Commensal bacteria make GPCR ligands that mimic human signalling molecules

Commensal bacteria are believed to have important roles in human health. The mechanisms by which they affect mammalian physiology remain poorly understood, but bacterial metabolites are likely to be key components of host interactions. Here we use bioinformatics and synthetic biology to mine the hum...
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Autor*in:	Cohen, Louis J [verfasserIn] Esterhazy, Daria Kim, Seong-Hwan Lemetre, Christophe Aguilar, Rhiannon R Gordon, Emma A Pickard, Amanda J Cross, Justin R Emiliano, Ana B Han, Sun M Chu, John Vila-Farres, Xavier Kaplitt, Jeremy Rogoz, Aneta Calle, Paula Y Hunter, Craig Bitok, J. Kipchirchir Brady, Sean F

Format:	Artikel
Sprache:	Englisch

Erschienen:	2017

Schlagwörter:	Bacteria Ligands (Biochemistry) Microbiota (Symbiotic organisms) Physiological aspects Disease Gene therapy Lipids Physiology Receptors Animal models Enzymes Metabolites Cell culture Homeostasis Hormones Amides Genes G protein-coupled receptors Genetic engineering Proteins Peptides Bioinformatics Gastrointestinal tract Metabolism Ligands Signalling

Übergeordnetes Werk:	Enthalten in: Nature - London : Macmillan Publishers Limited, part of Springer Nature, 1869, 549(2017), 7670, Seite 48
Übergeordnetes Werk:	volume:549 ; year:2017 ; number:7670 ; pages:48

