Multiple acyl-CoA dehydrogenase deficiency kills Mycobacterium tuberculosis in vitro and during infection

The pathogen Mycobacterium tuberculosis depends on host fatty acids and cholesterol as carbon sources. Here, Beites et al. identify a protein complex that is essential for fatty acid and cholesterol utilization and thus for survival of M. tuberculosis during infection, supporting this pathway as a p...

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Autores principales:	Tiago Beites, Robert S. Jansen, Ruojun Wang, Adrian Jinich, Kyu Y. Rhee, Dirk Schnappinger, Sabine Ehrt
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/56aca39f6d034a83b6674d2ac18e0572
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spelling	oai:doaj.org-article:56aca39f6d034a83b6674d2ac18e05722021-11-21T12:34:14ZMultiple acyl-CoA dehydrogenase deficiency kills Mycobacterium tuberculosis in vitro and during infection10.1038/s41467-021-26941-12041-1723https://doaj.org/article/56aca39f6d034a83b6674d2ac18e05722021-11-01T00:00:00Zhttps://doi.org/10.1038/s41467-021-26941-1https://doaj.org/toc/2041-1723The pathogen Mycobacterium tuberculosis depends on host fatty acids and cholesterol as carbon sources. Here, Beites et al. identify a protein complex that is essential for fatty acid and cholesterol utilization and thus for survival of M. tuberculosis during infection, supporting this pathway as a potential target for tuberculosis drug development.Tiago BeitesRobert S. JansenRuojun WangAdrian JinichKyu Y. RheeDirk SchnappingerSabine EhrtNature PortfolioarticleScienceQENNature Communications, Vol 12, Iss 1, Pp 1-10 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Tiago Beites Robert S. Jansen Ruojun Wang Adrian Jinich Kyu Y. Rhee Dirk Schnappinger Sabine Ehrt Multiple acyl-CoA dehydrogenase deficiency kills Mycobacterium tuberculosis in vitro and during infection
description	The pathogen Mycobacterium tuberculosis depends on host fatty acids and cholesterol as carbon sources. Here, Beites et al. identify a protein complex that is essential for fatty acid and cholesterol utilization and thus for survival of M. tuberculosis during infection, supporting this pathway as a potential target for tuberculosis drug development.
format	article
author	Tiago Beites Robert S. Jansen Ruojun Wang Adrian Jinich Kyu Y. Rhee Dirk Schnappinger Sabine Ehrt
author_facet	Tiago Beites Robert S. Jansen Ruojun Wang Adrian Jinich Kyu Y. Rhee Dirk Schnappinger Sabine Ehrt
author_sort	Tiago Beites
title	Multiple acyl-CoA dehydrogenase deficiency kills Mycobacterium tuberculosis in vitro and during infection
title_short	Multiple acyl-CoA dehydrogenase deficiency kills Mycobacterium tuberculosis in vitro and during infection
title_full	Multiple acyl-CoA dehydrogenase deficiency kills Mycobacterium tuberculosis in vitro and during infection
title_fullStr	Multiple acyl-CoA dehydrogenase deficiency kills Mycobacterium tuberculosis in vitro and during infection
title_full_unstemmed	Multiple acyl-CoA dehydrogenase deficiency kills Mycobacterium tuberculosis in vitro and during infection
title_sort	multiple acyl-coa dehydrogenase deficiency kills mycobacterium tuberculosis in vitro and during infection
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/56aca39f6d034a83b6674d2ac18e0572
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Multiple acyl-CoA dehydrogenase deficiency kills Mycobacterium tuberculosis in vitro and during infection

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