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Merck
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主要文件

SAB2702342

Sigma-Aldrich

Monoclonal Anti-HIF2 alpha antibody produced in mouse

clone GT125, affinity isolated antibody

别名:

ECYT4, HIF2A, HLF, MOP2

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About This Item

分類程式碼代碼:
12352203
NACRES:
NA.41

生物源

mouse

品質等級

共軛

unconjugated

抗體表格

affinity isolated antibody

抗體產品種類

primary antibodies

無性繁殖

GT125, monoclonal

形狀

buffered aqueous solution

分子量

96kDa

物種活性

rat, mouse, human

濃度

3mg/mL

技術

immunoprecipitation (IP): suitable
indirect immunofluorescence: suitable
western blot: 500-3000

同型

IgG1

UniProt登錄號

運輸包裝

wet ice

儲存溫度

−20°C

目標翻譯後修改

unmodified

基因資訊

human ... EPAS1(2034)

一般說明

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.

免疫原

Recombinant protein encompassing a sequence within the center region of human HIF2 alpha.

應用

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.

生化/生理作用

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.

特點和優勢

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.

其他說明

Purification: Affinity purified by Protein G

外觀

Phosphate-buffered saline, no preservative added.

免責聲明

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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儲存類別代碼

12 - Non Combustible Liquids

水污染物質分類(WGK)

WGK 2

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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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
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
Huihui Liu et al.
Blood cells, molecules & diseases, 84, 102446-102446 (2020-05-30)
Excessive erythrocytosis (EE) is a characteristic of chronic mountain sickness (CMS). Currently, the pathogenesis of CMS remains unclear. This study was intended to investigate the role of EPAS1 in the proliferation of erythroblasts in CMS. Changes of HIF-1α and EPAS1/HIF-2α
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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