Links:	Volltext Link aufrufen

DOI / URN:	10.1038/nature23874

Katalog-ID:	OLC1997471329

Internformat


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520			\|a Commensal bacteria are believed to have important roles in human health. The mechanisms by which they affect mammalian physiology remain poorly understood, but bacterial metabolites are likely to be key components of host interactions. Here we use bioinformatics and synthetic biology to mine the human microbiota for N-acyl amides that interact with G-protein-coupled receptors (GPCRs). We found that N-acyl amide synthase genes are enriched in gastrointestinal bacteria and the lipids that they encode interact with GPCRs that regulate gastrointestinal tract physiology. Mouse and cell-based models demonstrate that commensal GPR119 agonists regulate metabolic hormones and glucose homeostasis as efficiently as human ligands, although future studies are needed to define their potential physiological role in humans. Our results suggest that chemical mimicry of eukaryotic signalling molecules may be common among commensal bacteria and that manipulation of microbiota genes encoding metabolites that elicit host cellular responses represents a possible small-molecule therapeutic modality (microbiome-biosynthetic gene therapy).
650		4	\|a Bacteria
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allfields	10.1038/nature23874 doi PQ20171228 (DE-627)OLC1997471329 (DE-599)GBVOLC1997471329 (PRQ)g1460-4791a12984c907580add0c21178402360c6330b7444030c7bd255664f77ca2250 (KEY)0072945020170000549767000048commensalbacteriamakegpcrligandsthatmimichumansign DE-627 ger DE-627 rakwb eng 070 500 DE-101 500 AVZ BIODIV fid Cohen, Louis J verfasserin aut Commensal bacteria make GPCR ligands that mimic human signalling molecules 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Commensal bacteria are believed to have important roles in human health. The mechanisms by which they affect mammalian physiology remain poorly understood, but bacterial metabolites are likely to be key components of host interactions. Here we use bioinformatics and synthetic biology to mine the human microbiota for N-acyl amides that interact with G-protein-coupled receptors (GPCRs). We found that N-acyl amide synthase genes are enriched in gastrointestinal bacteria and the lipids that they encode interact with GPCRs that regulate gastrointestinal tract physiology. Mouse and cell-based models demonstrate that commensal GPR119 agonists regulate metabolic hormones and glucose homeostasis as efficiently as human ligands, although future studies are needed to define their potential physiological role in humans. Our results suggest that chemical mimicry of eukaryotic signalling molecules may be common among commensal bacteria and that manipulation of microbiota genes encoding metabolites that elicit host cellular responses represents a possible small-molecule therapeutic modality (microbiome-biosynthetic gene therapy). Bacteria Ligands (Biochemistry) Microbiota (Symbiotic organisms) Physiological aspects Disease Gene therapy Lipids Physiology Receptors Animal models Enzymes Metabolites Cell culture Homeostasis Hormones Amides Genes G protein-coupled receptors Genetic engineering Proteins Peptides Bioinformatics Gastrointestinal tract Metabolism Ligands Signalling Esterhazy, Daria oth Kim, Seong-Hwan oth Lemetre, Christophe oth Aguilar, Rhiannon R oth Gordon, Emma A oth Pickard, Amanda J oth Cross, Justin R oth Emiliano, Ana B oth Han, Sun M oth Chu, John oth Vila-Farres, Xavier oth Kaplitt, Jeremy oth Rogoz, Aneta oth Calle, Paula Y oth Hunter, Craig oth Bitok, J. Kipchirchir oth Brady, Sean F oth Enthalten in Nature London : Macmillan Publishers Limited, part of Springer Nature, 1869 549(2017), 7670, Seite 48 (DE-627)129292834 (DE-600)120714-3 (DE-576)014473941 0028-0836 nnns volume:549 year:2017 number:7670 pages:48 http://dx.doi.org/10.1038/nature23874 Volltext https://search.proquest.com/docview/1937363162 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_22 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_135 GBV_ILN_154 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_252 GBV_ILN_290 GBV_ILN_294 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2002 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2016 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2095 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4320 GBV_ILN_4324 AR 549 2017 7670 48
