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- Table of Contents
Facts about Transcriptional regulator ERG.
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Human | |
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Gene Name: | ERG |
Uniprot: | P11308 |
Entrez: | 2078 |
Belongs to: |
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ETS family |
transcriptional regulator ERG; 10ets-related; erg-3; p55; TMPRSS2-ERG prostate cancer specific; transcriptional regulator ERG; Transforming protein ERG; v-ets erythroblastosis virus E26 oncogene homolog (avian); v-ets erythroblastosis virus E26 oncogene like (avian); v-ets erythroblastosis virus E26 oncogene like
Mass (kDA):
54.608 kDA
Human | |
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Location: | 21q22.2 |
Sequence: | 21; NC_000021.9 (38367261..38661783, complement) |
Nucleus. Cytoplasm. Localized in cytoplasmic mRNP granules containing untranslated mRNAs.
The Boster Bio: Best Uses of The ERG Marker is an award-winning online resource. Boster Bio allows scientists the ability to submit results of species-specific or general applications. Scientists may be eligible for product credits or special samples in exchange. This free tool is available to Boster scientists all over the world. Continue reading to find out more. Here are some examples from Boster Bio: The Best Uses of ERG Marker.
Wild-type ERG markers have a unique feature: they are associated with direct AR-regulated genes. Affymetrix array was used for the evaluation of a subset these genes. This was done by identifying their ERG binding site. Comparing the expression of nine of these genes to that of a control line of cells was done. In this study, five of these genes were also compared in DHT-treated VCaP cells.
Transgenic expression of ERG in PCa cells increased cell invasion and proliferation. ERG's downstream effector, SOX9, was identified. ERG indirectly regulates SOX9 through opening a cryptic AR regulated enhancer in SOX9. ERG also redirects AR to genes that have not been stimulated. PCa progression is linked to Sox9 expression.
These findings are not the only ones that have been made. Numerous studies have also shown ERG's function in prostate progenitors. ERG-dependent proteins can be identified using organoids and Click-chemistry. This could possibly create the conditions that encourage prostate cancer. In 5-30% of HGPIN prostate lesion lesions, genomic rearrangements were shown to increase ERG expression. The gene could play a critical role in the initial stages of PCa.
Boster Bio ERG marker DS contains 56 genes that harbor ERG binding spots within 20 kb. 46 of these 66 genes contain ERG binding sites that are highly enriched. ERG binding can also be facilitated by AR binding sites specific to VCaP. The DS of the wild-type ERG marker Boster Bio can be used for identifying genes that have abnormal expression of VCaP.
The MSKCC dataset showed that SOX9 was correlated with ERG. Sox9 immunohistochemistry was performed on a primary PCa tissue microarray. The tumors were scored according to the percentage of cells that were positive and their intensity. A tumor's addscore was calculated based on these numbers. In the study, SOX9 expression was also higher among fusion-positive samples than those that were not.
We have done DS analysis of genes derived form Ewing sarcoma cellular cells in order to identify novel gene expression patterns. These gene expression patterns were associated to aberrant transcriptional regulation as well as DNA binding. The candidate gene for this disease is the EWSFLI1 fusion proteins. Its junction region plays a role in DNA methylation and transcriptional regulation as well as cell proliferation. This paper contains the DS results.
The DS analysis of EWSFLI1 protein demonstrated that the junction region is composed three amino acids, one of which was predicted be a ligand binding spot. The DS from wild-type FLI1 also showed circular Dichroism. It consists two ordered regions separated with a junction. Below is a description of the DS EWSFLI1.
We can also find a DS for ETS-FUS fusion. This fusion affects both wildtype and ETS/fusion partners. While the ERG is downregulated in the ES2 samples, the expression of FLI1 is not. The rMATS analysis is a powerful tool for discovering novel functional features in wild-type FLI1 human cells.
DS events may play a role in transcriptional activation. DS events are implicated in gene expression regulation during muscle development and neural stem cells proliferation. DS also affects the activities the PRC2 & BAF complexes. Moreover, the PRC2 complex, which contains three DS genes (CDC27, ANAPC77 and CDC23), is antagonistic towards BAF.
In a previous study we identified a functional fusion protein that combines NR0B1 and EWS-FlI1. The fusion did not alter the DS in wild-type FLI1; however, mutated proteins showed decreased tumorigenicity or cell proliferation. Ewing's syndrome patients may benefit from the novel FLI1 fusion proteins.
