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Fish Polyclonal EPAS1 Primary Antibody für 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 532 Pubmed References
Hamster Monoclonal EPAS1 Primary Antibody für 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 154 Pubmed References
Hamster Monoclonal EPAS1 Primary Antibody für 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 für ELISA, ICC - ABIN250055
Mekhail, Gunaratnam, Bonicalzi, Lee: HIF activation by pH-dependent nucleolar sequestration of VHL. in Nature cell biology 2004
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Fish Polyclonal EPAS1 Primary Antibody für 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 für 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
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Monoclonal EPAS1 Primary Antibody für 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
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Human Monoclonal EPAS1 Primary Antibody für 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
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Polyclonal EPAS1 Primary Antibody für 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
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Human Polyclonal EPAS1 Primary Antibody für IF (p), IHC (p) - ABIN686662
Li, Chen, Shao, Tang, Chen, Chen, Xu: Oxidative stress induces the decline of brain EPO expression in aging rats. in Experimental gerontology 2016
Study found that chronic hypoxia enhanced the resistance of breast cancer cells to Paclitaxel (PTX) and induced high expression of HIF-2alpha, but not HIF-1alpha. Furthermore, HIF-2alpha promoted the stem cell properties of breast cancer cells with increased expression of stem cells markers and induced resistance to PTX by activating Wnt and Notch signaling pathways.
CPT1A is repressed by HIF1 and HIF2, reducing fatty acid transport into the mitochondria, and forcing fatty acids to lipid droplets for storage.
PD-L1 tumor cell expression is strongly associated with increased HIF-2alpha expression and presence of dense lymphocytic infiltration in clear cell renal cell carcinoma.
Hypoxia-induced angiogenesis is a complex process that involves distinct but also overlapping functions of HIF-1alpha and HIF- 2alpha in regard to angiogenesis, bioenergetic adaption and the redundant transcriptional induction of MIF.
High HIF2A expression is associated with high Collagen I Fibers in Triple Negative Breast Cancer.
The studies indicate that HIF2-alpha induces myocardial AREG expression in cardiac myocytes, which increases myocardial ischemia tolerance.
High HIF2A expression is associated with Cervical Cancer.
Data found that overexpression of HIF-2alpha up-regulate the level of NEAT1 and promote EMT and metastasis in hepatoma cell under hypoxia, and inhibition of HIF-2alpha reverse the results. These indicated that HIF-2alpha can promote EMT and metastasis in hepatocellular carcinoma under hypoxia.
Studies have shown that both HIF1alpha and HIF2alpha may contribute to the regulation of cellular adaptation to hypoxia and resistance to cancer therapies with their potential to exert significant effects on the maintenance and evolution of cancer stem cells. Also, HIF1alpha and HIF2alpha seemed to have significant prognostic and predictive value. [review]
HIF-2alpha expression may be associated with the carcinogenesis of colorectal cancer (CRC), which is higher in males than in females, negatively linked to tumor differentiation, and correlated with a worse disease-free survival of CRC - Systematic Analysis
Overexpression of VHL was more successful at inhibiting fibrosis compared with silencing HIF-1a plus HIF-2a. Normoxia-active HIF-1a or HIF-2a prevented the inhibitory effect of VHL on liver fibrosis, indicating that attenuating fibrosis via VHL is HIF-1a- and HIF-2a-dependent to some extent.
HDX negatively regulates EPAS1 expression through a release-of-inhibition mechanism.
sing imputed data, we found that this SNP remained significant in the entire TRICL-ILCCO consortium (p=.03). Additional functional studies are warranted to better understand interrelationships among genetic polymorphisms, DNA methylation status, and EPAS1 expression.
Results suggest an interplay of the production and action of hydrogen sulfide during hypoxia with subsequent erythropoietin production regulated by HIF-1alpha and HIF-2alpha.
This suggests that higher aerobic capacities are caused by the presence of at least one minor A-Allele of the EPAS1 gene in the genome of an athlete
we report a rare case of renal-cell carcinoma and hereditary polycythemia. Genotyping revealed that the patient carried both a germline HIF2A mutation and a somatic VHL mutation. Both mutations result in overactivation of HIF2A and its downstream target genes
Identification of gain-of-function somatic mutations of EPAS1, which encodes for HIF-2alpha, in pheochromocytomas and paragangliomas in patients who presented with cyanotic congenital heart disease.
HIF-2a regulates non-canonical glutamine metabolism via activation of PI3K/mTORC2 pathway and GOT1 expression in human pancreatic ductal adenocarcinoma.
epigenomic profiling of clear cell renal cell carcinoma (ccRCC) establishes a compendium of somatically altered cis-regulatory elements, uncovering new potential targets including ZNF395. Loss of VHL, a ccRCC signature event, causes pervasive enhancer malfunction, with binding of enhancer-centric HIF2a and recruitment of histone acetyltransferase p300 at preexisting lineage-specific promoter-enhancer complexes
We studied the hypoxic activation of the transcription factors HIF-1alpha and HIF-2alpha in endothelial cells within a spatial linear gradient of oxygen. Quantification of the nuclear to cytosolic ratio of HIF immunofluorescent staining demonstrated that the threshold for HIF-1alpha activation was below 2.5% O2 while HIF-2alpha was activated throughout the entire linear gradient.
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.
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.
Data suggest that chronic hypoxia enhances HIF-2alpha stability, which causes increased arginase expression and dysregulates normal vascular NO homeostasis.
Data show that Tet1 modulates HIF-2alpha and HIF-1alpha through different mechanisms.
intestine HIF-2alpha regulates ceramide metabolism mainly from the salvage pathway, by positively regulating the expression of Neu3, the gene encoding neuraminidase 3. These results suggest that intestinal HIF-2alpha could be a viable target for hepatic steatosis therapy
endothelial EPAS1 has a global protective role during glomerular hypertensive injuries without influencing the hypertensive effect of angiotensin II
findings indicate that HIF-2alpha increases cancer cell growth by up-regulating YAP1 activity
Chronic activity of HIF2 in stromal progenitors impairs kidney development. Finally, these data confirm the concept that normal stroma function is essential for normal tubular differentiation.
this study shows that HIF-2alpha acts in resting macrophages as a phagocytosis suppressor implying an important relationship between the levels of HIF-2alpha and susceptibility to infection
in neurons HIF-1 and HIF-2 have redundant functions for cellular survival under ischemic conditions. By contrast, lack of anti-survival factors in Hif1a/Hif2a-deficient mice might protect from early acute neuronal cell death and neurological impairment, indicating a benefit of HIF-pathway inhibition in neurons in the very acute phase after ischemic stroke
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