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SAB2702342

Sigma-Aldrich

Monoclonal Anti-HIF2 alpha antibody produced in mouse

clone GT125, affinity isolated antibody

Sinónimos:

ECYT4, HIF2A, HLF, MOP2

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

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

12 - Non Combustible Liquids

wgk_germany

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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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
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
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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