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FLASH GENE
Symbol ERG contributors: mct/npt/pgu - updated : 09-04-2016
HGNC name v-ets erythroblastosis virus E26 oncogene homolog (avian)
HGNC id 3446
RNA
TRANSCRIPTS type messenger
identificationnb exonstypebpproduct
ProteinkDaAAspecific expressionYearPubmed
10 - 4945 - 479 - 2009 19156837
11 - 5042 - 462 - 2009 19156837
12 - 5114 54.5 486 - 2009 19156837
9 - 4727 44 387 - 2009 19156837
12 - 1520 - 317 - 2009 19156837
12 - 5139 - 486 - 2009 19156837
9 - 4703 - 363 - 2009 19156837
EXPRESSION
Type ubiquitous
   expressed in (based on citations)
organ(s)
SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
Cardiovascularvessel   highly Homo sapiens
Endocrineparathyroid   highly
Lymphoid/Immunespleen   highly
Reproductivemale systemtestis   
Urinarybladder   highly
tissue
SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
Blood / hematopoieticbone marrow   
Muscularsmoothvessel highly Homo sapiens
cells
SystemCellPubmedSpeciesStageRna symbol
Cardiovascularendothelial cell Homo sapiens
cell lineage
cell lines
fluid/secretion
at STAGE
physiological period perinatal
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • ETS DNA-binding and helix-loop-helix (HLH) domains
  • HOMOLOGY
    intraspecies homolog to avian erythroblastosis virus E26 (v-ets) oncogene
    Homologene
    FAMILY
  • Ets family of transcription factors
  • CATEGORY transcription factor , protooncogene
    SUBCELLULAR LOCALIZATION extracellular
        intracellular
    intracellular,cytoplasm
    intracellular,nucleus
    text its protein expression is predominantly found in prostate carcinomas with ERG gene rearrangement and does not occur in benign glands
    basic FUNCTION
  • transcription regulator, through SETDB1-mediated histone methylation
  • required for endothelial tube formation
  • involved in a new pathway regulating angiogenesis and endothelial survival, via the adhesion molecule VE-cadherin
  • is at the center of a distinct regulatory program that is not required for hematopoietic specification or differentiation but is critical for hematopoietic stem cell maintenance during embryonic development
  • Ets-transcription factor required for normal blood stem cell development
  • promotes T-ALL (T-acute lymphoblastic leukemia) and failure to extinguish activity of stem cell enhancers associated with regulatory transcription factors such as ERG can contribute to the development of leukemia
  • plays a pivotal role in regulating endothelial cells (EC) barrier function and this effect is mediated in part through its regulation of CLDN5 gene expression
  • role for ERG as a gatekeeper controlling vascular inflammation, thus providing an important barrier to protect against inappropriate endothelial activation
  • in primary leukemic cells, ERG may contribute to the dysregulation of kinase signaling, which results in resistance to kinase inhibitors
  • is critically important for maintenance of the hematopoietic stem cell population
  • CELLULAR PROCESS nucleotide, transcription
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • SETDB1
  • WNT11 is a direct target of ERG (potent ERG induction promoted morphological transformation through WNT11 signals
  • from the fetal period, ERG acts as a direct upstream regulator of GATA2 and RUNX1 gene activity
  • CLDN5 is a downstream target of ERG in EC
  • TDRD1 is the first identified upregulated direct ERG target gene that is strongly associated with ERG overexpression in primary prostate cancer
  • ERG redirects AR to a set of genes including SOX9 that are not normally androgen stimulated, and SOX9 is a critical downstream effector of ERG in TMPRSS2:ERG fusion-positive prostate cancer (PCa)
  • LEF1 is a direct target of ERG and LEF1 inhibition fully abolished ERG-induced WNT signaling and target gene expression
  • SPOP functions as a tumor suppressor to negatively regulate the stability of the ERG oncoprotein in prostate cancer
  • ERG is recruited to mRNAs via interaction with RBPMS, and it promotes mRNA decay by binding CNOT2, a component of the CCR4-NOT deadenylation complex
  • role for inflammation-induced oxidative stress in the formation of DNA breaks leading to recurrent TMPRSS2-ERG gene fusions
  • cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral fusion translocation    
    Loss of PTEN and concomitant activation of AKTcould act in partnership with the TMPRSS2-ERG fusion protein to promote progression to prostatecancer
    tumoral     --over  
    overexpression in prostate tumor cells may contribute to the neoplastic process by activating MYC and by abrogating prostate epithelial differentiation as indicated by prostate epithelial specific markers
    tumoral fusion      
    NDRG1-ERG fusion in prostate carcinoma is predicted to encode a chimeric protein
    tumoral fusion      
    TMPRSS2:ERG gene fusion predicts subsequent detection of prostate cancer in patients with high-grade prostatic intraepithelial neoplasia (P
    tumoral     --over  
    may deregulate several signaling cascades in acute leukemia
    tumoral fusion      
    TMPRSS2-ERG gene fusions were observed in 44p 100 of prostate cancer, and over 90p100 of these fusions occurred in ERG exons 3 or 4
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS