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BMI1 (BMI1 polycomb ring finger oncogene)

Written2009-03Lina Han, Szabolcs Fatrai, Jan Jacob Schuringa
Department of Hematology, University Medical Center Groningen, Hanzeplein 1, 9700 RB, The Netherlands

(Note : for Links provided by Atlas : click)


polycomb group ring finger 4
B lymphoma Mo-MLV insertion region 1 homolog (mouse)
Alias_symbol (synonym)RNF51
Other aliasMGC12685
HGNC (Hugo) BMI1
LocusID (NCBI) 648
Atlas_Id 807
Location 10p12.2  [Link to chromosome band 10p12]
Location_base_pair Starts at 22321210 and ends at 22331485 bp from pter ( according to hg19-Feb_2009)  [Mapping BMI1.png]
Local_order MLLT10 gene is one of the neighboring genes of BMI1. It locates 786566 base pairs downstream from the start site of BMI1. MLLT10 or AF10 is a transcription factor which is also one of the fusion proteins of ALL. ALL-AF10 can result in the development of T-cell ALL, AML FAB 0, AML FAB 1, AML FAB 5 and AML FAB 7.
PIP4K2A is the gene for Phosphatidylinositol-4-phosphate 5-kinase. The protein transcribed from this gene is catalyzing the phosphorylation of phosphatidylinositol-5-phosphate on the fourth hydroxyl of the myo-inositol ring to form phosphatidylinositol-5,4-bisphosphate. Phosphatidylinositol-5,4-bisphosphate is a precursor to second messengers in the phosphoinositide signal transduction pathways and it is involved in the regulation of secretion, cell proliferation, differentiation and motility.
Fusion genes
(updated 2017)
Data from Atlas, Mitelman, Cosmic Fusion, Fusion Cancer, TCGA fusion databases with official HUGO symbols (see references in chromosomal bands)
BMI1 (10p12.2) / ABI1 (10p12.1)COMMD3 (10p12.2) / BMI1 (10p12.2)GNA13 (17q24.1) / BMI1 (10p12.2)
STPG1 (1p36.11) / BMI1 (10p12.2)ZEB1 (10p11.22) / BMI1 (10p12.2)


Description DNA size: 10.04 kb with 10 exons.
The BMI1 gene is a highly conserved gene. The cDNA shows 86% identity to the mouse sequence.
Transcription mRNA size: 3199 bp.


Note 326 amino acids
Molecular weight of the protein: 36949 Da.
Description The ring finger domain is a cysteine-rich domain that binds two atoms of zinc and plays a key role in the process of ubiquitination. In hematopoietic stem cells BMI1 interacts with a proliferation inhibitor E4F through the IE4F site.
Expression Hematopoietic system: BMI1 is expressed in adult and embryonic fetal liver hematopoietic stem cells (HSC). During hematopoietic development the expression of BMI1 declines. Bmi1-/- mice are born with a hypocellular bone marrow, they have normal number of myeloid cells in the peripheral blood but lower number of lymphocytes. In the bone marrow of Bmi1-/- mice the total HSC number is decreased with 10-fold and transplanted bone marrow and fetal liver cells were able to contribute to hematopoiesis only transiently. Bmi1-depleted mice die within two months after birth. Adult HSCs from Bmi1-/- mice lack self-renewal potential. Furthermore, expression of stem cell-associated genes, cell survival genes, transcription factors and genes modulating proliferation was altered in the bone marrow cells. BMI1 overexpression was studied in transgenic mice and human CB models. In these mouse models 14% of the mice developed lymphoma. BMI1 overexpression in CD34+ cord blood cells resulted in long term maintenance and self-renewal of human hematopoietic stem and progenitor cells. These cells engrafted more efficiently in NOD-SCID mice and gave a rise to secondary engraftment.
