Use your antibodies-online credentials, if available.
抗Mouse (Murine) 抗体:
抗Rat (Rattus) 抗体:
Human Polyclonal ETS2 Primary Antibody for FACS, IHC (p) - ABIN653803
Kabbout, Garcia, Fujimoto, Liu, Woods, Chow, Mendoza, Momin, James, Solis, Behrens, Lee, Wistuba, Kadara: ETS2 mediated tumor suppressive function and MET oncogene inhibition in human non-small cell lung cancer. in Clinical cancer research : an official journal of the American Association for Cancer Research 2013
Human Monoclonal ETS2 Primary Antibody for IHC, WB - ABIN2720577
Wang, Huang, Liu, Cai, Millard, Wang, Chang, Peng, Fan: Cardiomyocytes mediate anti-angiogenesis in type 2 diabetic rats through the exosomal transfer of miR-320 into endothelial cells. in Journal of molecular and cellular cardiology 2014
a new layer of regulation whereby Yan and Pointed co-occupy regulatory elements to repress gene expression in a coordinated manner, with Pointed being unexpectedly required for the genome-wide occupancy of both Yan and the co-repressor Groucho.
results demonstrate that PntP1 prevents both the premature differentiation and the dedifferentiation of INPs by regulating the expression of distinct target genes at different stages of imINP development.
Both PntP1 and PntP2 are required for oenocyte specification. Since PntP1 is a downstream effector of EGF signaling, these findings provide insight into how a Hox factor can both trigger and potentiate the EGF signal to promote an essential cell fate along the body plan.
PntP2 transcription factor plays a role in air sac development by regulation of the EGF ligand Vein protein.
These studies identify Cic, Pnt, and Ets21C as critical downstream effectors of EGFR signaling in Drosophila Intestinal Stem Cells
Btd prevents the premature differentiation by suppressing the expression of Prospero in immature intermediate neural progenitor cells. Btd functions cooperatively with Pointed P1 to promote the generation of the above cells.
instances of co-expressed Yan and Pnt-GFP in tissues with high RTK signaling cannot be explained by the current model, and thus they provide important contexts for future investigation of how context-specific differences in RTK signaling
Data show that Appl is directly regulated by the Ras/MAPK pathway through a mechanism mediated by PntP2.
Specific disruption of either pntP1 or pntP2 resulted in the same R8-only phenotype, demonstrating that both Pnt isoforms are essential for photoreceptor recruitment
a low level of Notch signaling functions to maintain the neuroepithelial cell identity by suppressing the expression of pointedP1 gene through the transcriptional repressor Anterior open.
Demonstrate that the Pointed-P2 PNT domain contains a dynamic N-terminal helix H0 appended to a core conserved five-helix bundle diagnostic of the SAM domain fold.
The MAPK/ERK pathway acts via the ETS-1 transcription factor Pointed. This mechanism permits physiological adjustment of insulin sensitivity and subsequent maintenance of circulating glucose at appropriate levels.
PntP1 is both necessary and sufficient for the suppression of Ase in type II NBs and the generation of intermediate neural progenitor cells in Drosophila larval brains
Pointed directly regulates the transcription of string and thereby cell proliferation
In different types of glial cells, REPO can act alone, or cooperate with either TTK69 or PNTP1 to regulate different target genes.
Data show that pannier acts upstream of pointed P2 in a developmental pathway in which pannier promotes cardiac mesoderm formation, and pointed acts subsequently to distinguish between cardioblast and pericardial cell fates.
Efficient phosphorylation and consequent activation of Pnt-P2 requires a three-dimensional docking surface on its SAM domain for the MAP kinase but Mae binding to Pnt-P2 occludes this docking surface.
Homozygous deletion of Ets2 in p53 mutant mice resulted in strong down-regulation of snoRNAs and reversed the prometastatic phenotype of mutant p53 but had no effect on osteosarcoma development, which remained 100% penetrant.
These results suggest an unappreciated role for ETS2 in fibroblasts in establishing an immune-suppressive microenvironment in response to oncogenic Kras(G12D) signaling during the initial stages of tumor development.
The differentiation of ERF-overexpressing trophoblast stem cell lines also suggests that ERF may have an FGF2-independent effect during the commitment towards syncytiotrophoblasts.
MicroRNA 17-92 cluster mediates ETS1 and ETS2-dependent RAS-oncogenic transformation
Elf5 and Ets2 have roles in maintaining the mouse extraembryonic ectoderm in a dosage dependent synergistic manner
identified Ets2 as a key novel regulator in both the positive and negative control of miR-155 in the inflammatory response.
The data reveals a key function for Ets2 in tumor fibroblasts in signaling to endothelial cells to promote tumor angiogenesis.
Data indicate that differences between the N termini of transcription factors Ets1 and Ets2, rather than differences in the DNA binding domains, determine whether the proteins are capable of blocking antibody-secreting cells (ASCs) formation or not.
propose a model that provides a genetic explanation as to how Ets2 in trophoblast mediates the progression of gastrulation within the epiblast
Ets-2 play a key role in transcriptional regulation of CTRP5 in muscle cells.