spelling	10.1038/nature23874 doi PQ20171228 (DE-627)OLC1997471329 (DE-599)GBVOLC1997471329 (PRQ)g1460-4791a12984c907580add0c21178402360c6330b7444030c7bd255664f77ca2250 (KEY)0072945020170000549767000048commensalbacteriamakegpcrligandsthatmimichumansign DE-627 ger DE-627 rakwb eng 070 500 DE-101 500 AVZ BIODIV fid Cohen, Louis J verfasserin aut Commensal bacteria make GPCR ligands that mimic human signalling molecules 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Commensal bacteria are believed to have important roles in human health. The mechanisms by which they affect mammalian physiology remain poorly understood, but bacterial metabolites are likely to be key components of host interactions. Here we use bioinformatics and synthetic biology to mine the human microbiota for N-acyl amides that interact with G-protein-coupled receptors (GPCRs). We found that N-acyl amide synthase genes are enriched in gastrointestinal bacteria and the lipids that they encode interact with GPCRs that regulate gastrointestinal tract physiology. Mouse and cell-based models demonstrate that commensal GPR119 agonists regulate metabolic hormones and glucose homeostasis as efficiently as human ligands, although future studies are needed to define their potential physiological role in humans. Our results suggest that chemical mimicry of eukaryotic signalling molecules may be common among commensal bacteria and that manipulation of microbiota genes encoding metabolites that elicit host cellular responses represents a possible small-molecule therapeutic modality (microbiome-biosynthetic gene therapy). Bacteria Ligands (Biochemistry) Microbiota (Symbiotic organisms) Physiological aspects Disease Gene therapy Lipids Physiology Receptors Animal models Enzymes Metabolites Cell culture Homeostasis Hormones Amides Genes G protein-coupled receptors Genetic engineering Proteins Peptides Bioinformatics Gastrointestinal tract Metabolism Ligands Signalling Esterhazy, Daria oth Kim, Seong-Hwan oth Lemetre, Christophe oth Aguilar, Rhiannon R oth Gordon, Emma A oth Pickard, Amanda J oth Cross, Justin R oth Emiliano, Ana B oth Han, Sun M oth Chu, John oth Vila-Farres, Xavier oth Kaplitt, Jeremy oth Rogoz, Aneta oth Calle, Paula Y oth Hunter, Craig oth Bitok, J. Kipchirchir oth Brady, Sean F oth Enthalten in Nature London : Macmillan Publishers Limited, part of Springer Nature, 1869 549(2017), 7670, Seite 48 (DE-627)129292834 (DE-600)120714-3 (DE-576)014473941 0028-0836 nnns volume:549 year:2017 number:7670 pages:48 http://dx.doi.org/10.1038/nature23874 Volltext https://search.proquest.com/docview/1937363162 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_22 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_135 GBV_ILN_154 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_252 GBV_ILN_290 GBV_ILN_294 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2002 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2016 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2095 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4320 GBV_ILN_4324 AR 549 2017 7670 48
allfields_unstemmed	10.1038/nature23874 doi PQ20171228 (DE-627)OLC1997471329 (DE-599)GBVOLC1997471329 (PRQ)g1460-4791a12984c907580add0c21178402360c6330b7444030c7bd255664f77ca2250 (KEY)0072945020170000549767000048commensalbacteriamakegpcrligandsthatmimichumansign DE-627 ger DE-627 rakwb eng 070 500 DE-101 500 AVZ BIODIV fid Cohen, Louis J verfasserin aut Commensal bacteria make GPCR ligands that mimic human signalling molecules 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Commensal bacteria are believed to have important roles in human health. The mechanisms by which they affect mammalian physiology remain poorly understood, but bacterial metabolites are likely to be key components of host interactions. Here we use bioinformatics and synthetic biology to mine the human microbiota for N-acyl amides that interact with G-protein-coupled receptors (GPCRs). We found that N-acyl amide synthase genes are enriched in gastrointestinal bacteria and the lipids that they encode interact with GPCRs that regulate gastrointestinal tract physiology. Mouse and cell-based models demonstrate that commensal GPR119 agonists regulate metabolic hormones and glucose homeostasis as efficiently as human ligands, although future studies are needed to define their potential physiological role in humans. Our results suggest that chemical mimicry of eukaryotic signalling molecules may be common among commensal bacteria and that manipulation of microbiota genes encoding metabolites that elicit host cellular responses represents a possible small-molecule therapeutic modality (microbiome-biosynthetic gene therapy). Bacteria Ligands (Biochemistry) Microbiota (Symbiotic organisms) Physiological aspects Disease Gene therapy Lipids Physiology Receptors Animal models Enzymes Metabolites Cell culture Homeostasis Hormones Amides Genes G protein-coupled receptors Genetic engineering Proteins Peptides Bioinformatics Gastrointestinal tract Metabolism Ligands Signalling Esterhazy, Daria oth Kim, Seong-Hwan oth Lemetre, Christophe oth Aguilar, Rhiannon R oth Gordon, Emma A oth Pickard, Amanda J oth Cross, Justin R oth Emiliano, Ana B oth Han, Sun M oth Chu, John oth Vila-Farres, Xavier oth Kaplitt, Jeremy oth Rogoz, Aneta oth Calle, Paula Y oth Hunter, Craig oth Bitok, J. Kipchirchir oth Brady, Sean F oth Enthalten in Nature London : Macmillan Publishers Limited, part of Springer Nature, 1869 549(2017), 7670, Seite 48 (DE-627)129292834 (DE-600)120714-3 (DE-576)014473941 0028-0836 nnns volume:549 year:2017 number:7670 pages:48 http://dx.doi.org/10.1038/nature23874 Volltext https://search.proquest.com/docview/1937363162 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_22 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_135 GBV_ILN_154 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_252 GBV_ILN_290 GBV_ILN_294 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2002 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2016 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2095 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4320 GBV_ILN_4324 AR 549 2017 7670 48
