ArticlePloS one2014
BEX1 promotes imatinib-induced apoptosis by binding to and antagonizing BCL-2.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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
18 citing papers in PubMed, 26 citations in OpenAlex.
- Biological potential and mechanisms of Brain-Expressed X-linked family proteins in cancers: an updated review.Journal of advanced research · 2026Review
- BEX2 influences the MCL1-Hedgehog signaling axis to regulate the potential of stemness characterization in colorectal cancer.Cancer biology & medicine · 2026Article
- Outcome prediction of oestrogen receptor-positive breast cancer based on a panel of oestrogen receptor-regulated genes.Histopathology · 2025Article
- Exploring the Genetic Orchestra of Cancer: The Interplay Between Oncogenes and Tumor-Suppressor Genes.Cancers · 2025Review
- Yeast as a tool to decipher the molecular mechanisms underlying the functions of Bcl-2 family.Exploration of targeted anti-tumor therapy · 2022Review
- Systems Approaches to Treatment Response to Imatinib in Severe Asthma: A Pilot Study.Journal of personalized medicine · 2021Article
- Article
- Aberrant brain-expressed X-linked 4 (BEX4) expression is a novel prognostic biomarker in gastric cancer.Medicine · 2020Article
- Silencing of brain-expressed X-linked 2 (BEX2) promotes colorectal cancer metastasis through the Hedgehog signaling pathway.International journal of biological sciences · 2020Article
- Defined factors to reactivate cell cycle activity in adult mouse cardiomyocytes.Scientific reports · 2019Article
- Diagnostic and prognostic value of the BEX family in lung adenocarcinoma.Oncology letters · 2019Article
- ANGPTL1 attenuates colorectal cancer metastasis by up-regulating microRNA-138.Journal of experimental & clinical cancer research : CR · 2017Article
- BEX2 promotes tumor proliferation in colorectal cancer.International journal of biological sciences · 2017Article
- Combination of Imatinib Mesylate and AKT Inhibitor Provides Synergistic Effects in Preclinical Study of Gastrointestinal Stromal Tumor.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Decreased brain-expressed X-linked 4 (BEX4) expression promotes growth of oral squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2016Article
- BEX1 acts as a tumor suppressor in acute myeloid leukemia.Oncotarget · 2015Article
- Brain expressed and X-linked (Bex) proteins are intrinsically disordered proteins (IDPs) and form new signaling hubs.PloS one · 2015Article
- Computational deconvolution of genome wide expression data from Parkinson's and Huntington's disease brain tissues using population-specific expression analysis.Frontiers in neuroscience · 2014Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
An enhanced anti-apoptotic capacity of tumor cells plays an important role in the process of breakpoint cluster region/Abelson tyrosine kinase gene (BCR/ABL)-independent imatinib resistance. We have previously demonstrated that brain expressed X-linked 1 (BEX1) was silenced in secondary imatinib-resistant K562 cells and that re-expression of BEX1 can restore imatinib sensitivity resulting in the induction of apoptosis. However, the mechanism by which BEX1 executes its pro-apoptotic function remains unknown. We identified B-cell lymphoma 2 (BCL-2) as a BEX1-interacting protein using a yeast two-hybrid screen. The interaction between BEX1 and BCL-2 was subsequently confirmed by co-immunoprecipitation assays. Like BCL-2, BEX1 was localized to the mitochondria. The region between 33K and 64Q on BEX1 is important for its localization to the mitochondria and its ability to interact with BCL-2. Additionally, we found that this region is essential for BEX1-regulated imatinib-induced apoptosis. Furthermore, we demonstrated that the interaction between BCL-2 and BEX1 promotes imatinib-induced apoptosis by suppressing the formation of anti-apoptotic BCL-2/BCL-2-associated X protein (BAX) heterodimers. Our results revealed an interaction between BEX1 and BCL-2 and a novel mechanism of imatinib resistance mediated by the BEX1/BCL-2 pathway.
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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.