DS is characterized by splicing of the FLI1 gene. In this study, DS from EWSR1–FLI1 was not found to be significantly different from wild-type FLI1. The wild-type FLI1 gene's DS showed a preference for ES cells. It showed less bidirectional transcripting in the wild type FLI1 gene.
Overexpression of EZH2 has been associated with poor prognosis for prostate cancer. It has also been linked to breast, bladder, endometrial and melanoma tumors. Tumor growth is directly related to EZH2 protein levels. Several transcription factors of the E2F family, the ETS transcription factor ERG, and c-MYC activate EZH2 transcription.
Mutations of EZH2 result in reduced methylation activities. This gene mutation can cause skeletal defects and developmental delays. DS of wild type EZH2 has not yet been linked to Sotos syndrome. This is because Sotos syndrome results from mutations within the NSD1 gene. Researchers have struggled to find wild-type complexes.
Moreover, mice that were overexpressed EZH2 had a greater proliferative capacity of leukemic cells. However, mice with EZH2 overexpression had higher levels of MPNs. In conclusion, DS of wild-type EZH2 represses H3K27me3 and has anti-proliferative effects similar to those observed in cells harboring EZH2-mutation.
DS of wild-type EZH2, Y641 single allele-mutated EZH2, exhibits increased activity in subsequent reactions. The A677G activating mutation has also been identified in GC-NHL, and has been linked to enhanced H3K27 tri-methylation. DS for mutant EZH2 is also more stable that wild-type EZH2.
The DS of wild-type EZH2, Y557 and Y603, is the catalytic component of polycomb repressive complex 2. The SET domain is essential for EZH2's histone methyltransferase activation. It can only gain histone methyltransferase activities when it complexes the other PRC2 subunits EED or SUZ12.
The regulator of tumorigenesis is the polycomb-repressive complex 2(PRC2). EZH2 is a member the PRC2 family of proteins and mediates gene suppression. EZH2 initially was identified as a gene that was overexpressed in breast cancer and prostate cancer. Later studies found that it was upregulated when there were hematological malignancies (leukemia and lymphoma). Moreover, stably transfected cells expressing EZH2 showed increased cell growth and H3K27-trimehtylation.
Suz12 is a developmental protein that controls the proliferation and survival of cells. The DS level of wild-type SUZ12 SUZ12 cellular cells is lower than that of mutant SUZ12 cellular cells. Moreover, mutant cells have lower levels of AEBP2 or RBAP48. These findings underscore the importance for further research. You can read more about the mechanism of DS for wild-type SUZ12.
SUZ12 activates RAS/ERK signaling pathways in cells. It activates the PKA/Rap1/ERK signaling pathways. These actions are likely triggered through the SUZ12 mutation. Moreover deletion of SUZ12 can cause an increase in cAMP/PKA/Rap1 Activity. The mechanism by SUZ12 activation is still unknown.
The genetic rearrangement JAZF1 & SUZ12 produces a chimeric proteins, JAZF1 – SUZ12. This represses the transcription by interfacing with TR4, the nuclear orphan protein. The DS of wild-type SUZ12. SUZ12 also has a conserved VEFSbox and Znfinger domain. It plays a role in cell cycle and X-chromosome inactivation.
In the absence EZH2, H3K27me3 deposited only at the borders SUZ12 peaks. In addition, there were no signs of 5' spreading in the absence of EZH2 or PRC2. This indicates that SUZ12 can associate to chromatin independently from its catalytic activation. In this sense, DS for wild-type SUZ12 is a better predictor for SUZ12-mediated transcript.
DS of wild type SUZ12.mutated cells also showed significantly lower H3K27me3 levels and increased Rap1 expression. This suggests that SUZ12 DS can upregulate RAS signaling via ADCY1/cAMP/Rap1/ERK. However, SUZ12 can be overexpressed, which increases the production cAMP, a product ADCY1.
SUZ12 in 293T cells was silenced using a retroviral virus vector containing the siRNA complex sequence 5' GATCCGACATGAGAGAA. The production and transfection of retroviral structures into packaging cells was possible using a cellbased RNAi–pSIREN–RetroQ promor. The supernatant of the retroviral constructs was collected for further research.
PMID: 3299708 by Rao V.N., et al. erg, a human ets-related gene on chromosome 21: alternative splicing, polyadenylation, and translation.
PMID: 3476934 by Reddy E.S.P., et al. The erg gene: a human gene related to the ets oncogene.