allfieldsGer	10.1038/nature23874 doi PQ20171228 (DE-627)OLC1997471329 (DE-599)GBVOLC1997471329 (PRQ)g1460-4791a12984c907580add0c21178402360c6330b7444030c7bd255664f77ca2250 (KEY)0072945020170000549767000048commensalbacteriamakegpcrligandsthatmimichumansign DE-627 ger DE-627 rakwb eng 070 500 DE-101 500 AVZ BIODIV fid Cohen, Louis J verfasserin aut Commensal bacteria make GPCR ligands that mimic human signalling molecules 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Commensal bacteria are believed to have important roles in human health. The mechanisms by which they affect mammalian physiology remain poorly understood, but bacterial metabolites are likely to be key components of host interactions. Here we use bioinformatics and synthetic biology to mine the human microbiota for N-acyl amides that interact with G-protein-coupled receptors (GPCRs). We found that N-acyl amide synthase genes are enriched in gastrointestinal bacteria and the lipids that they encode interact with GPCRs that regulate gastrointestinal tract physiology. Mouse and cell-based models demonstrate that commensal GPR119 agonists regulate metabolic hormones and glucose homeostasis as efficiently as human ligands, although future studies are needed to define their potential physiological role in humans. Our results suggest that chemical mimicry of eukaryotic signalling molecules may be common among commensal bacteria and that manipulation of microbiota genes encoding metabolites that elicit host cellular responses represents a possible small-molecule therapeutic modality (microbiome-biosynthetic gene therapy). Bacteria Ligands (Biochemistry) Microbiota (Symbiotic organisms) Physiological aspects Disease Gene therapy Lipids Physiology Receptors Animal models Enzymes Metabolites Cell culture Homeostasis Hormones Amides Genes G protein-coupled receptors Genetic engineering Proteins Peptides Bioinformatics Gastrointestinal tract Metabolism Ligands Signalling Esterhazy, Daria oth Kim, Seong-Hwan oth Lemetre, Christophe oth Aguilar, Rhiannon R oth Gordon, Emma A oth Pickard, Amanda J oth Cross, Justin R oth Emiliano, Ana B oth Han, Sun M oth Chu, John oth Vila-Farres, Xavier oth Kaplitt, Jeremy oth Rogoz, Aneta oth Calle, Paula Y oth Hunter, Craig oth Bitok, J. Kipchirchir oth Brady, Sean F oth Enthalten in Nature London : Macmillan Publishers Limited, part of Springer Nature, 1869 549(2017), 7670, Seite 48 (DE-627)129292834 (DE-600)120714-3 (DE-576)014473941 0028-0836 nnns volume:549 year:2017 number:7670 pages:48 http://dx.doi.org/10.1038/nature23874 Volltext https://search.proquest.com/docview/1937363162 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_22 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_135 GBV_ILN_154 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_252 GBV_ILN_290 GBV_ILN_294 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2002 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2016 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2095 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4320 GBV_ILN_4324 AR 549 2017 7670 48
allfieldsSound	10.1038/nature23874 doi PQ20171228 (DE-627)OLC1997471329 (DE-599)GBVOLC1997471329 (PRQ)g1460-4791a12984c907580add0c21178402360c6330b7444030c7bd255664f77ca2250 (KEY)0072945020170000549767000048commensalbacteriamakegpcrligandsthatmimichumansign DE-627 ger DE-627 rakwb eng 070 500 DE-101 500 AVZ BIODIV fid Cohen, Louis J verfasserin aut Commensal bacteria make GPCR ligands that mimic human signalling molecules 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Commensal bacteria are believed to have important roles in human health. The mechanisms by which they affect mammalian physiology remain poorly understood, but bacterial metabolites are likely to be key components of host interactions. Here we use bioinformatics and synthetic biology to mine the human microbiota for N-acyl amides that interact with G-protein-coupled receptors (GPCRs). We found that N-acyl amide synthase genes are enriched in gastrointestinal bacteria and the lipids that they encode interact with GPCRs that regulate gastrointestinal tract physiology. Mouse and cell-based models demonstrate that commensal GPR119 agonists regulate metabolic hormones and glucose homeostasis as efficiently as human ligands, although future studies are needed to define their potential physiological role in humans. Our results suggest that chemical mimicry of eukaryotic signalling molecules may be common among commensal bacteria and that manipulation of microbiota genes encoding metabolites that elicit host cellular