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Validated All-in-One™ qPCR Primer for ETS2(NM_005239.5) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
ETS transcriptions factors, such as ETS2, regulate numerous genes and are involved in stem cell development, cell senescence and death, and tumorigenesis. The conserved ETS domain within these proteins is a winged helix-turn-helix DNA-binding domain that recognizes the core consensus DNA sequence GGAA/T of target genes (Dwyer et al., 2007 [PubMed 17986575]).[supplied by OMIM].
Gene References into function
- Linkage of elevated expression to hepatocarcinogenesis
- Two closely spaced Ets-2 binding sites in the proximal promoter of the human chorionic gonadotropin beta5 (hCGbeta5) gene constitute a major enhancer for hCGbeta gene expression in JAr and JEG-3 human choriocarcinoma cells and in mouse NIH3T3 cells.
- Overexpression of ETS2 in human esophageal squamous cell carcinoma in both mRNA and protein levels.
- ets-2 has a role as a repressor and indicate that components of the mammalian SNF/SWI complex are required as co-repressors
- ETS2 is a target of protein kinase C and upregulates GM-CSF
- Ets-2 and its targets play essential roles in endothelial cell function
- Ras/mitogen-activated kinase signaling activates ETS2 by CBP/p300 recruitment.
- Coexpression of Ets-2 and SRC-1 significantly associated with the rate of recurrence and HER expression in breast cancer
- Phosphorylated ERK1/2 was further associated with the presence of VEGFR2 (cohorts II and III) and the degree of phosphorylated Ets-2, indicating in vivo, a signalling cascade from VEGFR2 via ERK1/2 to Ets-2 phosphorylation
- analysis of Ets2 in cell-seeded three-dimensional bone constructs
- c-Myb and c-Ets family members (Ets-1/2, PU.1, and Spi-B) control hGR 1A promoter regulation in T- and B-lymphoblast cells
- Data show that transcription of the putative tumor suppressor gene HCCS1 requires binding of ETS-2 to its consensus near the transcription start site.
- Results suggest that there is a strong interplay of Ets2 with bone-specific proteins in cell-seeded three-dimensional bone constructs.
- data of study population indicate a higher ETS2 RNA concentration compared with uPA in the case of bladder cancer, resulting in an increased ETS2:uPA RNA ratio in urine
- Data show that there are combinatorial effects of Ets2, PKA, and CBP/p300 and triggered via growth factors released from maternal endometrium.
- Expression of Ets-2, SRC-1 and c-Myc individually are all associated with reduced disease-free survival in breast cancer
- In erythroleukemia cells, induction of ETS2 caused an erythroid-to-megakaryocytic phenotypic switch, cytokine & transcription factor upregulation,& sensitivity to ara-C & daunorubicin.
- hTERT gene expression is maintained by a mechanism involving Ets2 interactions with the c-Myc transcription factor and the hTERT gene promoter, a protein-DNA complex critical for hTERT gene expression and breast cancer cell proliferation.
- Hepatitis B virus-induced hFGL2 transcription is dependent on c-Ets-2 and MAPK signal pathway
- These results indicate that intron 1 of DUSP6 plays a crucial role in transcriptional regulation of DUSP6 in a feedback loop manner responding to MAPK1 via ETS2 in human cells.
