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Status: Bibliographieeintrag

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Verfasst von:Kashif, Muhammed [VerfasserIn]   i
 Hellwig, Andrea [VerfasserIn]   i
 Kumar, Varun [VerfasserIn]   i
 Bock, Fabian [VerfasserIn]   i
 Bierhaus, Angelika [VerfasserIn]   i
 Nawroth, Peter Paul [VerfasserIn]   i
Titel:Nuclear factor erythroid-derived 2 (Nfe2) regulates JunD DNA-binding activity via acetylation
Titelzusatz:a novel mechanism regulating trophoblast differentiation
Verf.angabe:Muhammed Kashif, Andrea Hellwig, Said Hashemolhosseini, Varun Kumar, Fabian Bock, Hongjie Wang, Khurrum Shahzad, Satish Ranjan, Juliane Wolter, Thati Madhusudhan, Angelika Bierhaus, Peter Nawroth and Berend Isermann
Jahr:2012
Jahr des Originals:2011
Umfang:12 S.
Teil:volume:287
 year:2012
 number:8
 pages:5400-5411
 extent:12
Fussnoten:Published, JBC Papers in Press, December 15, 2011 ; Gesehen am 02.07.2018
Titel Quelle:Enthalten in: The journal of biological chemistry
Ort Quelle:Bethesda, Md. : Soc., 1905
Jahr Quelle:2012
Band/Heft Quelle:287(2012), 8, Seite 5400-5411
ISSN Quelle:1083-351X
Abstract:We recently demonstrated that the bZip transcription factor nuclear factor erythroid-derived 2 (Nfe2) represses protein acetylation and expression of the transcription factor glial cell missing 1 (Gcm1) in trophoblast cells, preventing excess syncytiotrophoblast formation and permitting normal placental vascularization and embryonic growth. However, the Gcm1 promoter lacks a Nfe2-binding site and hence the mechanisms linking Nfe2 and Gcm1 expression remained unknown. Here we show that Nfe2 represses JunD DNA-binding activity to the Gcm1 promoter during syncytiotrophoblast differentiation. Interventional studies using knockdown and knockin approaches show that enhanced JunD DNA-binding activity is required for increased expression of Gcm1 and syncytiotrophoblast formation as well as impaired placental vascularization and reduced growth of Nfe2−/− embryos. Induction of Gcm1 expression requires binding of JunD to the −1441 site within the Gcm1 promoter, which is distinct from the −1314 site previously shown to induce Gcm1 expression by other bZip transcription factors. Nfe2 modulates JunD binding to the Gcm1 promoter via acetylation, as reducing JunD acetylation using the histone acetyltransferase inhibitor curcumin reverses the increased JunD DNA-binding activity observed in the absence of Nfe2. This identifies a novel mechanism through which bZip transcription factors interact. Within the placenta this interaction regulates Gcm1 expression, syncytiotrophoblast formation, placental vascularization, and embryonic growth.
DOI:doi:10.1074/jbc.M111.289801
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Kostenfrei: Volltext ; Verlag: http://dx.doi.org/10.1074/jbc.M111.289801
 Kostenfrei: Volltext: http://www.jbc.org/content/287/8/5400
 DOI: https://doi.org/10.1074/jbc.M111.289801
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Acetylation
 AP1 Transcription Factor
 Development
 Embryo
 Gcm1
 JunD
 Nfe2
 Placenta
 Syncytiotrophoblast Differentiation
 Trophoblast
K10plus-PPN:1577083555
Verknüpfungen:→ Zeitschrift

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