ArticleMolecular and cellular biology1996
Transformation by the Bmi-1 oncoprotein correlates with its subnuclear localization but not its transcriptional suppression activity.
Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 62 citations in OpenAlex.
- BMI-1 modulation and trafficking during M phase in diffuse intrinsic pontine glioma.FEBS open bio · 2026Article
- Targeting LSD1 suppresses stem cell-like properties and sensitizes head and neck squamous cell carcinoma to PD-1 blockade.Cell death & disease · 2021Article
- Regulation of gene transcription of B lymphoma Mo-MLV insertion region 1 homolog (Review).Biomedical reports · 2021Review
- BMI1 Drives Steroidogenesis Through Epigenetically Repressing the p38 MAPK Pathway.Frontiers in cell and developmental biology · 2021Article
- Mitochondrial BMI1 maintains bioenergetic homeostasis in cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- BMI1 regulates PRC1 architecture and activity through homo- and hetero-oligomerization.Nature communications · 2016Article
- Overexpression of Bmi1 in Lymphocytes Stimulates Skeletogenesis by Improving the Osteogenic Microenvironment.Scientific reports · 2016Article
- Bmi-1: At the crossroads of physiological and pathological biology.Genes & diseases · 2015Article
- The Bmi-1 helix-turn and ring finger domains are required for Bmi-1 antagonism of (-) epigallocatechin-3-gallate suppression of skin cancer cell survival.Cellular signalling · 2015Article
- Article
- BMI1 expression identifies subtypes of Merkel cell carcinoma.Virchows Archiv : an international journal of pathology · 2012Article
- Clinicopathologic characteristics of high expression of Bmi-1 in esophageal adenocarcinoma and squamous cell carcinoma.BMC gastroenterology · 2012Article
- Polycomb group proteins are key regulators of keratinocyte function.The Journal of investigative dermatology · 2011Review
- Bmi-1 extends the life span of normal human oral keratinocytes by inhibiting the TGF-beta signaling.Experimental cell research · 2010Article
- Deletion analysis of BMI1 oncoprotein identifies its negative regulatory domain.Molecular cancer · 2010Article
- Identification of a polymorphism in the RING finger of human Bmi-1 that causes its degradation by the ubiquitin-proteasome system.FEBS letters · 2009Article
- Severe growth retardation and early lethality in mice lacking the nuclear localization sequence and C-terminus of PTH-related protein.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Epidermal growth factor receptor 1 (EGFR1) and its variant EGFRvIII regulate TATA-binding protein expression through distinct pathways.Molecular and cellular biology · 2008Article
- Expression of Bmi-1 in epidermis enhances cell survival by altering cell cycle regulatory protein expression and inhibiting apoptosis.The Journal of investigative dermatology · 2008Article
- Contribution of polycomb homologues Bmi-1 and Mel-18 to medulloblastoma pathogenesis.Molecular and cellular biology · 2007Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The bmi-1 oncogene cooperates with c-myc in transgenic mice, resulting in accelerated lymphoma development. Altering the expression of Bmi-1 affects normal embryogenesis. The protein product of bmi-1 is homologous to certain Drosophila Polycomb group proteins that regulate homeotic gene expression through alteration of chromatin structure. Chimeric LexA-Bmi-1 protein has previously been shown to repress transcription. How Bmi-1 functions in embryogenesis and whether this relates to the ability of Bmi-1 to mediate cellular transformation is unknown. We demonstrate here that Bmi-1 is able to transform rodent fibroblasts in vitro, providing a system that has allowed us to correlate its molecular properties with its ability to transform cells. We map functional domains of Bmi-1 involved in transcriptional suppression by using the GAL4 chimeric transcriptional regulator system. Deletion analysis shows that the centrally located helix-turn-helix-turn-helix-turn (HTHTHT) motif is necessary for transcriptional suppression whereas the N-terminal RING finger domain is not required. We demonstrate that nuclear localization requires KRMK (residues 230 to 233) and that the absence of nuclear entry ablates transformation. In addition, we find that the subnuclear localization of wild-type Bmi-1 to the rim of the nucleus requires the RING finger domain and correlates with its ability to transform. Our studies with Bmi-1 deletion mutants suggest that the ability of Bmi-1 to mediate cellular transformation correlates with its unique subnuclear localization but not its transcriptional suppression activity.
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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.