Nervous system: BMI1 is required for neural stem cell self-renewal but it does not influence their survival and differentiation. BMI1 is strongly expressed in proliferating cerebellar precursor cells in mice and humans. The absence of BMI1 was related to the low level of p16 Ink4 as well as to low proliferation rate of neural stem cells. BMI1-deficient mice develop balance disorders, tremor, behavior disorders and they have a severe reduction in total postnatal brain mass.
Fibroblasts: In BMI1-deficient primary mouse embryonic fibroblast cell cycle progression to S phase was impaired and cells entered early senescence.
Localisation In nucleus and in the cytoplasm.
Function BMI1 is a member of the Polycomb group (PcG) genes, which are transcriptional repressors that play essential roles in the maintenance of appropriate gene expression during development. Two distinct multiprotein PcG complexes have been identified, the Polycomb Repression Complex (PRC) 1 and PRC2. The PRC2 complex is involved in initiation of silencing and contains histone deacetylases and methyltransferases that can methylate H3 lysine 9 and 27 (H3K27). Deletion of PRC2 genes in mice results in embryonic lethality, emphasizing their importance in development. PRC1 is implicated in stable maintenance of gene repression and recognizes the methylation marks set by PRC2. Mice mutant for most PRC1 genes survive until birth as result of partial functional redundancy provided by their homologues, but developmental defects do arise thereafter as is e.g. the case in the hematopoietic compartment after deletion of BMI1. Targeted deletion of BMI1 has shown that although the numbers of fetal liver-derived HSCs is normal in these mice, their proliferative and self-renewal capacity is severely impaired. In adult BMI1-deficient mice, the HSCs are less frequent and display an impaired competitive repopulation capacity. Gain-of-function studies demonstrated enhanced self-renewal of murine HSC and with a shift in balance towards more symmetric stem cell divisions. Constitutive expression of BMI1 in human cord blood cells results in prolonged maintenance of the stem cell pool and enhances self-renewal of human stem and progenitor cells. BMI1 is potent negative regulator of the Ink4a/Arf locus in embryonic fibroblasts. This locus encodes the cell cycle regulators and tumor suppressor p16 and p19/p14. Increased expression of these genes was observed in the BMI1-deficient mice. However, INK4A/ARF-independent BMI1-targets must exist as well since overexpression of BMI1 in p16/p19-deficient cells still altered HSC self-renewal phenotypes.


