Redox regulation of methylthioadenosine phosphorylase in liver cells: molecular mechanism and functional implications

MTAP (5'-methylthioadenosine phosphorylase) catalyses the reversible phosphorolytic cleavage of methylthioadenosine leading to the production of methylthioribose-1-phosphate and adenine. Deficient MTAP activity has been correlated with human diseases including cirrhosis and hepatocellular carci...

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Autores: Fernandez-Irigoyen, J. (Joaquín)|||/items/700f4366-d68f-4161-af03-2cac47ea718d, Santamaria, M. (Mónica)|||/items/072812e5-8222-4bfc-96cd-c78ee9d883e3, Sanchez-Quiles, V. (Virginia)|||/items/9e99781c-bce3-459d-a1d9-c08700f11905, Latasa, M.U. (María Ujué)|||/items/e1e74596-1598-4722-a96a-7bdd7cdec356, Santamaria, E. (Enrique)|||/items/fc2c70d6-973c-4d67-8185-6c56a59477c8, Muñoz, J. (Javier)|||/items/a5dea34b-9970-44b5-a405-4031315a288f, Sanchez-del-Pino, M.M. (Manuel M.)|||/items/ebbc885a-5036-4bc0-b697-16ada2926964, Valero, M.L. (María L.)|||/items/c3c591d8-b983-4945-a27e-56cd23813d70, Prieto, J. (Jesús)|||/items/0d9c3dec-4a09-400d-8c83-23ece1096c71, Avila, M.A. (Matías Antonio)|||/items/3ad9abbb-c18d-445b-86cf-cb76be15419f, Corrales, F.J. (Fernando José)|||/items/96b34843-1185-4837-be4b-d1d63e688ec2
Tipo de recurso: artículo
Fecha de publicación:2008
País:España
Institución:Universidad de Navarra
Repositorio:Dadun. Depósito Académico Digital de la Universidad de Navarra
Idioma:inglés
OAI Identifier:oai:dadun.unav.edu:10171/21417
Acceso en línea:https://hdl.handle.net/10171/21417
Access Level:acceso abierto
Palabra clave:Cysteine oxidation,
Inflammatio
Methylthioadenosine
Methylthioadenosine phosphorylase
Oxidative stress
Sulfenic acid
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spelling Redox regulation of methylthioadenosine phosphorylase in liver cells: molecular mechanism and functional implicationsFernandez-Irigoyen, J. (Joaquín)|||/items/700f4366-d68f-4161-af03-2cac47ea718dSantamaria, M. (Mónica)|||/items/072812e5-8222-4bfc-96cd-c78ee9d883e3Sanchez-Quiles, V. (Virginia)|||/items/9e99781c-bce3-459d-a1d9-c08700f11905Latasa, M.U. (María Ujué)|||/items/e1e74596-1598-4722-a96a-7bdd7cdec356Santamaria, E. (Enrique)|||/items/fc2c70d6-973c-4d67-8185-6c56a59477c8Muñoz, J. (Javier)|||/items/a5dea34b-9970-44b5-a405-4031315a288fSanchez-del-Pino, M.M. (Manuel M.)|||/items/ebbc885a-5036-4bc0-b697-16ada2926964Valero, M.L. (María L.)|||/items/c3c591d8-b983-4945-a27e-56cd23813d70Prieto, J. (Jesús)|||/items/0d9c3dec-4a09-400d-8c83-23ece1096c71Avila, M.A. (Matías Antonio)|||/items/3ad9abbb-c18d-445b-86cf-cb76be15419fCorrales, F.J. (Fernando José)|||/items/96b34843-1185-4837-be4b-d1d63e688ec2Cysteine oxidation,InflammatioMethylthioadenosineMethylthioadenosine phosphorylaseOxidative stressSulfenic acidMTAP (5'-methylthioadenosine phosphorylase) catalyses the reversible phosphorolytic cleavage of methylthioadenosine leading to the production of methylthioribose-1-phosphate and adenine. Deficient MTAP activity has been correlated with human diseases including cirrhosis and hepatocellular carcinoma. In the present study we have investigated the regulation of MTAP by ROS (reactive oxygen species). The results of the present study support the inactivation of MTAP in the liver of bacterial LPS (lipopolysaccharide)-challenged mice as well as in HepG2 cells after exposure to t-butyl hydroperoxide. Reversible inactivation of purified MTAP by hydrogen peroxide results from a reduction of V(max) and involves the specific oxidation of Cys(136) and Cys(223) thiols to sulfenic acid that may be further stabilized to sulfenyl amide intermediates. Additionally, we found that Cys(145) and Cys(211) were disulfide bonded upon hydrogen peroxide