ArticleScientific reports2013
Lys63-linked polyubiquitination of BRAF at lysine 578 is required for BRAF-mediated signaling.
Article in Scientific reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 13 citations in OpenAlex.
- MARCH2-mediated Lys63-linked polyubiquitination promotes metastasis by modulating the catalytic activity of TGF-β type I receptor.Cell death & disease · 2025Article
- The evolution of BRAF-targeted therapies in melanoma: overcoming hurdles and unleashing novel strategies.Frontiers in oncology · 2024Review
- The ubiquitin system: orchestrating cellular signals in non-small-cell lung cancer.Cellular & molecular biology letters · 2020Review
- UBE2N plays a pivotal role in maintaining melanoma malignancy.Oncotarget · 2018Article
- UBE2N Promotes Melanoma Growth via MEK/FRA1/SOX10 Signaling.Cancer research · 2018Article
- TRAF1 Is Critical for Regulating the BRAF/MEK/ERK Pathway in Non-Small Cell Lung Carcinogenesis.Cancer research · 2018Article
- Oncogenic mutations in IKKβ function through global changes induced by K63-linked ubiquitination and result in autocrine stimulation.PloS one · 2018Article
- Oncogenic role of rab escort protein 1 through EGFR and STAT3 pathway.Cell death & disease · 2017Article
- Phospho-proteomic analyses of B-Raf protein complexes reveal new regulatory principles.Oncotarget · 2016Article
- EcSTAT3ic about K63-Linked Ubiquitylation of IKKβ.Cell cycle (Georgetown, Tex.) · 2015Article
- BRAF kinase domain mutations are present in a subset of chronic myelomonocytic leukemia with wild-type RAS.American journal of hematology · 2014Article
- Novel Lys63-linked ubiquitination of IKKβ induces STAT3 signaling.Cell cycle (Georgetown, Tex.) · 2014Article
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Authors and funding
13 authors at 7 institutions in 2 countries.
Funding
Abstract
The RAF kinase family is essential in mediating signal transduction from RAS to ERK. BRAF constitutively active mutations correlate with human cancer development. However, the precise molecular regulation of BRAF activation is not fully understood. Here we report that BRAF is modified by Lys63-linked polyubiquitination at lysine 578 within its kinase domain once it is activated by gain of constitutively active mutation or epidermal growth factor (EGF) stimulation. Substitution of BRAF lysine 578 with arginine (K578R) inhibited BRAF-mediated ERK activation. Furthermore, ectopic expression of BRAF K578R mutant inhibited anchorage-independent colony formation of MCF7 breast cancer cell line. Our studies have identified a previously unrecognized regulatory role of Lys63-linked polyubiquitination in BRAF-mediated normal and oncogenic signalings.
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Registered trials
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