicrobial defences

Peptidoglycan recognition proteins (PGRPs) are innate immune receptors that are highly conserved from insects to mammals. Recent studies have revealed that, despite this conservation, insect and mammalian PGRPs defend host cells against infection by different mechanisms. Julien Royet and Roman Dziarski review these contrasting modes of action.

Julien Royet
Roman Dziarski
Reviews01 Apr 2007
Nature Reviews Microbiology

Volume: 5, P: 264-277
Peptidoglycan recognition proteins: modulators of the microbiome and inflammation

This Review discusses how invertebrate and vertebrate members of the PGRP family have developed an amazing variety of mechanisms to coordinate the host response to mutualistic, commensal and parasitic microorganisms.

Julien Royet
Dipika Gupta
Roman Dziarski
Reviews11 Nov 2011
Nature Reviews Immunology

Volume: 11, P: 837-851
Peptidoglycan recognition proteins kill bacteria by activating protein-sensing two-component systems

Mammalian peptidoglycan recognition proteins (PGRPs) are innate immune effectors that kill bacteria by unclear mechanisms. Kashyap et al. now provide insight into this question and report that PGRPs activate the bacterial two-component system that normally rids the cell of unfolded proteins. PGRP activation of this system abrogates metabolic functions, leading to accumulation of hydroxyl radicals and bacterial cell death.

Des Raj Kashyap
Minhui Wang
Roman Dziarski
Research22 May 2011
Nature Medicine

Volume: 17, P: 676-683
Deadly plague versus mild-mannered TLR4

Yersinia pestis evades lipopolysaccharide (LPS)-induced inflammation and establishes deadly infection mediated by myriad virulence factors. Virulence can be completely neutralized, however, if Y. pestis expresses a Toll-like receptor 4–stimulating LPS.

Roman Dziarski
News & Views01 Oct 2006
Nature Immunology

Volume: 7, P: 1017-1019
Nod2 protects mice from inflammation and obesity-dependent liver cancer

Serdar A. Gurses
Sunil Banskar
Dipika Gupta
ResearchOpen Access25 Nov 2020
Scientific Reports

Volume: 10, P: 1-17
Respiratory chain components are required for peptidoglycan recognition protein-induced thiol depletion and killing in Bacillus subtilis and Escherichia coli

Chun-Kai Yang
Des R. Kashyap
Roman Dziarski
ResearchOpen Access08 Jan 2021
Scientific Reports

Volume: 11, P: 1-18
Formate dehydrogenase, ubiquinone, and cytochrome bd-I are required for peptidoglycan recognition protein-induced oxidative stress and killing in Escherichia coli

Des R. Kashyap
Dominik A. Kowalczyk
Roman Dziarski
ResearchOpen Access06 Feb 2020
Scientific Reports

Volume: 10, P: 1-16
Nod2 and Nod2-regulated microbiota protect BALB/c mice from diet-induced obesity and metabolic dysfunction

Ivan Rodriguez-Nunez
Tiffany Caluag
Dipika Gupta
ResearchOpen Access03 Apr 2017
Scientific Reports

Volume: 7, P: 1-18
Author Correction: Nod2 and Nod2-regulated microbiota protect BALB/c mice from diet-induced obesity and metabolic dysfunction

Ivan Rodriguez-Nunez
Tiffany Caluag
Dipika Gupta
Amendments and CorrectionsOpen Access16 Apr 2018
Scientific Reports

Volume: 8, P: 1-4

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Peptidoglycan recognition proteins: pleiotropic sensors and effectors of antimicrobial defences

Peptidoglycan recognition proteins: modulators of the microbiome and inflammation

Peptidoglycan recognition proteins kill bacteria by activating protein-sensing two-component systems

Deadly plague versus mild-mannered TLR4

Nod2 protects mice from inflammation and obesity-dependent liver cancer

Respiratory chain components are required for peptidoglycan recognition protein-induced thiol depletion and killing in Bacillus subtilis and Escherichia coli

Formate dehydrogenase, ubiquinone, and cytochrome bd-I are required for peptidoglycan recognition protein-induced oxidative stress and killing in Escherichia coli

Nod2 and Nod2-regulated microbiota protect BALB/c mice from diet-induced obesity and metabolic dysfunction

Author Correction: Nod2 and Nod2-regulated microbiota protect BALB/c mice from diet-induced obesity and metabolic dysfunction

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