exposure. However, this modification is not relevant to the mediation of the loss of MTAP activity as assessed by site-directed mutagenesis. Regulation of MTAP by ROS might participate in the redox regulation of the methionine catabolic pathway in the liver. Reduced MTA (5'-deoxy-5'-methylthioadenosine)-degrading activity may compensate for the deficient production of the precursor S-adenosylmethionine, allowing maintenance of intracellular MTA levels that may be critical to ensure cellular adaptation to physiopathological conditions such as inflammation.Portland PressDadun. Depósito Académico Digital Universidad de Navarra20122012-03-2920082008-01-0120082008-01-01journal articlehttp://purl.org/coar/resource_type/c_6501info:eu-repo/semantics/articleapplication/pdfhttps://hdl.handle.net/10171/21417reponame:Dadun. Depósito Académico Digital de la Universidad de Navarrainstname:Universidad de NavarraInglésengopen accesshttp://purl.org/coar/access_right/c_abf2info:eu-repo/semantics/openAccessoai:dadun.unav.edu:10171/214172026-06-21T12:47:57Z
dc.title.none.fl_str_mv Redox regulation of methylthioadenosine phosphorylase in liver cells: molecular mechanism and functional implications
title Redox regulation of methylthioadenosine phosphorylase in liver cells: molecular mechanism and functional implications
spellingShingle Redox regulation of methylthioadenosine phosphorylase in liver cells: molecular mechanism and functional implications
Fernandez-Irigoyen, J. (Joaquín)|||/items/700f4366-d68f-4161-af03-2cac47ea718d
Cysteine oxidation,
Inflammatio
Methylthioadenosine
Methylthioadenosine phosphorylase
Oxidative stress
Sulfenic acid
title_short Redox regulation of methylthioadenosine phosphorylase in liver cells: molecular mechanism and functional implications
title_full Redox regulation of methylthioadenosine phosphorylase in liver cells: molecular mechanism and functional implications
title_fullStr Redox regulation of methylthioadenosine phosphorylase in liver cells: molecular mechanism and functional implications
title_full_unstemmed Redox regulation of methylthioadenosine phosphorylase in liver cells: molecular mechanism and functional implications
title_sort Redox regulation of methylthioadenosine phosphorylase in liver cells: molecular mechanism and functional implications
dc.creator.none.fl_str_mv Fernandez-Irigoyen, J. (Joaquín)|||/items/700f4366-d68f-4161-af03-2cac47ea718d
Santamaria, M. (Mónica)|||/items/072812e5-8222-4bfc-96cd-c78ee9d883e3
Sanchez-Quiles, V. (Virginia)|||/items/9e99781c-bce3-459d-a1d9-c08700f11905
Latasa, M.U. (María Ujué)|||/items/e1e74596-1598-4722-a96a-7bdd7cdec356
Santamaria, E. (Enrique)|||/items/fc2c70d6-973c-4d67-8185-6c56a59477c8
Muñoz, J. (Javier)|||/items/a5dea34b-9970-44b5-a405-4031315a288f
Sanchez-del-Pino, M.M. (Manuel M.)|||/items/ebbc885a-5036-4bc0-b697-16ada2926964
Valero, M.L. (María L.)|||/items/c3c591d8-b983-4945-a27e-56cd23813d70
Prieto, J. (Jesús)|||/items/0d9c3dec-4a09-400d-8c83-23ece1096c71
Avila, M.A. (Matías Antonio)|||/items/3ad9abbb-c18d-445b-86cf-cb76be15419f
Corrales, F.J. (Fernando José)|||/items/96b34843-1185-4837-be4b-d1d63e688ec2
author Fernandez-Irigoyen, J. (Joaquín)|||/items/700f4366-d68f-4161-af03-2cac47ea718d
author_facet Fernandez-Irigoyen, J. (Joaquín)|||/items/700f4366-d68f-4161-af03-2cac47ea718d
Santamaria, M. (Mónica)|||/items/072812e5-8222-4bfc-96cd-c78ee9d883e3
Sanchez-Quiles, V. (Virginia)|||/items/9e99781c-bce3-459d-a1d9-c08700f11905
Latasa, M.U. (María Ujué)|||/items/e1e74596-1598-4722-a96a-7bdd7cdec356
Santamaria, E. (Enrique)|||/items/fc2c70d6-973c-4d67-8185-6c56a59477c8
Muñoz, J. (Javier)|||/items/a5dea34b-9970-44b5-a405-4031315a288f
Sanchez-del-Pino, M.M. (Manuel M.)|||/items/ebbc885a-5036-4bc0-b697-16ada2926964
Valero, M.L. (María L.)|||/items/c3c591d8-b983-4945-a27e-56cd23813d70
Prieto, J. (Jesús)|||/items/0d9c3dec-4a09-400d-8c83-23ece1096c71
Avila, M.A. (Matías Antonio)|||/items/3ad9abbb-c18d-445b-86cf-cb76be15419f
Corrales, F.J. (Fernando José)|||/items/96b34843-1185-4837-be4b-d1d63e688ec2
author_role author
author2 Santamaria, M. (Mónica)|||/items/072812e5-8222-4bfc-96cd-c78ee9d883e3
Sanchez-Quiles, V. (Virginia)|||/items/9e99781c-bce3-459d-a1d9-c08700f11905
Latasa, M.U. (María Ujué)|||/items/e1e74596-1598-4722-a96a-7bdd7cdec356
Santamaria, E. (Enrique)|||/items/fc2c70d6-973c-4d67-8185-6c56a59477c8
Muñoz, J. (Javier)|||/items/a5dea34b-9970-44b5-a405-4031315a288f
Sanchez-del-Pino, M.M. (Manuel M.)|||/items/ebbc885a-5036-4bc0-b697-16ada2926964
Valero, M.L. (María L.)|||/items/c3c591d8-b983-4945-a27e-56cd23813d70
Prieto, J. (Jesús)|||/items/0d9c3dec-4a09-400d-8c83-23ece1096c71
Avila, M.A. (Matías Antonio)|||/items/3ad9abbb-c18d-445b-86cf-cb76be15419f
Corrales, F.J. (Fernando José)|||/items/96b34843-1185-4837-be4b-d1d63e688ec2
author2_role author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Dadun. Depósito Académico Digital Universidad de Navarra
dc.subject.none.fl_str_mv Cysteine oxidation,
Inflammatio
Methylthioadenosine
Methylthioadenosine phosphorylase
Oxidative stress
Sulfenic acid
topic Cysteine oxidation,
Inflammatio
Methylthioadenosine
Methylthioadenosine phosphorylase
Oxidative stress
Sulfenic acid
description MTAP (5'-methylthioadenosine phosphorylase) catalyses the reversible phosphorolytic cleavage of methylthioadenosine leading to the production of methylthioribose-1-phosphate and adenine. Deficient MTAP activity has been correlated with human diseases including cirrhosis and hepatocellular carcinoma. In the present study we have investigated the regulation of MTAP by ROS (reactive oxygen species). The results of the present study support the inactivation of MTAP in the liver of bacterial LPS (lipopolysaccharide)-challenged mice as well as in HepG2 cells after exposure to t-butyl hydroperoxide. Reversible inactivation of purified MTAP by hydrogen peroxide results from a reduction of V(max) and involves the specific oxidation of Cys(136) and Cys(223) thiols to sulfenic acid that may be further stabilized to sulfenyl amide intermediates. Additionally, we found that Cys(145) and Cys(211) were disulfide bonded upon hydrogen peroxide exposure. However, this modification is not relevant to the mediation of the loss of MTAP activity as assessed by site-directed mutagenesis. Regulation of MTAP by ROS might participate in the redox regulation of the methionine catabolic pathway in the liver. Reduced MTA (5'-deoxy-5'-methylthioadenosine)-degrading activity may compensate for the deficient production of the precursor S-adenosylmethionine, allowing maintenance of intracellular MTA levels that may be critical to ensure cellular adaptation to physiopathological conditions such as inflammation.
publishDate 2008
dc.date.none.fl_str_mv 2008
2008-01-01
2008
2008-01-01
2012
2012-03-29
dc.type.none.fl_str_mv journal article
http://purl.org/coar/resource_type/c_6501
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://hdl.handle.net/10171/21417
url https://hdl.handle.net/10171/21417
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Portland Press
publisher.none.fl_str_mv Portland Press
dc.source.none.fl_str_mv reponame:Dadun. Depósito Académico Digital de la Universidad de Navarra
instname:Universidad de Navarra
instname_str Universidad de Navarra
reponame_str Dadun. Depósito Académico Digital de la Universidad de Navarra
collection Dadun. Depósito Académico Digital de la Universidad de Navarra
repository.name.fl_str_mv
repository.mail.fl_str_mv
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