responses represents a possible small-molecule therapeutic modality (microbiome-biosynthetic gene therapy). Bacteria Ligands (Biochemistry) Microbiota (Symbiotic organisms) Physiological aspects Disease Gene therapy Lipids Physiology Receptors Animal models Enzymes Metabolites Cell culture Homeostasis Hormones Amides Genes G protein-coupled receptors Genetic engineering Proteins Peptides Bioinformatics Gastrointestinal tract Metabolism Ligands Signalling Esterhazy, Daria oth Kim, Seong-Hwan oth Lemetre, Christophe oth Aguilar, Rhiannon R oth Gordon, Emma A oth Pickard, Amanda J oth Cross, Justin R oth Emiliano, Ana B oth Han, Sun M oth Chu, John oth Vila-Farres, Xavier oth Kaplitt, Jeremy oth Rogoz, Aneta oth Calle, Paula Y oth Hunter, Craig oth Bitok, J. Kipchirchir oth Brady, Sean F oth Enthalten in Nature London : Macmillan Publishers Limited, part of Springer Nature, 1869 549(2017), 7670, Seite 48 (DE-627)129292834 (DE-600)120714-3 (DE-576)014473941 0028-0836 nnns volume:549 year:2017 number:7670 pages:48 http://dx.doi.org/10.1038/nature23874 Volltext https://search.proquest.com/docview/1937363162 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_22 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_135 GBV_ILN_154 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_252 GBV_ILN_290 GBV_ILN_294 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2002 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2016 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2095 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4320 GBV_ILN_4324 AR 549 2017 7670 48
language	English
source	Enthalten in Nature 549(2017), 7670, Seite 48 volume:549 year:2017 number:7670 pages:48
sourceStr	Enthalten in Nature 549(2017), 7670, Seite 48 volume:549 year:2017 number:7670 pages:48
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Bacteria Ligands (Biochemistry) Microbiota (Symbiotic organisms) Physiological aspects Disease Gene therapy Lipids Physiology Receptors Animal models Enzymes Metabolites Cell culture Homeostasis Hormones Amides Genes G protein-coupled receptors Genetic engineering Proteins Peptides Bioinformatics Gastrointestinal tract Metabolism Ligands Signalling
dewey-raw	070
isfreeaccess_bool	false
container_title	Nature
authorswithroles_txt_mv	Cohen, Louis J @@aut@@ Esterhazy, Daria @@oth@@ Kim, Seong-Hwan @@oth@@ Lemetre, Christophe @@oth@@ Aguilar, Rhiannon R @@oth@@ Gordon, Emma A @@oth@@ Pickard, Amanda J @@oth@@ Cross, Justin R @@oth@@ Emiliano, Ana B @@oth@@ Han, Sun M @@oth@@ Chu, John @@oth@@ Vila-Farres, Xavier @@oth@@ Kaplitt, Jeremy @@oth@@ Rogoz, Aneta @@oth@@ Calle, Paula Y @@oth@@ Hunter, Craig @@oth@@ Bitok, J. Kipchirchir @@oth@@ Brady, Sean F @@oth@@
publishDateDaySort_date	2017-01-01T00:00:00Z
hierarchy_top_id	129292834
dewey-sort	270
id	OLC1997471329
language_de	englisch
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author	Cohen, Louis J
spellingShingle	Cohen, Louis J ddc 070 ddc 500 fid BIODIV misc Bacteria misc Ligands (Biochemistry) misc Microbiota (Symbiotic organisms) misc Physiological aspects misc Disease misc Gene therapy misc Lipids misc Physiology misc Receptors misc Animal models misc Enzymes misc Metabolites misc Cell culture misc Homeostasis misc Hormones misc Amides misc Genes misc G protein-coupled receptors misc Genetic engineering misc Proteins misc Peptides misc Bioinformatics misc Gastrointestinal tract misc Metabolism misc Ligands misc Signalling Commensal bacteria make GPCR ligands that mimic human signalling molecules
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topic_title	070 500 DE-101 500 AVZ BIODIV fid Commensal bacteria make GPCR ligands that mimic human signalling molecules Bacteria Ligands (Biochemistry) Microbiota (Symbiotic organisms) Physiological aspects Disease Gene therapy Lipids Physiology Receptors Animal models Enzymes Metabolites Cell culture Homeostasis Hormones Amides Genes G protein-coupled receptors Genetic engineering Proteins Peptides Bioinformatics Gastrointestinal tract Metabolism Ligands Signalling
topic	ddc 070 ddc 500 fid BIODIV misc Bacteria misc Ligands (Biochemistry) misc Microbiota (Symbiotic organisms) misc Physiological aspects misc Disease misc Gene therapy misc Lipids misc Physiology misc Receptors misc Animal models misc Enzymes misc Metabolites misc Cell culture misc Homeostasis misc Hormones misc Amides misc Genes misc G protein-coupled receptors misc Genetic engineering misc Proteins misc Peptides misc Bioinformatics misc Gastrointestinal tract misc Metabolism misc Ligands misc Signalling
topic_unstemmed	ddc 070 ddc 500 fid BIODIV misc Bacteria misc Ligands (Biochemistry) misc Microbiota (Symbiotic organisms) misc Physiological aspects misc Disease misc Gene therapy misc Lipids misc Physiology misc Receptors misc Animal models misc Enzymes misc Metabolites misc Cell culture misc Homeostasis misc Hormones misc Amides misc Genes misc G protein-coupled receptors misc Genetic engineering misc Proteins misc Peptides misc Bioinformatics misc Gastrointestinal tract misc Metabolism misc Ligands misc Signalling