Results identify ETS2 as a functionally important transcription factor in adipogenesis.
These data indicate the importance of phosphorylated ets-2 in the pathogenesis of pulmonary fibrosis through the expression of Type I collagen and (myo)fibroblast activation.
transcriptional cofactor that enhances inflammatory lymphangiogenesis
silencing of Smad2 is able to prevent the suppression of both HO-1 and Ets-2 by TGF-beta1 during exposure to lipopolysaccharide.
Provide evidence for the plaque-destabilizing role of Ets2 in atherosclerosis development by induction of an intraplaque proinflammatory phenotype in endothelial cells.
Ets2 regulates colonic stem cells and sensitivity to tumorigenesis.
This study uncovers new roles for Ets2 in trophoblast stem cell self-renewal and differentiation
decrease in ETS2 protein levels after exposure to electromagnetic fields
Ets2 expression pattern in E8.5 to E13.5 embryos
Ets2 plays a role in the proliferation and survival of thymocytes probably via a Myc-dependent pathway.
High ETS2 expression predicts poor prognosis in acute myeloid leukemia patients undergoing allogeneic hematopoietic stem cell transplantation.
ETS2 is of potential value as a molecular target for RCC treatment.
ETS2 functions as an oncogene and plays a key role in the progression of hypopharyngeal cancer.
ETS2 (high) is a poor prognostic factor in acute myeloid leukemia and may guide treatment decisions towards allogeneic hematopoietic stem cell transplantation.
Findings strongly suggest a critical role of Ets2 in human esophageal squamous cell carcinoma pathogenesis via the inactivation of the mTOR/p70S6K signaling pathway.
Authors demonstrate that mtp53 prevents the COP1/DET1 complex from ubiquitinating ETS2 and thereby marking it for destruction. Authors show that mtp53 destabilizes DET1 and also disrupts the DET1/ETS2 complex thereby preventing ETS2 degradation.
These findings suggest that ETS2 rs461155A>G, could be used as a biomarker predicting the clinical outcomes of non-small cell lung cancer patients treated with first-line paclitaxel-cisplatin chemotherapy.
Interaction with ZMYND11 mediates opposing roles of Ras-responsive ETS1 and ETS2.
Data suggest marked changes in DNA methylation occur at a single CpG site (CpG4) in promoter region of ESR1 as breast cancer cells become resistant to hormonal/aromatase inhibitor antineoplastic agents; this CpG region is completely conserved among species, suggesting that it acts as a methylation-sensitive ETS2 transcription factor binding site/response element. (ESR1 = estrogen receptor 1; ETS2 = ETS proto-oncogene 2)
ETS2 and Twist1 promote invasiveness of Helicobacter pylori-infected gastric cancer cells by inducing Siah2
Neuronal C-ETS2 senses oxidative stress, activates TFEB transcription, and mediates the upregulation of lysosomal genes.
ETS2, HNF4A and JUNB are synergistic master regulators of epithelial-to-mesenchymal transition in cancer.
ATO treatment upregulated Ets-2 and miR-126 expression in HUVECs.
RNA-seq evidence of biallelic expression of ETS2 and 10 neighboring genes in at least one primary human tissue tested indicates that the expression of ETS2 is uncoupled from the control of the maternally inherited 5mCpG imprints at the WRB differentially methylated region (DMR) in disomic controls or trisomy (Down syndrome) individuals.
Data show that NF-kappa-B p52 subunit (p52) interacts with ets transcription factors ETS1/2 factors at the C250T telomerase (TERT) promoter to mediate TERT reactivation.
ETS-1/ETS-2 and C/EBPalpha could interact with corresponding binding sites.
c-ETS transcription factors appear to be key regulators of MCM4 origin where c-ETS2 seems to promote DNA replication whereas c-ETS1 functions as a negative regulator.
These data suggested that Ets-2, a genuine cancer-specific transcription factor, is actively involved in EGFR kinase-induced hTERT overexpression pathway in lung cancer cells.
The crystal structure of a DNA complex of the Ets-2 Ets domain.
DLX3 has a central role in controlling IFNT gene expression by associating with ETS2 on the IFNT promoter.
This gene encodes a transcription factor which regulates genes involved in development and apoptosis. The encoded protein is also a protooncogene and shown to be involved in regulation of telomerase. A pseudogene of this gene is located on the X chromosome. Alternative splicing results in multiple transcript variants.
, Ets at 58AB
, Ets protein pointed P2
, no terminal cell clones-R
, pointed P2
, avian leukemia oncogene 2
, protein C-ets-2
, oncogene ETS-2
, v-ets avian erythroblastosis virus E2 oncogene homolog 2
, v-ets erythroblastosis virus E26 oncogene homolog 2
, E26 avian leukemia oncogene 2, 3' domain
, avian erythroblastosis virus E26 (v-ets) oncogene homolog 2
, v-ets avian erythroblastosis virus E26 oncogene homolog 2