ArticleNature communications2024
MEF2B C-terminal mutations enhance transcriptional activity and stability to drive B cell lymphomagenesis.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- The Growth Supporting Role of ZDHHC11 Is Linked to the MEF2B-BCL6 Regulatory Circuit in Burkitt Lymphoma.International journal of cancer · 2026Article
- Article
- Identification and validation of prognostic genes related to centrosome amplification in multiple myeloma.PeerJ · 2026Article
- Mouse models of B cell lymphomas on the basis of genetic features.Frontiers in immunology · 2026Review
- Transcriptomic and differential gene analysis investigating the differences in biological behaviour between subtypes of feline alimentary lymphoma.Frontiers in veterinary science · 2026Article
- Role of human Myocyte Enhancer Factor 2 (MEF2) proteins in cancer: structural insights, functional diversity, and regulatory mechanisms.Cancer cell international · 2025Review
- Identification of IGF2BP3 and CENPA as key regulators of immunophenotypes in renal clear cell carcinoma.Frontiers in genetics · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
The myocyte enhancer factor 2B (MEF2B) transcription factor is frequently mutated in germinal center (GC)-derived B-cell lymphomas. Its ammino (N)-terminal mutations drive lymphomagenesis by escaping interaction with transcriptional repressors, while the function of carboxy (C)-terminal mutations remains to be elucidated. Here, we show that MEF2B C-tail is physiologically phosphorylated at specific residues and phosphorylation at serine (S)324 is impaired by lymphoma-associated mutations. Lack of phosphorylation at S324 enhances the interaction of MEF2B with the SWI/SNF chromatin remodeling complex, leading to higher transcriptional activity. In addition, these mutants show an increased protein stability due to impaired interaction with the CUL3/KLHL12 ubiquitin complex. Mice expressing a phosphorylation-deficient lymphoma-associated MEF2B mutant display GC enlargement and develop GC-derived lymphomas, when crossed with Bcl2 transgenic mice. These results unveil converging mechanisms of action for a diverse spectrum of MEF2B mutations, all leading to its dysregulation and GC B-cell lymphomagenesis.
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