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anti-Human EPAS1 Antibodies:
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Fish Polyclonal EPAS1 Primary Antibody for ChIP, ELISA - ABIN151051
Conrad, Freeman, Beitner-Johnson, Millhorn: EPAS1 trans-activation during hypoxia requires p42/p44 MAPK. in The Journal of biological chemistry 1999
Show all 584 Pubmed References
Hamster Monoclonal EPAS1 Primary Antibody for ChIP, ELISA - ABIN151063
Bernhardt, Wiesener, Weidemann, Schmitt, Weichert, Lechler, Campean, Ong, Willam, Gretz, Eckardt: Involvement of hypoxia-inducible transcription factors in polycystic kidney disease. in The American journal of pathology 2007
Show all 162 Pubmed References
Hamster Monoclonal EPAS1 Primary Antibody for ELISA, IHC - ABIN250056
Harvey, Kind, Pantaleon, Armstrong, Thompson: Oxygen-regulated gene expression in bovine blastocysts. in Biology of reproduction 2004
Show all 19 Pubmed References
Hamster Monoclonal EPAS1 Primary Antibody for ELISA, ICC - ABIN250055
Mekhail, Gunaratnam, Bonicalzi, Lee: HIF activation by pH-dependent nucleolar sequestration of VHL. in Nature cell biology 2004
Show all 15 Pubmed References
Fish Polyclonal EPAS1 Primary Antibody for ELISA, ICC - ABIN249868
Alvarez-Tejado, Naranjo-Suarez, Jiménez, Carrera, Landázuri, del Peso: Hypoxia induces the activation of the phosphatidylinositol 3-kinase/Akt cell survival pathway in PC12 cells: protective role in apoptosis. in The Journal of biological chemistry 2001
Show all 17 Pubmed References
Polyclonal EPAS1 Primary Antibody for IHC (fro), WB - ABIN540396
Sears, Hoppe, Ebrahem, Anand-Apte: Prolyl hydroxylase inhibition during hyperoxia prevents oxygen-induced retinopathy. in Proceedings of the National Academy of Sciences of the United States of America 2008
Show all 6 Pubmed References
Monoclonal EPAS1 Primary Antibody for FACS, IHC (p) - ABIN534071
Wiesener, Turley, Allen, Willam, Eckardt, Talks, Wood, Gatter, Harris, Pugh, Ratcliffe, Maxwell: Induction of endothelial PAS domain protein-1 by hypoxia: characterization and comparison with hypoxia-inducible factor-1alpha. in Blood 1998
Show all 5 Pubmed References
Human Monoclonal EPAS1 Primary Antibody for IHC (fro), IHC (p) - ABIN1742588
Giatromanolaki, Koukourakis, Sivridis, Turley, Wykoff, Gatter, Harris: DEC1 (STRA13) protein expression relates to hypoxia- inducible factor 1-alpha and carbonic anhydrase-9 overexpression in non-small cell lung cancer. in The Journal of pathology 2003
Show all 4 Pubmed References
Polyclonal EPAS1 Primary Antibody for IHC (fro), IF - ABIN540619
Tian, McKnight, Russell: Endothelial PAS domain protein 1 (EPAS1), a transcription factor selectively expressed in endothelial cells. in Genes & development 1997
Show all 3 Pubmed References
Human Monoclonal EPAS1 Primary Antibody for IHC, WB - ABIN2722736
Liu, Wang, Tong, Liu, Yuan, Zhang, Ye, Zhang, Yuan, Feng, Zhang, Jiang: A Somatic HIF2α Mutation-Induced Multiple and Recurrent Pheochromocytoma/Paraganglioma with Polycythemia: Clinical Study with Literature Review. in Endocrine pathology 2017
Hypoxia-induced elevation of sFlt-1 secretion from the cytotrophoblasts was inhibited by silencing the HIF-2alpha, but not HIF-1alpha mRNA.
FSTL1 plays a tumor suppression role possibly via repressing the NF-kB and HIF-2a signaling pathways. To increase FSTL1 expression might be a candidate therapeutic strategy for metastatic clear-cell renal cell carcinoma.
