دورية أكاديمية

The E3 Ligase RNF34 is a Novel Negative Regulator of the NOD1 Pathway

التفاصيل البيبلوغرافية
العنوان: The E3 Ligase RNF34 is a Novel Negative Regulator of the NOD1 Pathway
المؤلفون: Rui Zhang, Jian Zhao, Yuhua Song, Xu Wang, Lili Wang, Jian Xu, Chun Song, Fang Liu
المصدر: Cellular Physiology and Biochemistry, Vol 33, Iss 6, Pp 1954-1962 (2014)
بيانات النشر: Cell Physiol Biochem Press GmbH & Co KG, 2014.
سنة النشر: 2014
المجموعة: LCC:Physiology
LCC:Biochemistry
مصطلحات موضوعية: NOD1, RNF34, NF-κB, Physiology, QP1-981, Biochemistry, QD415-436
الوصف: Background/Aims: To identify the regulator of nucleotide-binding oligomerization domain-containing protein 1 (NOD1) and its regulatory function. Methods and Results: We performed a yeast two-hybrid screening assay and identified the E3 ligase RNF34 as a candidate partner of NOD1. Using co-immunoprecipitation (co-IP) and glutathione S transferase (GST)-pull down assays, we further confirmed that RNF34 is associated with NOD1. Western blotting showed that RNF34 downregulated the stability of NOD1 and promoted its ubiquitination. Functional analysis demonstrated that RNF34 overexpression inhibited NOD1-dependent activation of nuclear factor-kappa B (NF-γB), whereas knockdown of RNF34 using small interfering RNA increased NF-γB activation following stimulation from NOD1 overexpression or transfection of γ-D-glutamyl-meso-diaminopimelic acid. Conclusion: These findings confirm that RNF34 is a negative regulator of the NOD1 pathway through direct interaction and ubiquitination of NOD1, and suggest a novel regulatory mechanism of NOD1.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1015-8987
1421-9778
Relation: http://www.karger.com/Article/FullText/362972; https://doaj.org/toc/1015-8987; https://doaj.org/toc/1421-9778
DOI: 10.1159/000362972
URL الوصول: https://doaj.org/article/ca2840abf5ce42a5a74851bf39a66da4
رقم الأكسشن: edsdoj.2840abf5ce42a5a74851bf39a66da4
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:10158987
14219778
DOI:10.1159/000362972