Note A mutation in BMI1 that results in a cysteine into tyrosine substitution at position 18 within the RING domain has been identified, which is associated with a decrease in BMI1 expression levels and elevated ubiquitination.

Implicated in

Entity Hematological malignancies
Disease BMI1 overexpression has been demonstrated in several hematological malignancies, mainly including mantle cell lymphoma, myeloid dysplastic syndrome (MDS), chronic myeloid leukemia (CML) and acute myeloid leukemia (AML).
Prognosis In general, high BMI1 expression levels are associated with a poor prognosis and increased aggressiveness of the tumors. In CML, the level of BMI1 at diagnosis correlated with time to transformation to blast crisis. In MDS, patients with RA and RARS with a higher percentage of BMI1-positive cells showed disease progression to RAEB. Intriguingly, in CML post allo-SCT, high BMI1 at diagnosis predicts better overall survival, which might be ascribed to the neutralized effects against BMI1 by an immune response in donor cells.
Cytogenetics Different chromosomal translocations involving the 10p11-13 region have also been identified in infant leukemias, occurring in children < 12 months of age and T cell lymphoproliferative disorders, including mainly adult T cell leukemia/lymphomas and occasional cutaneous T cell lymphomas. It was demonstrated that BMI1 was overexpressed with MEIS1 in 11q23 (MLL) rearrangements, suggesting that p16/p19 suppression maybe involved in MLL-associated leukemia.
Oncogenesis See below.
Entity Solid tumors
Disease BMI1 overexpression was implicated in various solid tumors, including ovarian cancer, bladder cancer, squamous cell carcinoma, prostate cancer, breast carcinomas, non-small-cell lung cancer and GI cancer.
Prognosis The oncogenic role of the BMI1 activation may contribute to progression of many types of solid tumors. The median survival is 46 months and 5-year survival is 37.5% in BMI1/EZH2-positive prostate cancer patients after radical prostatectomy (The 5-year survival is 72.4% in BMI1/EZH2-negative prostate cancer patients). But in breast cancer, increased BMI1 expression is associated with a good prognosis, which might be because BMI1 overexpression correlates with higher ER expression and lower TP53 mutations.
Oncogenesis See below.
Entity Neural stem cells renewal
Note BMI1 promotes the maintenance of adult neural stem cells (NSCs) by repressing the cyclin-dependent kinase inhibitors, p16Ink4a and p19ARF. Recent study showed that BMI1 was also important for NSCs in the embryo, using lentiviral-delivered shRNAs in vitro and in vivo. These defects caused by BMI1 downregulation were unexpectedly mediated by p21.
Oncogenesis Gene-profiling studies show that BMI-/- HSC displayed altered expression of multiple genes important for stem cell fate decisions. The tumor suppressor locus p16Ink4a/p19ARF is one of the important targets that is repressed by BMI1. The p16Ink4a protein blocks the cyclinD-CDK complexes by binding directly to CDK4 and CDK6, enabling p21CIP1 and p27KIP1 to associate with and inhibit cyclin E-CDK2 and cyclin A-CDK2, which results the hypophosphorylated pRb. The E2F transcription factors will be sequestered and their target genes will be repressed, ultimately leading to G1-phase cell cycle arrest, senescence, or apoptosis. p19ARF binds to MDM2 and inhibits its ubiquitin ligase activity, resulting in activation of p53 target genes, including Wig1 and p21, leading to cell cycle arrest and apoptosis. Furthermore, cells might undergo apoptosis as a result of downregulated apoptosis inhibitor AI-6 in the absence of BMI1. BMI1 was also demonstrated to upregulate the human telomerase RT gene (hTERT), which might also be relevant for the self-renewal ability of HSCs or LSCs.
Deregulated Hox gene expression caused by chromosomal translocations and MLL rearrangements, is involved in some types of leukemia. The skeletal defects of PcG mutant mice revealed PcG genes as Hox gene regulators. Knockout of BMI1 results in alterations in Hox gene expression, with 12 Hox genes significantly upregulated (for example, HoxA7-HoxA13 ; HoxC10-HoxC13) and 13 downregulated (for example, HoxA1-HoxA4 ). This study demonstrated that BMI1 and RING1A play important roles in H2A ubiquitylation and Hox gene silencing.
Overexpression of BMI1 is involved in tumor development and is used as an important marker for predicting prognosis. The mechanisms regulating BMI1 expression are not fully elucidated yet. In AML, BMI1 was demonstrated to be a direct target gene of SALL4, a zinc-finger transcription factor, which is expressed constitutively in human leukemia cell lines and primary AML cells. High levels of H3-K4 trimethylation and H3-K79 dimethylation were observed in the SALL4 binding region of the BMI1promoter. In normal and malignant human mammary stem cells activation of hedgehog signaling increases BMI1 expression and BMI1 overexpression promotes mammary stem cell self-renewal and proliferation. In CML, it was suggested that BMI1 was positively regulated by BCR-ABL as well as by additional posttranscriptional modification in the course of the disease progression.
Chromatin association and dissociation of BMI1 was also studied. BMI1 can be phosphorylated by 3pk (MAPKAP kinase 3), a convergence point downstream of activated ERK and p38 signaling pathways which are implicated in differentiation and developmental processes. BMI1 phosphorylation results in dissociation of BMI1 from chromatin, followed by de-repression of target genes.