We also summarize the current knowledge on the crosstalk between HIF-2 and angiogenesis, describing reported phenotypical changes of HIF-2alpha genetic models and HIF-2 target genes implicated in angiogenesis. Finally, we provide a survey of recent pharmacologic strategies to specifically target HIF-2 activity.
We also found that RCAN1.4 could regulate epithelial-mesenchymal transition (EMT) and the expression of HIF2alpha in sunitinib-resistant cell lines...these findings indicate that downregulation of RCAN1.4 may be crucial for the metastasis of Clear cell renal cell carcinoma and may induce sunitinib resistance.
ZMYND8 interacts with HIF-1alpha and HIF-2alpha and enhances elongation of the global HIF-induced oncogenic genes by increasing recruitment of BRD4 and subsequent release of paused RNA polymerase II in breast cancer cells.
with the current available data EPAS1/HIF2alpha should not be classified as a neuroblastoma oncogene and is less likely to represent a suitable drug target in this disease.
the work revealed surprisingly discrete binding patterns for HIF-1 and HIF-2. They suggest that the DNA-binding complexes function more independently than previously foreseen and rationalize the use of isoform-specific therapeutic inhibitors for specific indications
miR-363-3p is induced by HIF-2alpha to promote the stemness of melanoma cells via inhibiting p21.
identified WT1 as a downstream target of HIF-2alpha in Kelly neuroblastoma cells. In chromatin immunoprecipitation assays, HIF-2alpha bound to a HRE in intron 3 of the WT1 gene, but not to another predicted HIF binding site (HBS) in the first intron.
The function of HIF-2alpha in promoting tumor growth and metastasis.
Hypoxia suppressed cell growth and the recovery of clonogenic cells. Moreover, hypoxia up-regulated hypoxia-inducible factor (HIF) 1alpha and HIF2alpha expression while suppressing the expression and activation of NOTCH1, mechanistic target of rapamycin kinase (mTOR) activation, and nuclear factor-kappa B (NF-kappaB) phosphorylation
Our results indicate that EPAS1 mutations might have a potential causative effect on the development of Tibetan non-syndromic congenital heart disease .
lncRNA HIF2PUT may act as a tumour suppressor in osteosarcoma
HER2 overexpression in MCF7 cells leads to an increase in HIF-2alpha but not HIF-1alpha expression in normoxia and an increased upregulation of HIF-2alpha in hypoxia. Global gene expression analysis showed that HER2 overexpression in these cells promotes an exaggerated transcriptional response to both short-term and long-term hypoxia, with increased expression of numerous hypoxia response genes.
MiR-365 regulates IL-1beta-stimulated catabolic effects in human chondrocytes by modulating HIF-2alpha expression.
HIF2A, rather than HIF1A, is most affected by reduced oxygen level during syncytialization, and increases in HIF2A trigger a reduction of PlGF production.
HIF2alpha almost exclusively regulated a large and diverse subset of transcription factors.
The genetic variants in EPAS1, GPR126 may contribute to the physiological adaptations to hypobaric hypoxia, possibly by altering lung function.
late-stage renal tubular HIF-2alpha activation has protective effects on renal fibrosis and the resultant renal dysfunction, thus it could represent a therapeutic target in late stage of CKD.
In renal clear-cell carcinomas, HIF-2alpha selectively enriches polyunsaturated lipids, the rate-limiting substrates for lipid peroxidation, by activating the expression of hypoxia-inducible, lipid droplet-associated protein (HILPDA).
These findings demonstrate a molecular link between hepatic hepcidin and intestinal HIF-2alpha that controls physiological iron uptake and drives iron hyperabsorption during iron overload.
Signaling pathways important for acinar cell homeostasis are altered in HIF2alpha-overexpressing pancreata.
hypothalamic HIF2alpha responds to insulin, and the up-regulation is involved in adaptive metabolic regulation as age increases, whereas impairment of HIF2alpha in the hypothalamus contributes to weight gain and glucose disorders in age-dependent manners.
Hematopoietic-specific deficiency of Hif2alpha ameliorated pathological neovascularization in the OIR model, which was accompanied by enhanced endothelial cell apoptosis
The p75NTR enhances HIF1A/HIF2A-dependent signaling in glioma.
