The Ran-binding protein RanBPM can depress the NF-κB pathway by interacting with TRAF6

التفاصيل البيبلوغرافية
العنوان: The Ran-binding protein RanBPM can depress the NF-κB pathway by interacting with TRAF6
المؤلفون: Xin Wang, Yu-He Yuan, Hong Chen, Lan Wang, Bingren Huang, Chengbo Fu, Ying-Bin Cui, Yun-Fei Xie
المصدر: Molecular and cellular biochemistry. 359(1-2)
سنة النشر: 2011
مصطلحات موضوعية: Transcription, Genetic, Clinical Biochemistry, Plasma protein binding, Tropomyosin receptor kinase A, chemistry.chemical_compound, Ubiquitin, Protein Interaction Mapping, Humans, Nuclear protein, Molecular Biology, Adaptor Proteins, Signal Transducing, TNF Receptor-Associated Factor 6, biology, NF-kappa B, Nuclear Proteins, NF-κB, Cell Biology, General Medicine, NFKB1, Molecular biology, Cell biology, Cytoskeletal Proteins, Förster resonance energy transfer, chemistry, biology.protein, Signal transduction, Protein Binding, Signal Transduction
الوصف: Ran-binding protein in microtubule-organizing center (RanBPM) has been reported to interact with the neurotrophin receptors p75NTR and TrkA, meanwhile p75NTR and TrkA can also interact with TRAF6. Whether RanBPM interacts directly with TRAF6 has not yet been established. In this study, using a yeast two-hybrid system and glutathione-S: -transferase pull-down assays, we determined that RanBPM binds to the TRAF6 C-terminus through its SPRY motif. Complex formation between overexpressed RanBPM and TRAF6 was also confirmed with a co-immunoprecipitation assay, laser scanning confocal and fluorescence resonance energy transfer. Additional co-immunoprecipitation experiments verified that endogenous RanBPM and TRAF6 interact in several mammalian cell lines. A series of experiments revealed that RanBPM influences TRAF6 ubiquitination and the TRAF6-triggered NF-κB signaling pathway through RanBPM's interaction with TRAF6. These data suggest that RanBPM participates in gene transcription by binding to TRAF6.
تدمد: 1573-4919
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ef5204bccbf437e164eccf41dc6b2823
https://pubmed.ncbi.nlm.nih.gov/21805090
Rights: CLOSED
رقم الانضمام: edsair.doi.dedup.....ef5204bccbf437e164eccf41dc6b2823
قاعدة البيانات: OpenAIRE