FIH Regulates Cellular Metabolism through Hydroxylation of the Deubiquitinase OTUB1.

The asparagine hydroxylase, factor inhibiting HIF (FIH), confers oxygen-dependence upon the hypoxia-inducible factor (HIF), a master regulator of the cellular adaptive response to hypoxia. Studies investigating whether asparagine hydroxylation is a general regulatory oxygen-dependent modification ha...

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Main Authors: Carsten C Scholz, Javier Rodriguez, Christina Pickel, Stephen Burr, Jacqueline-Alba Fabrizio, Karen A Nolan, Patrick Spielmann, Miguel A S Cavadas, Bianca Crifo, Doug N Halligan, James A Nathan, Daniel J Peet, Roland H Wenger, Alex Von Kriegsheim, Eoin P Cummins, Cormac T Taylor
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2016-01-01
Series:PLoS Biology
Online Access:https://doi.org/10.1371/journal.pbio.1002347
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author Carsten C Scholz
Javier Rodriguez
Christina Pickel
Stephen Burr
Jacqueline-Alba Fabrizio
Karen A Nolan
Patrick Spielmann
Miguel A S Cavadas
Bianca Crifo
Doug N Halligan
James A Nathan
Daniel J Peet
Roland H Wenger
Alex Von Kriegsheim
Eoin P Cummins
Cormac T Taylor
author_facet Carsten C Scholz
Javier Rodriguez
Christina Pickel
Stephen Burr
Jacqueline-Alba Fabrizio
Karen A Nolan
Patrick Spielmann
Miguel A S Cavadas
Bianca Crifo
Doug N Halligan
James A Nathan
Daniel J Peet
Roland H Wenger
Alex Von Kriegsheim
Eoin P Cummins
Cormac T Taylor
author_sort Carsten C Scholz
collection DOAJ
description The asparagine hydroxylase, factor inhibiting HIF (FIH), confers oxygen-dependence upon the hypoxia-inducible factor (HIF), a master regulator of the cellular adaptive response to hypoxia. Studies investigating whether asparagine hydroxylation is a general regulatory oxygen-dependent modification have identified multiple non-HIF targets for FIH. However, the functional consequences of this outside of the HIF pathway remain unclear. Here, we demonstrate that the deubiquitinase ovarian tumor domain containing ubiquitin aldehyde binding protein 1 (OTUB1) is a substrate for hydroxylation by FIH on N22. Mutation of N22 leads to a profound change in the interaction of OTUB1 with proteins important in cellular metabolism. Furthermore, in cultured cells, overexpression of N22A mutant OTUB1 impairs cellular metabolic processes when compared to wild type. Based on these data, we hypothesize that OTUB1 is a target for functional hydroxylation by FIH. Additionally, we propose that our results provide new insight into the regulation of cellular energy metabolism during hypoxic stress and the potential for targeting hydroxylases for therapeutic benefit.
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institution Kabale University
issn 1544-9173
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language English
publishDate 2016-01-01
publisher Public Library of Science (PLoS)
record_format Article
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spelling doaj-art-195eb6b4e4534a8d981fea77cbdb36dd2025-08-20T03:46:42ZengPublic Library of Science (PLoS)PLoS Biology1544-91731545-78852016-01-01141e100234710.1371/journal.pbio.1002347FIH Regulates Cellular Metabolism through Hydroxylation of the Deubiquitinase OTUB1.Carsten C ScholzJavier RodriguezChristina PickelStephen BurrJacqueline-Alba FabrizioKaren A NolanPatrick SpielmannMiguel A S CavadasBianca CrifoDoug N HalliganJames A NathanDaniel J PeetRoland H WengerAlex Von KriegsheimEoin P CumminsCormac T TaylorThe asparagine hydroxylase, factor inhibiting HIF (FIH), confers oxygen-dependence upon the hypoxia-inducible factor (HIF), a master regulator of the cellular adaptive response to hypoxia. Studies investigating whether asparagine hydroxylation is a general regulatory oxygen-dependent modification have identified multiple non-HIF targets for FIH. However, the functional consequences of this outside of the HIF pathway remain unclear. Here, we demonstrate that the deubiquitinase ovarian tumor domain containing ubiquitin aldehyde binding protein 1 (OTUB1) is a substrate for hydroxylation by FIH on N22. Mutation of N22 leads to a profound change in the interaction of OTUB1 with proteins important in cellular metabolism. Furthermore, in cultured cells, overexpression of N22A mutant OTUB1 impairs cellular metabolic processes when compared to wild type. Based on these data, we hypothesize that OTUB1 is a target for functional hydroxylation by FIH. Additionally, we propose that our results provide new insight into the regulation of cellular energy metabolism during hypoxic stress and the potential for targeting hydroxylases for therapeutic benefit.https://doi.org/10.1371/journal.pbio.1002347
spellingShingle Carsten C Scholz
Javier Rodriguez
Christina Pickel
Stephen Burr
Jacqueline-Alba Fabrizio
Karen A Nolan
Patrick Spielmann
Miguel A S Cavadas
Bianca Crifo
Doug N Halligan
James A Nathan
Daniel J Peet
Roland H Wenger
Alex Von Kriegsheim
Eoin P Cummins
Cormac T Taylor
FIH Regulates Cellular Metabolism through Hydroxylation of the Deubiquitinase OTUB1.
PLoS Biology
title FIH Regulates Cellular Metabolism through Hydroxylation of the Deubiquitinase OTUB1.
title_full FIH Regulates Cellular Metabolism through Hydroxylation of the Deubiquitinase OTUB1.
title_fullStr FIH Regulates Cellular Metabolism through Hydroxylation of the Deubiquitinase OTUB1.
title_full_unstemmed FIH Regulates Cellular Metabolism through Hydroxylation of the Deubiquitinase OTUB1.
title_short FIH Regulates Cellular Metabolism through Hydroxylation of the Deubiquitinase OTUB1.
title_sort fih regulates cellular metabolism through hydroxylation of the deubiquitinase otub1
url https://doi.org/10.1371/journal.pbio.1002347
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