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Coactivation of GR and NFKB alters the repertoire of their binding sites and target genes

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Coactivation of GR and NFKB alters the repertoire of their binding sites and target genes
Moulos, Panagiotis
Francoijs, Kees-Jan
Stunnenberg, Hendrik G.
Αλέξης, Μιχαήλ Ν.
Μήτσιου, Δήμητρα
McCalman, Melysia T.
Rao, Nagesha A. S.
Χατζηιωάννου, Αριστοτέλης
Κολίσης, Φραγκίσκος Ν.
Άρθρο σε επιστημονικό περιοδικό
2011-09
Glucocorticoid receptor (GR) exerts anti-inflammatory action in part by antagonizing proinflammatory transcription factors such as the nuclear factor kappa-b (NFKB). Here, we assess the crosstalk of activated GR and RELA (p65, major NFKB component) by global identification of their binding sites and target genes. We show that coactivation of GR and p65 alters the repertoire of regulated genes and results in their association with novel sites in a mutually dependent manner. These novel sites predominantly cluster with p65 target genes that are antagonized by activated GR and vice versa. Our data show that coactivation of GR and NFKB alters signaling pathways that are regulated by each factor separately and provide insight into the networks underlying the GR and NFKB crosstalk.
Cold Spring Harbor
Βιολογία (Γενικά) (EL)
Βιοτεχνολογία (EL)
Biology (General) (EN)
Biotechnology (EN)
Genetics & Heredity
English
Cold Spring Harbor Laboratory Press, Publications Department
Genome Research
© COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
© COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT (EN)
National Hellenic Research Foundation (NHRF)
Helios - Repository of the National Hellenic Research Foundation (NHRF)



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