Ink4a and Arf differentially affect cell proliferation and neural stem cell self-renewal in Bmi1-deficient mice.
Bruggeman SW, Valk-Lingbeek ME, van der Stoop PP, Jacobs JJ, Kieboom K, Tanger E, Hulsman D, Leung C, Arsenijevic Y, Marino S, van Lohuizen M.
Genes Dev. 2005 Jun 15;19(12):1438-43.
PMID 15964995
E4F1: a novel candidate factor for mediating BMI1 function in primitive hematopoietic cells.
Chagraoui J, Niessen SL, Lessard J, Girard S, Coulombe P, Sauvageau M, Meloche S, Sauvageau G.
Genes Dev. 2006 Aug 1;20(15):2110-20.
PMID 16882984
Novel zinc finger gene implicated as myc collaborator by retrovirally accelerated lymphomagenesis in E mu-myc transgenic mice.
Haupt Y, Alexander WS, Barri G, Klinken SP, Adams JM.
Cell. 1991 May 31;65(5):753-63.
PMID 1904009
bmi-1 transgene induces lymphomas and collaborates with myc in tumorigenesis.
Haupt Y, Bath ML, Harris AW, Adams JM.
Oncogene. 1993 Nov;8(11):3161-4.
PMID 8414519
Control of the replicative life span of human fibroblasts by p16 and the polycomb protein Bmi-1.
Itahana K, Zou Y, Itahana Y, Martinez JL, Beausejour C, Jacobs JJ, Van Lohuizen M, Band V, Campisi J, Dimri GP.
Mol Cell Biol. 2003 Jan;23(1):389-401.
PMID 12482990
Enhanced self-renewal of hematopoietic stem cells mediated by the polycomb gene product Bmi-1.
Iwama A, Oguro H, Negishi M, Kato Y, Morita Y, Tsukui H, Ema H, Kamijo T, Katoh-Fukui Y, Koseki H, van Lohuizen M, Nakauchi H.
Immunity. 2004 Dec;21(6):843-51.
PMID 15589172
The oncogene and Polycomb-group gene bmi-1 regulates cell proliferation and senescence through the ink4a locus.
Jacobs JJ, Kieboom K, Marino S, DePinho RA, van Lohuizen M.
Nature. 1999 Jan 14;397(6715):164-8.
PMID 9923679
Bmi1 is essential for cerebellar development and is overexpressed in human medulloblastomas.
Leung C, Lingbeek M, Shakhova O, Liu J, Tanger E, Saremaslani P, Van Lohuizen M, Marino S.
Nature. 2004 Mar 18;428(6980):337-41.
PMID 15029199
Bmi-1 promotes neural stem cell self-renewal and neural development but not mouse growth and survival by repressing the p16Ink4a and p19Arf senescence pathways.
Molofsky AV, He S, Bydon M, Morrison SJ, Pardal R.
Genes Dev. 2005 Jun 15;19(12):1432-7.
PMID 15964994
Bmi-1 is required for maintenance of adult self-renewing haematopoietic stem cells.
Park IK, Qian D, Kiel M, Becker MW, Pihalja M, Weissman IL, Morrison SJ, Clarke MF.
Nature. 2003 May 15;423(6937):302-5. Epub 2003 Apr 20.
PMID 12714971
Long-term maintenance of human hematopoietic stem/progenitor cells by expression of BMI1.
Rizo A, Dontje B, Vellenga E, de Haan G, Schuringa JJ.
Blood. 2008 Mar 1;111(5):2621-30. Epub 2007 Dec 21.
PMID 18156489
Posterior transformation, neurological abnormalities, and severe hematopoietic defects in mice with a targeted deletion of the bmi-1 proto-oncogene.
van der Lugt NM, Domen J, Linders K, van Roon M, Robanus-Maandag E, te Riele H, van der Valk M, Deschamps J, Sofroniew M, van Lohuizen M, et al.
Genes Dev. 1994 Apr 1;8(7):757-69.
PMID 7926765


This paper should be referenced as such :
Han, L ; Fatrai, S ; Schuringa, JJ
BMI1 (BMI1 polycomb ring finger oncogene)
Atlas Genet Cytogenet Oncol Haematol. 2010;14(2):87-90.
Free journal version : [ pdf ]   [ DOI ]
On line version :

Other Leukemias implicated (Data extracted from papers in the Atlas) [ 2 ]
  t(10;10)(p11;p12) ZEB1/BMI1
t(10;14)(p12;q32) IGH/BMI1

Other Solid tumors implicated (Data extracted from papers in the Atlas) [ 2 ]
  BMI1/ABI1 (10p12)
t(10;17)(p12;q24) GNA13/BMI1

