SAB2702342
Monoclonal Anti-HIF2 alpha antibody produced in mouse
clone GT125, affinity isolated antibody
Synonym(s):
ECYT4, HIF2A, HLF, MOP2
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All Photos(5)
About This Item
UNSPSC Code:
12352203
NACRES:
NA.41
Recommended Products
biological source
mouse
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
GT125, monoclonal
form
buffered aqueous solution
mol wt
96kDa
species reactivity
rat, mouse, human
concentration
3mg/mL
technique(s)
immunoprecipitation (IP): suitable
indirect immunofluorescence: suitable
western blot: 500-3000
isotype
IgG1
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... EPAS1(2034)
General description
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
Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.
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.
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Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 2
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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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)
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
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
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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