ERG
ERG (ETS transcription factor ERG, also known as erg-3 and p55) is a nuclear transcriptional regulator of the ETS family. It acts in vascular remodelling and haematopoiesis, and its gene is a frequent partner in oncogenic fusions. Browse Assay Genie's current range of ERG research reagents below, or read on for the biology behind the target.
ERG is a transcriptional regulator. UniProt annotates it as possibly participating in transcriptional regulation through recruitment of the SETDB1 histone methyltransferase, which would modify local chromatin structure. The protein is mainly found in the nucleus, with a cytoplasmic pool also recorded. It contains an ETS DNA-binding domain and a PNT (pointed) domain, the latter implicated in the self-association of chimeric oncoproteins.
The ERG gene encodes a member of the erythroblast transformation-specific (ETS) family. Members of this family are key regulators of embryonic development, cell proliferation, differentiation, angiogenesis, inflammation and apoptosis. The ERG protein is required for platelet adhesion to the subendothelium, where it induces vascular cell remodelling. It also regulates haematopoiesis and the differentiation and maturation of megakaryocytic cells. More than two dozen transcript variants have been reported, generated by three alternative promoters and multiple alternative splicing events, although the full-length nature of many of them has not been determined.
The gene takes its earlier names, v-ets avian erythroblastosis virus E26 oncogene related and oncogene homolog, from its relationship to the viral E26 oncogene. ERG is involved in chromosomal translocations that produce fusion genes, including TMPRSS2-ERG and NDRG1-ERG in prostate cancer, EWS-ERG in Ewing's sarcoma and FUS-ERG in acute myeloid leukaemia. These rearrangements make ERG a recurring subject in cancer biology as well as vascular and blood-cell research.
ERG is fused to partners such as TMPRSS2 and NDRG1 in prostate cancer, making it a focus for studies of translocation-driven disease.
EWS-ERG in Ewing's sarcoma and FUS-ERG in acute myeloid leukaemia link ERG to fusion oncoprotein biology in these malignancies.
ERG regulates haematopoiesis and the differentiation and maturation of megakaryocytic cells, so it is relevant to blood-cell development studies.
ERG is required for platelet adhesion to the subendothelium and induces vascular cell remodelling, linking it to angiogenesis and vessel function.
ERG is an ETS family transcriptional regulator. It may act by recruiting the SETDB1 histone methyltransferase to alter local chromatin. It is required for platelet adhesion to the subendothelium, induces vascular cell remodelling, and regulates haematopoiesis and megakaryocytic differentiation and maturation.
ERG is also called erg-3 and p55, and was formerly named v-ets avian erythroblastosis virus E26 oncogene related or homolog. UniProt lists it as Transcriptional regulator ERG. More than two dozen transcript variants have been reported, from three alternative promoters and alternative splicing.
The ERG gene is involved in chromosomal translocations that create fusion genes. Examples are TMPRSS2-ERG and NDRG1-ERG in prostate cancer, EWS-ERG in Ewing's sarcoma and FUS-ERG in acute myeloid leukaemia. The PNT domain is implicated in self-association of such chimeric oncoproteins.
Fusion partners, chromatin regulators and other targets connected to ERG biology in cancer and development.
Gene and protein annotations from HGNC, NCBI Gene and UniProt P11308; product specifications from Assay Genie datasheets.