The MEF2A and MEF2D isoforms are differentially regulated in muscle and adipose tissue during states of insulin deficiency

Previously we have demonstrated that striated muscle GLUT4 gene expression decreased following streptozotocin-induced diabetes due to a loss of MEF2A transcription factor expression without any significant effect on the MEF2D isoform (Mora, S. and J. E. Pessin (2000) J Biol Chem, 275:16323-16328). I...

Descripción completa

Detalles Bibliográficos
Autores: Mora Fayos, Sílvia, Yang, Chunmei, Ryder, Jeffrey W., Boeglin, Diana, Pessin, Jeffrey E.
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2001
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/176702
Acceso en línea:https://hdl.handle.net/2445/176702
Access Level:acceso abierto
Palabra clave:Teixit adipós
Insulina
Diabetis
Adipose tissues
Insulin
Diabetes
id ES_29983e726d64dffeb8a20530c31c1a56
oai_identifier_str oai:recercat.cat:2445/176702
network_acronym_str ES
network_name_str España
repository_id_str
spelling The MEF2A and MEF2D isoforms are differentially regulated in muscle and adipose tissue during states of insulin deficiencyMora Fayos, SílviaYang, ChunmeiRyder, Jeffrey W.Boeglin, DianaPessin, Jeffrey E.Teixit adipósInsulinaDiabetisAdipose tissuesInsulinDiabetesPreviously we have demonstrated that striated muscle GLUT4 gene expression decreased following streptozotocin-induced diabetes due to a loss of MEF2A transcription factor expression without any significant effect on the MEF2D isoform (Mora, S. and J. E. Pessin (2000) J Biol Chem, 275:16323-16328). In contrast to both cardiac and skeletal muscle, adipose tissue displays a selective decrease in MEF2D expression in diabetes without any significant alteration in MEF2A protein content. Adipose tissue also expresses very low levels of the MEF2 transcription factors and nuclear extracts from white adipose tissue exhibit poor in vitro binding to the MEF2 element. However, addition of in vitro synthesized MEF2A to adipose nuclear extracts results in the formation of the expected MEF2/DNA complex. More importantly, binding to the MEF2 element was also compromised in the diabetic condition. Furthermore, in vivo overexpression of MEF2A selectively in adipose tissue did not affect GLUT4 or MEF2D expression and was not sufficient to prevent GLUT4 down-regulation that occurred in insulin-deficient states.Association for the Study of Internal Secretions2021202120012021info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion6 p.application/pdfhttps://hdl.handle.net/2445/176702Articles publicats en revistes (Bioquímica i Biomedicina Molecular)reponame:Recercat. Dipósit de la Recerca de Catalunyainstname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)InglésReproducció del document publicat a: https://doi.org/10.1210/endo.142.5.8160Endocrinology, 2001, vol. 142, p. 1999-2004https://doi.org/10.1210/endo.142.5.8160(c) Association for the Study of Internal Secretions, 2001info:eu-repo/semantics/openAccessoai:recercat.cat:2445/1767022026-05-29T05:05:01Z
dc.title.none.fl_str_mv The MEF2A and MEF2D isoforms are differentially regulated in muscle and adipose tissue during states of insulin deficiency
title The MEF2A and MEF2D isoforms are differentially regulated in muscle and adipose tissue during states of insulin deficiency
spellingShingle The MEF2A and MEF2D isoforms are differentially regulated in muscle and adipose tissue during states of insulin deficiency
Mora Fayos, Sílvia
Teixit adipós
Insulina
Diabetis
Adipose tissues
Insulin
Diabetes
title_short The MEF2A and MEF2D isoforms are differentially regulated in muscle and adipose tissue during states of insulin deficiency
title_full The MEF2A and MEF2D isoforms are differentially regulated in muscle and adipose tissue during states of insulin deficiency
title_fullStr The MEF2A and MEF2D isoforms are differentially regulated in muscle and adipose tissue during states of insulin deficiency
title_full_unstemmed The MEF2A and MEF2D isoforms are differentially regulated in muscle and adipose tissue during states of insulin deficiency
title_sort The MEF2A and MEF2D isoforms are differentially regulated in muscle and adipose tissue during states of insulin deficiency
dc.creator.none.fl_str_mv Mora Fayos, Sílvia
Yang, Chunmei
Ryder, Jeffrey W.
Boeglin, Diana
Pessin, Jeffrey E.
author Mora Fayos, Sílvia
author_facet Mora Fayos, Sílvia
Yang, Chunmei
Ryder, Jeffrey W.
Boeglin, Diana
Pessin, Jeffrey E.
author_role author
author2 Yang, Chunmei
Ryder, Jeffrey W.
Boeglin, Diana
Pessin, Jeffrey E.
author2_role author
author
author
author
dc.subject.none.fl_str_mv Teixit adipós
Insulina
Diabetis
Adipose tissues
Insulin
Diabetes
topic Teixit adipós
Insulina
Diabetis
Adipose tissues
Insulin
Diabetes
description Previously we have demonstrated that striated muscle GLUT4 gene expression decreased following streptozotocin-induced diabetes due to a loss of MEF2A transcription factor expression without any significant effect on the MEF2D isoform (Mora, S. and J. E. Pessin (2000) J Biol Chem, 275:16323-16328). In contrast to both cardiac and skeletal muscle, adipose tissue displays a selective decrease in MEF2D expression in diabetes without any significant alteration in MEF2A protein content. Adipose tissue also expresses very low levels of the MEF2 transcription factors and nuclear extracts from white adipose tissue exhibit poor in vitro binding to the MEF2 element. However, addition of in vitro synthesized MEF2A to adipose nuclear extracts results in the formation of the expected MEF2/DNA complex. More importantly, binding to the MEF2 element was also compromised in the diabetic condition. Furthermore, in vivo overexpression of MEF2A selectively in adipose tissue did not affect GLUT4 or MEF2D expression and was not sufficient to prevent GLUT4 down-regulation that occurred in insulin-deficient states.
publishDate 2001
dc.date.none.fl_str_mv 2001
2021
2021
2021
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/176702
url https://hdl.handle.net/2445/176702
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Reproducció del document publicat a: https://doi.org/10.1210/endo.142.5.8160
Endocrinology, 2001, vol. 142, p. 1999-2004
https://doi.org/10.1210/endo.142.5.8160
dc.rights.none.fl_str_mv (c) Association for the Study of Internal Secretions, 2001
info:eu-repo/semantics/openAccess
rights_invalid_str_mv (c) Association for the Study of Internal Secretions, 2001
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 6 p.
application/pdf
dc.publisher.none.fl_str_mv Association for the Study of Internal Secretions
publisher.none.fl_str_mv Association for the Study of Internal Secretions
dc.source.none.fl_str_mv Articles publicats en revistes (Bioquímica i Biomedicina Molecular)
reponame:Recercat. Dipósit de la Recerca de Catalunya
instname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
instname_str Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
reponame_str Recercat. Dipósit de la Recerca de Catalunya
collection Recercat. Dipósit de la Recerca de Catalunya
repository.name.fl_str_mv
repository.mail.fl_str_mv
_version_ 1869405013344780288
score 15,811543

Similares en LA Referencia