Mice with stromal deletion of Hif2a (Hif2a-sKO mice) showed infertility with impaired embryo invasion and those with epithelial deletion of Hif2a (Hif2a-eKO mice) showed normal fertility, suggesting the importance of stromal HIF2alpha in embryo invasion.
These findings suggest that HIF2A is a pivotal mediator of hypoxia signaling in satellite cells and may be therapeutically targeted to improve muscle regeneration.
the reversal of erythrocytosis/polycythemia to translational repression of Hif2alpha expression by Tempol-mediated increases in the IRE-binding activity of Irp1, as reversal of polycythemia was abrogated in VhlR200W mice in which Irp1 was genetically ablated.
High HIF-2A expression is associated with metabolic diseases.
we demonstrated that hypoxia significantly induced the GSC mesenchymal transition, increased the expression levels of the pluripotent transcription factor OCT4 and migration-associated proteins..he underlying mechanism involved significant IGF-1/IGF-1R activation of OCT4/CXCR4 expression through HIF-2alpha regulation.
Increased HIF-2alpha expression is associated with the development of severe pulmonary hypertension.
The studies indicate that HIF2-alpha induces myocardial AREG expression in cardiac myocytes, which increases myocardial ischemia tolerance.
EPAS1 links DOCK8 deficiency to atopic skin inflammation via IL-31 induction in CD4thorn T cells.
Myeloid-specific deletion of Epas1 had no impact on the number of myeloid cells migrating into the eye.
Defect in nephron formation in PHD2/PHD3 double mutants required intact hypoxia-inducible factor-2 signaling and was dependent on the extent of stromal hypoxia-inducible factor activation. Thus, hypoxia-inducible factor prolyl-4-hydroxylation in renal interstitial cells is critical for normal nephron formation.
Absence of Hif2a in retinal neuroprogenitor cells causes a marked reduction of proliferating endothelial cells at the angiogenic front. This results in delayed retinal vascular development, fewer major retinal vessels and reduced density of the peripheral deep retinal vascular plexus.
HIF2alpha is linked to tumor suppression in neuroblastoma.
The pseudo-hypoxic phenotype of stem-like glioma cells is achieved by stabilization of HIF-2a through interaction with CD44, independently of oxygen.
HIF-1alpha-dependent, HIF-2alpha-independent angiogenesis and constitutive diuresis is caused by Vhl deletion in renal epithelia
A novel biological pathway has been discovered of soluble biglycan inducing HIF-2alpha protein stabilization and Epo production presumably in an oxygen-independent manner, ultimately giving rise to secondary polycythemia.
immunostaining for HIF-1alpha and HIF-2alpha was observed during endochondral ossification; only HIF-2alpha was present at sites of intramembranous ossification
There was an association of an EPAS1 (HIF2alpha) double variant in the oxygen degradation domain of EPAS1 in Angus cattle with high altitude pulmonary hypertension (HAPH). There was upregulation of 26 of 27 HIF2alpha target genes in EPAS1 carriers with HAPH.
This gene encodes a transcription factor involved in the induction of genes regulated by oxygen, which is induced as oxygen levels fall. The encoded protein contains a basic-helix-loop-helix domain protein dimerization domain as well as a domain found in proteins in signal transduction pathways which respond to oxygen levels. Mutations in this gene are associated with erythrocytosis familial type 4.
endothelial PAS domain protein 1
, endothelial PAS domain-containing protein 1-like
, HIF-1-alpha-like factor
, HIF-1alpha-like factor
, PAS domain-containing protein 2
, basic-helix-loop-helix-PAS protein MOP2
, class E basic helix-loop-helix protein 73
, endothelial PAS domain-containing protein 1
, hypoxia-inducible factor 2 alpha
, hypoxia-inducible factor 2-alpha
, member of PAS protein 2
, HIF-related factor
, HIF1 alpha-like factor
, HIF1alpha-like factor
, HLF (HIF1alpha-like factor)
, Hif like protein
, hypoxia inducible transcription factor 2alpha
, HIF-2 alpha
, HIF2 alpha
, hypoxia inducible factor 2, alpha subunit
, hypoxia inducible factor 2a