External links

HGNC (Hugo)BMI1   1066
Entrez_Gene (NCBI)BMI1  648  BMI1 proto-oncogene, polycomb ring finger
AliasesFLVI2/BMI1; PCGF4; RNF51; flvi-2/bmi-1
GeneCards (Weizmann)BMI1
Ensembl hg19 (Hinxton)ENSG00000168283 [Gene_View]
Ensembl hg38 (Hinxton)ENSG00000168283 [Gene_View]  ENSG00000168283 [Sequence]  chr10:22321210-22331485 [Contig_View]  BMI1 [Vega]
ICGC DataPortalENSG00000168283
TCGA cBioPortalBMI1
AceView (NCBI)BMI1
Genatlas (Paris)BMI1
SOURCE (Princeton)BMI1
Genetics Home Reference (NIH)BMI1
Genomic and cartography
GoldenPath hg38 (UCSC)BMI1  -     chr10:22321210-22331485 +  10p12.2   [Description]    (hg38-Dec_2013)
GoldenPath hg19 (UCSC)BMI1  -     10p12.2   [Description]    (hg19-Feb_2009)
GoldenPathBMI1 - 10p12.2 [CytoView hg19]  BMI1 - 10p12.2 [CytoView hg38]
Mapping of homologs : NCBIBMI1 [Mapview hg19]  BMI1 [Mapview hg38]
Gene and transcription
Genbank (Entrez)AH004292 AI274830 BC011652 BE008203 BT019450
RefSeq transcript (Entrez)NM_005180
RefSeq genomic (Entrez)
Consensus coding sequences : CCDS (NCBI)BMI1
Cluster EST : UnigeneHs.731287 [ NCBI ]
CGAP (NCI)Hs.731287
Alternative Splicing GalleryENSG00000168283
Gene ExpressionBMI1 [ NCBI-GEO ]   BMI1 [ EBI - ARRAY_EXPRESS ]   BMI1 [ SEEK ]   BMI1 [ MEM ]
Gene Expression Viewer (FireBrowse)BMI1 [ Firebrowse - Broad ]
SOURCE (Princeton)Expression in : [Datasets]   [Normal Tissue Atlas]  [carcinoma Classsification]  [NCI60]
GenevestigatorExpression in : [tissues]  [cell-lines]  [cancer]  [perturbations]  
BioGPS (Tissue expression)648
GTEX Portal (Tissue expression)BMI1
Human Protein AtlasENSG00000168283-BMI1 [pathology]   [cell]   [tissue]
Protein : pattern, domain, 3D structure
UniProt/SwissProtP35226   [function]  [subcellular_location]  [family_and_domains]  [pathology_and_biotech]  [ptm_processing]  [expression]  [interaction]
NextProtP35226  [Sequence]  [Exons]  [Medical]  [Publications]
With graphics : InterProP35226
Splice isoforms : SwissVarP35226
Domaine pattern : Prosite (Expaxy)ZF_RING_1 (PS00518)    ZF_RING_2 (PS50089)   
Domains : Interpro (EBI)RAWUL    Znf_RING    Znf_RING/FYVE/PHD    Znf_RING_CS   
Domain families : Pfam (Sanger)RAWUL (PF16207)   
Domain families : Pfam (NCBI)pfam16207   
Domain families : Smart (EMBL)RING (SM00184)  
Conserved Domain (NCBI)BMI1
DMDM Disease mutations648
Blocks (Seattle)BMI1
PDB (RSDB)2H0D    2NA1    3RPG    4R8P    5FR6   
PDB Europe2H0D    2NA1    3RPG    4R8P    5FR6   
PDB (PDBSum)2H0D    2NA1    3RPG    4R8P    5FR6   
PDB (IMB)2H0D    2NA1    3RPG    4R8P    5FR6   
Structural Biology KnowledgeBase2H0D    2NA1    3RPG    4R8P    5FR6   
SCOP (Structural Classification of Proteins)2H0D    2NA1    3RPG    4R8P    5FR6   
CATH (Classification of proteins structures)2H0D    2NA1    3RPG    4R8P    5FR6   
Human Protein Atlas [tissue]ENSG00000168283-BMI1 [tissue]
Peptide AtlasP35226
IPIIPI00017299   IPI00514181   IPI00646013   IPI00643353   IPI00643590   IPI00640733   
Protein Interaction databases
IntAct (EBI)P35226
Ontologies - Pathways
Ontology : AmiGOnegative regulation of transcription by RNA polymerase II  negative regulation of transcription by RNA polymerase II  ubiquitin ligase complex  protein binding  nucleus  nucleoplasm  cytosol  chromatin silencing  segment specification  zinc ion binding  regulation of gene expression  nuclear body  hemopoiesis  PcG protein complex  PRC1 complex  PRC1 complex  histone H2A-K119 monoubiquitination  histone H2A-K119 monoubiquitination  negative regulation of gene expression, epigenetic  positive regulation of fibroblast proliferation  positive regulation of ubiquitin-protein transferase activity  negative regulation of G0 to G1 transition  RING-like zinc finger domain binding  promoter-specific chromatin binding  promoter-specific chromatin binding  
Ontology : EGO-EBInegative regulation of transcription by RNA polymerase II  negative regulation of transcription by RNA polymerase II  ubiquitin ligase complex  protein binding  nucleus  nucleoplasm  cytosol  chromatin silencing  segment specification  zinc ion binding  regulation of gene expression  nuclear body  hemopoiesis  PcG protein complex  PRC1 complex  PRC1 complex  histone H2A-K119 monoubiquitination  histone H2A-K119 monoubiquitination  negative regulation of gene expression, epigenetic  positive regulation of fibroblast proliferation  positive regulation of ubiquitin-protein transferase activity  negative regulation of G0 to G1 transition  RING-like zinc finger domain binding  promoter-specific chromatin binding  promoter-specific chromatin binding  
Pathways : KEGGTranscriptional misregulation in cancer    MicroRNAs in cancer   
REACTOMEP35226 [protein]
REACTOME PathwaysR-HSA-8953750 [pathway]   
NDEx NetworkBMI1
Atlas of Cancer Signalling NetworkBMI1
Wikipedia pathwaysBMI1
Orthology - Evolution
GeneTree (enSembl)ENSG00000168283
Phylogenetic Trees/Animal Genes : TreeFamBMI1
Homologs : HomoloGeneBMI1
Homology/Alignments : Family Browser (UCSC)BMI1
Gene fusions - Rearrangements
Fusion : MitelmanGNA13/BMI1 [17q24.1/10p12.2]  [t(10;17)(p12;q24)]  
Fusion : MitelmanIGH/BMI1 [14q32.33/10p12.2]  [t(10;14)(p12;q32)]  
Fusion : MitelmanZEB1/BMI1 [10p11.22/10p12.2]  [t(10;10)(p11;p12)]  
Fusion PortalGNA13 17q24.1 BMI1 10p12.2 HNSC
Fusion : FusionGDB14826    4224   
Fusion : Fusion_HubABI1--BMI1    BMI1--BTG1    BMI1--DDX5    BMI1--DIP2A    BMI1--HK1    BMI1--IGH@    BMI1--PCGF5    BMI1--PIP4K2A    BMI1--SEC24B    BMI1--SORBS1    BMI1--SRP72    BMI1--UBR3    COMMD3--BMI1    FAM20C--BMI1    GNA13--BMI1   
HERC4--BMI1    PIP4K2A--BMI1    SMARCD2--BMI1    ZFAND3--BMI1   
Fusion : QuiverBMI1
Polymorphisms : SNP and Copy number variants
NCBI Variation ViewerBMI1 [hg38]
dbSNP Single Nucleotide Polymorphism (NCBI)BMI1
Exome Variant ServerBMI1
ExAC (Exome Aggregation Consortium)ENSG00000168283
GNOMAD BrowserENSG00000168283
Varsome BrowserBMI1
Genetic variants : HAPMAP648
Genomic Variants (DGV)BMI1 [DGVbeta]
DECIPHERBMI1 [patients]   [syndromes]   [variants]   [genes]  
CONAN: Copy Number AnalysisBMI1 
ICGC Data PortalBMI1 
TCGA Data PortalBMI1 
Broad Tumor PortalBMI1
OASIS PortalBMI1 [ Somatic mutations - Copy number]
Somatic Mutations in Cancer : COSMICBMI1  [overview]  [genome browser]  [tissue]  [distribution]  
Somatic Mutations in Cancer : COSMIC3DBMI1
Mutations and Diseases : HGMDBMI1
LOVD (Leiden Open Variation Database)Whole genome datasets
LOVD (Leiden Open Variation Database)LOVD 3.0 shared installation
BioMutasearch BMI1
DgiDB (Drug Gene Interaction Database)BMI1
DoCM (Curated mutations)BMI1 (select the gene name)
CIViC (Clinical Interpretations of Variants in Cancer)BMI1 (select a term)
NCG5 (London)BMI1
Cancer3DBMI1(select the gene name)
Impact of mutations[PolyPhen2] [Provean] [Buck Institute : MutDB] [Mutation Assessor] [Mutanalyser]
Genetic Testing Registry BMI1
NextProtP35226 [Medical]
Target ValidationBMI1
Huge Navigator BMI1 [HugePedia]
snp3D : Map Gene to Disease648
BioCentury BCIQBMI1
Clinical trials, drugs, therapy
Chemical/Protein Interactions : CTD648
Chemical/Pharm GKB GenePA25376
Clinical trialBMI1
canSAR (ICR)BMI1 (select the gene name)
DataMed IndexBMI1
PubMed499 Pubmed reference(s) in Entrez
GeneRIFsGene References Into Functions (Entrez)
REVIEW articlesautomatic search in PubMed
Last year publicationsautomatic search in PubMed

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