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ERG encodes a member of the erythroblast transformation-specific (ETS) family of transcriptions factors. Zusätzlich bieten wir Ihnen V-Ets erythroblastosis Virus E26 Oncogene Homolog (Avian) Antikörper (115) und V-Ets erythroblastosis Virus E26 Oncogene Homolog (Avian) Proteine (17) und viele weitere Produktgruppen zu diesem Protein an.
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KLF2 (zeige KLF2 ELISA Kits) and ERG associate in a physical complex and the two proteins synergistically activate transcription of Flk1 (zeige KDR ELISA Kits).
loss of ERG and FLI1 (zeige FLI1 ELISA Kits) might contribute to the pathogenesis of vascular lung complications through the induction of inflammation.
Combined, these data suggest a possible pathway linking GDF5 (zeige GDF5 ELISA Kits), ERG and downstream factors in the processes of chondrocyte differentiation during articular joint formation.
Our study reveals that ERG has essential and cell autonomous roles in endothelial cell development and blood vessel maintenance.
We show that the gene expression signature specifically attributable to trisomy of Erg in the murine model is strongly correlated with gene expression changes in human Down syndrome hematopoietic cells.
Articular cartilage endurance and resistance to osteoarthritic changes require transcription factor Erg.
ERG plays a critical role in coordinating the balance between self-renewal and differentiation of HSCs.
ERG activates the transcriptional program regulated by YAP1 (zeige YAP1 ELISA Kits) of the Hippo signaling pathway and found that prostate-specific activation of either ERG or YAP1 (zeige YAP1 ELISA Kits) in mice induces similar transcriptional changes and results in age-related prostate tumors.
ERG and APLNR (zeige APLNR ELISA Kits) are essential for endothelial homeostasis in venules in the lung and that perturbation in ERG-APLNR (zeige APLNR ELISA Kits) signaling is crucial for the development of pulmonary veno-occlusive disease.
Regulation of Erg by TGF-beta (zeige TGFB1 ELISA Kits) was confirmed in these cells.
Ablation of the oncogenic transcription factor ERG by deubiquitinase inhibition in prostate cancer.
NOTCH (zeige NOTCH1 ELISA Kits) pathway inhibition antagonizes the growth and invasion of transmembrane protease serine 2 (TMPRSS2 (zeige TMPRSS2 ELISA Kits))-transforming protein ERG (ERG) (T2E) -positive prostate cancer cells.
findings have identified critical molecular mechanisms involving ERK (zeige EPHB2 ELISA Kits)-mediated ERG activation that could be exploited for therapeutic intervention in ERG-positive prostate cancers.
Detection of Gene Rearrangements in Circulating Tumor Cells: Examples of ALK (zeige ALK ELISA Kits)-, ROS1 (zeige ROS1 ELISA Kits)-, RET (zeige RET ELISA Kits)-Rearrangements in Non-Small-Cell Lung Cancer and ERG-Rearrangements in Prostate Cancer.(
The TMPRSS2 (zeige TMPRSS2 ELISA Kits)-ERG gene fusion is the most frequently observed genetic aberration in Prostate cancer.
Loss of ERG is associated with prostate tumors.
Data show that homogeneous ERG positivity is very rare in prostate cancer, especially in elderly patients. However, development of subpopulations with ERG fusions may be a much more frequent event in ERG negative cancer foci as previously believed.
Genome-wide gene expression profiling identified a network of VEGF (zeige VEGFA ELISA Kits)-responsive and ERG-dependent genes.
ERG deletion is associated with acute lymphoblastic leukemia.
Study provide evidence that PTEN deletion and TMPRSS2 (zeige TMPRSS2 ELISA Kits)-ERG gene fusion were mutually exclusive in patients with prostate neoplasm. TMPRSS2 (zeige TMPRSS2 ELISA Kits)-ERG gene fusion was rare compared to peripheral zone tumors and to PTEN inactivation in T1a (zeige PDPN ELISA Kits) transition zone tumors.
ERG rearrangement, but not PTEN loss, is present in a minority of potential neoplastic precursor lesions in the prostate.
fli1 (zeige FLI1 ELISA Kits), and etsrp, demonstrated that erg (zeige KCNH2 ELISA Kits) and fli1 (zeige FLI1 ELISA Kits) act cooperatively and are required for angiogenesis possibly via direct regulation of an endothelial cell junction molecule, VE-cadherin (zeige CDH5 ELISA Kits)
A combination of gain-of-function and loss-of-function studies suggested a redundant yet specific role for erg (zeige KCNH2 ELISA Kits) in both angioblast specification/proliferation and early angiogenesis, and a synergistic interaction with the critical ETS (zeige ETS1 ELISA Kits) factor etsrp.
This gene encodes a member of the erythroblast transformation-specific (ETS) family of transcriptions factors. All members of this family are key regulators of embryonic development, cell proliferation, differentiation, angiogenesis, inflammation, and apoptosis. The protein encoded by this gene is mainly expressed in the nucleus. It contains an ETS DNA-binding domain and a PNT (pointed) domain which is implicated in the self-association of chimeric oncoproteins. This protein is required for platelet adhesion to the subendothelium, inducing vascular cell remodeling. It also regulates hematopoesis, and the differentiation and maturation of megakaryocytic cells. This gene is involved in chromosomal translocations, resulting in different fusion gene products, such as TMPSSR2-ERG and NDRG1-ERG in prostate cancer, EWS-ERG in Ewing's sarcoma and FUS-ERG in acute myeloid leukemia. Multiple alternatively spliced transcript variants encoding different isoforms have been identified.
v-ets erythroblastosis virus E26 oncogene like
, Ether-a-go-go-related gene potassium channel 1
, Potassium voltage-gated channel subfamily H member 2
, v-ets erythroblastosis virus E26 oncogene homolog (avian)
, v-ets erythroblastosis virus E26 oncogene homolog
, erg gene (erg_E)
, vascular ETS factor
, transcriptional regulator ERG
, avian erythroblastosis virus E-26 (v-ets) oncogene related
, TMPRSS2/ERG fusion
, transcriptional regulator ERG (transforming protein ERG)
, v-ets avian erythroblastosis virus E26 oncogene related
, transcriptional regulator Erg