Hypoxia-inducible factor 2-α (HIF2) also known as endothelial PAS domain protein 1 (EPAS1) belongs to the helix-loop-helix/ Per-Arnt-Sim (PAS) transcription factor family. The HIF2 gene is mapped to human chromosome 2p21. HIF2 is expressed in endothelial cells, hepatocytes, lung, cardiomyocytes, and renal fibroblasts.
Immunogen
Recombinant protein encompassing a sequence within the center region of human HIF2 alpha.
Application
Suggested starting dilutions are as follows: ICC/IF: 1:100-1:1000, IP: 1:100-1:700, WB: 1:500-1:3000. Not yet tested in other applications. Optimal working dilutions should be determined experimentally by the end user.
Biochem/physiol Actions
Hypoxia-inducible factor 2-α (HIF2) regulates oxygen physiology and modulates the hypoxic response. It favors chondrosarcoma progression. Mutations in the HIF2 Phe-540 residue abolishes its interaction with von hippel lindau (VHL) and prolyl hydroxylase domain-2 (PHD2). HIF2 regulates erythropoietin synthesis and is implicated in the pathophysiology of excessive erythrocytosis (EE). Mutations in the HIF2 gene impair response to the changes in oxygen tension. A gain-of-function mutation of HIF2 results in Zhuang syndrome.
Features and Benefits
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Other Notes
Purification: Affinity purified by Protein G
Physical form
Phosphate-buffered saline, no preservative added.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Hypoxia-inducible factor-2α (HIF-2α, or EPAS1) is important for cancer progression, and is a putative biomarker for poor prognosis for non-small cell lung cancer (NSCLC). However, molecular mechanisms underlying the EPAS1 overexpression are not still fully understood. We explored a role
Patients with the EPAS1 gain-of-function mutation syndrome (or Pacak-Zhuang syndrome) present with multiple paragangliomas or pheochromocytomas, duodenal somatostatinoma, polycythemia, headaches, and sometimes diminished visual acuity at an early age. The characteristic phenotype and known genetic cause of the syndrome provide
Chondrosarcomas, malignant cartilaginous neoplasms, are capable of transitioning to highly aggressive, metastatic, and treatment-refractory states, resulting in significant patient mortality. Here, we aim to uncover the transcriptional program directing such tumor progression in chondrosarcomas. We conduct weighted correlation network analysis
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