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title	Commensal bacteria make GPCR ligands that mimic human signalling molecules
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title_full	Commensal bacteria make GPCR ligands that mimic human signalling molecules
author_sort	Cohen, Louis J
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title_sort	commensal bacteria make gpcr ligands that mimic human signalling molecules
title_auth	Commensal bacteria make GPCR ligands that mimic human signalling molecules
abstract	Commensal bacteria are believed to have important roles in human health. The mechanisms by which they affect mammalian physiology remain poorly understood, but bacterial metabolites are likely to be key components of host interactions. Here we use bioinformatics and synthetic biology to mine the human microbiota for N-acyl amides that interact with G-protein-coupled receptors (GPCRs). We found that N-acyl amide synthase genes are enriched in gastrointestinal bacteria and the lipids that they encode interact with GPCRs that regulate gastrointestinal tract physiology. Mouse and cell-based models demonstrate that commensal GPR119 agonists regulate metabolic hormones and glucose homeostasis as efficiently as human ligands, although future studies are needed to define their potential physiological role in humans. Our results suggest that chemical mimicry of eukaryotic signalling molecules may be common among commensal bacteria and that manipulation of microbiota genes encoding metabolites that elicit host cellular responses represents a possible small-molecule therapeutic modality (microbiome-biosynthetic gene therapy).
abstractGer	Commensal bacteria are believed to have important roles in human health. The mechanisms by which they affect mammalian physiology remain poorly understood, but bacterial metabolites are likely to be key components of host interactions. Here we use bioinformatics and synthetic biology to mine the human microbiota for N-acyl amides that interact with G-protein-coupled receptors (GPCRs). We found that N-acyl amide synthase genes are enriched in gastrointestinal bacteria and the lipids that they encode interact with GPCRs that regulate gastrointestinal tract physiology. Mouse and cell-based models demonstrate that commensal GPR119 agonists regulate metabolic hormones and glucose homeostasis as efficiently as human ligands, although future studies are needed to define their potential physiological role in humans. Our results suggest that chemical mimicry of eukaryotic signalling molecules may be common among commensal bacteria and that manipulation of microbiota genes encoding metabolites that elicit host cellular responses represents a possible small-molecule therapeutic modality (microbiome-biosynthetic gene therapy).
abstract_unstemmed	Commensal bacteria are believed to have important roles in human health. The mechanisms by which they affect mammalian physiology remain poorly understood, but bacterial metabolites are likely to be key components of host interactions. Here we use bioinformatics and synthetic biology to mine the human microbiota for N-acyl amides that interact with G-protein-coupled receptors (GPCRs). We found that N-acyl amide synthase genes are enriched in gastrointestinal bacteria and the lipids that they encode interact with GPCRs that regulate gastrointestinal tract physiology. Mouse and cell-based models demonstrate that commensal GPR119 agonists regulate metabolic hormones and glucose homeostasis as efficiently as human ligands, although future studies are needed to define their potential physiological role in humans. Our results suggest that chemical mimicry of eukaryotic signalling molecules may be common among commensal bacteria and that manipulation of microbiota genes encoding metabolites that elicit host cellular responses represents a possible small-molecule therapeutic modality (microbiome-biosynthetic gene therapy).
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title_short	Commensal bacteria make GPCR ligands that mimic human signalling molecules
url	http://dx.doi.org/10.1038/nature23874 https://search.proquest.com/docview/1937363162
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author2	Esterhazy, Daria Kim, Seong-Hwan Lemetre, Christophe Aguilar, Rhiannon R Gordon, Emma A Pickard, Amanda J Cross, Justin R Emiliano, Ana B Han, Sun M Chu, John Vila-Farres, Xavier Kaplitt, Jeremy Rogoz, Aneta Calle, Paula Y Hunter, Craig Bitok, J. Kipchirchir Brady, Sean F
author2Str	Esterhazy, Daria Kim, Seong-Hwan Lemetre, Christophe Aguilar, Rhiannon R Gordon, Emma A Pickard, Amanda J Cross, Justin R Emiliano, Ana B Han, Sun M Chu, John Vila-Farres, Xavier Kaplitt, Jeremy Rogoz, Aneta Calle, Paula Y Hunter, Craig Bitok, J. Kipchirchir Brady, Sean F
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up_date	2024-07-04T02:59:09.537Z
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Commensal bacteria make GPCR ligands that mimic human signalling molecules

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