کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10956673 | 1099395 | 2011 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
ERK-associated changes of AP-1 proteins during fear extinction
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کلمات کلیدی
CREDyad symmetry elementJunDRSKJDP2MSKSREHDAC1DSENMDARJnkc-fosAP-1ERKc-Jun N-terminal kinase - C-Jun N-terminal kinaseMitogen activated protein kinase kinase - Mitogen فعال پروتئین کیناز کینازExtinction - انقراضFear conditioning - تهدید ترسc-Jun - جون ژوئنSerum response element - عنصر پاسخ سرمMEK - مجاهدین خلقhistone deacetylase 1 - هیستون دیازتیلاز 1Hippocampus - هیپوکامپ activator protein-1 - پروتئین فعال کننده-1mitogen- and stress-activated protein kinase - پروتئین کیناز متیوژن و استرس فعالextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیN-methyl-d-aspartate receptor - گیرنده N-methyl-d-aspartate
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
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چکیده انگلیسی
Extensive research has unraveled the molecular basis of learning processes underlying contextual fear conditioning, but the mechanisms of fear extinction remain less known. Contextual fear extinction occurs when an aversive stimulus that initially caused fear is no longer present and depends on the activation of the extracellular signal-regulated kinase (ERK), among other molecules. Here we investigated how ERK signaling triggered by extinction affects its downstream targets belonging to the activator protein-1 (AP-1) transcription factor family. We found that extinction, when compared to conditioning of fear, markedly enhanced the interactions of active, phospho-ERK (pERK ) with c-Jun causing alterations of its phosphorylation state. The AP-1 binding of c-Jun was decreased whereas AP-1 binding of JunD, Jun dimerization protein 2 (JDP2) and ERK were significantly enhanced. The increased AP-1 binding of the inhibitory JunD and JDP2 transcription factors was paralleled by decreased levels of the AP-1 regulated proteins c-Fos and GluR2. These changes were specific for extinction and were MEK-dependent. Overall, fear extinction involves ERK/Jun interactions and a decrease of a subset of AP-1-regulated proteins that are typically required for fear conditioning. Facilitating the formation of inhibitory AP-1 complexes may thus facilitate the reduction of fear.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Neuroscience - Volume 47, Issue 2, June 2011, Pages 137-144
Journal: Molecular and Cellular Neuroscience - Volume 47, Issue 2, June 2011, Pages 137-144
نویسندگان
Anita L. Guedea, Christina Schrick, Yomayra F. Guzman, Katie Leaderbrand, Vladimir Jovasevic, Kevin A. Corcoran, Natalie C. Tronson, Jelena Radulovic,