SAB2702342
Monoclonal Anti-HIF2 alpha antibody produced in mouse
clone GT125, affinity isolated antibody
Synonyme(s) :
ECYT4, HIF2A, HLF, MOP2
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About This Item
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41
Produits recommandés
Source biologique
mouse
Niveau de qualité
Conjugué
unconjugated
Forme d'anticorps
affinity isolated antibody
Type de produit anticorps
primary antibodies
Clone
GT125, monoclonal
Forme
buffered aqueous solution
Poids mol.
96kDa
Espèces réactives
rat, mouse, human
Concentration
3mg/mL
Technique(s)
immunoprecipitation (IP): suitable
indirect immunofluorescence: suitable
western blot: 500-3000
Isotype
IgG1
Numéro d'accès UniProt
Conditions d'expédition
wet ice
Température de stockage
−20°C
Modification post-traductionnelle de la cible
unmodified
Informations sur le gène
human ... EPAS1(2034)
Description générale
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.
Immunogène
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.
Actions biochimiques/physiologiques
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.
Caractéristiques et avantages
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Autres remarques
Purification: Affinity purified by Protein G
Forme physique
Phosphate-buffered saline, no preservative added.
Clause de non-responsabilité
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.
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Code de la classe de stockage
12 - Non Combustible Liquids
Classe de danger pour l'eau (WGK)
WGK 2
Point d'éclair (°F)
Not applicable
Point d'éclair (°C)
Not applicable
Certificats d'analyse (COA)
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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.
Andika C Putra et al.
PloS one, 10(8), e0134496-e0134496 (2015-08-12)
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
Pauline M Dmitriev et al.
JAMA ophthalmology, 138(2), 148-155 (2019-12-27)
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
Two new mutations in the HIF2A gene associated with erythrocytosis.
Melanie J Percy et al.
American journal of hematology, 87(4), 439-442 (2012-03-01)
Hyeonkyeong Kim et al.
Nature communications, 11(1), 5023-5023 (2020-10-08)
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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