ArticleOncogene2016
The presence of C/EBPα and its degradation are both required for TRIB2-mediated leukaemia.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- FLT3-ITD signals for CEBPA and p53 proteolysis by the ubiquitin-proteosome pathway.Research square · 2026Article
- FLT3-ITD signals for CEBPA and p53 proteolysis by the ubiquitin-proteosome pathway.bioRxiv : the preprint server for biology · 2026Article
- Inducing TRIB2-targeted protein degradation to reverse chemoresistance in acute myeloid leukaemia.The Biochemical journal · 2026Article
- Tribbles Pseudokinases in Colorectal Cancer.Cancers · 2021Review
- Review
- Control of Cell Growth and Proliferation by the Tribbles Pseudokinase: Lessons from Drosophila.Cancers · 2021Review
- Trib1 promotes acute myeloid leukemia progression by modulating the transcriptional programs of Hoxa9.Blood · 2021Article
- Article
- Cataloguing the dead: breathing new life into pseudokinase research.The FEBS journal · 2020Review
- CCAAT enhancer binding protein alpha (CEBPA) biallelic acute myeloid leukaemia: cooperating lesions, molecular mechanisms and clinical relevance.British journal of haematology · 2020Review
- TRIB3 confers radiotherapy resistance in esophageal squamous cell carcinoma by stabilizing TAZ.Oncogene · 2020Article
- TRIB3 supports breast cancer stemness by suppressing FOXO1 degradation and enhancing SOX2 transcription.Nature communications · 2019Article
- TRIB2 regulates the differentiation of MLL-TET1 transduced myeloid progenitor cells.Journal of molecular medicine (Berlin, Germany) · 2018Article
- Covalent inhibitors of EGFR family protein kinases induce degradation of human Tribbles 2 (TRIB2) pseudokinase in cancer cells.Science signaling · 2018Article
- Substrate binding allosterically relieves autoinhibition of the pseudokinase TRIB1.Science signaling · 2018Article
- [Roles of CCAAT enhancer binding protein α in acute myeloblastic leukemia].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2018Review
- A Trib2-p38 axis controls myeloid leukaemia cell cycle and stress response signalling.Cell death & disease · 2018Article
- Trib2 expression in granulocyte-monocyte progenitors drives a highly drug resistant acute myeloid leukaemia linked to elevated Bcl2.Oncotarget · 2018Article
- Trib2 regulates the pluripotency of embryonic stem cells and enhances reprogramming efficiency.Experimental & molecular medicine · 2017Article
- Tribbles in the 21st Century: The Evolving Roles of Tribbles Pseudokinases in Biology and Disease.Trends in cell biology · 2017Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
C/EBPα (p42 and p30 isoforms) is commonly dysregulated in cancer via the action of oncogenes, and specifically in acute myeloid leukaemia (AML) by mutation. Elevated TRIB2 leads to the degradation of C/EBPα p42, leaving p30 intact in AML. Whether this relationship is a cooperative event in AML transformation is not known and the molecular mechanism involved remains elusive. Using mouse genetics, our data reveal that in the complete absence of C/EBPα, TRIB2 was unable to induce AML. Only in the presence of C/EBPα p42 and p30, were TRIB2 and p30 able to cooperate to decrease the latency of disease. We demonstrate that the molecular mechanism involved in the degradation of C/EBPα p42 requires site-specific direct interaction between TRIB2 and C/EBPα p42 for the K48-specific ubiquitin-dependent proteasomal degradation of C/EBPα p42. This interaction and ubiquitination is dependent on a critical C terminal lysine residue on C/EBPα. We show effective targeting of this pathway pharmacologically using proteasome inhibitors in TRIB2-positive AML cells. Together, our data show that excess p30 cooperated with TRIB2 only in the presence of p42 to accelerate AML, and the direct interaction and degradation of C/EBPα p42 is required for TRIB2-mediated AML.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.