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Merck

SAB3500126

Sigma-Aldrich

Monoclonal Anti-ORAI1 antibody produced in mouse

clone 3F6H5, purified immunoglobulin, buffered aqueous solution

別名:

抗TMEM142A抗体, 抗カルシウム放出-活性化カルシウムチャネルタンパク質1抗体, 抗膜貫通型タンパク質142A抗体

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100 μG
¥95,200

¥95,200


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100 μG
¥95,200

About This Item

UNSPSCコード:
12352203
NACRES:
NA.41

¥95,200


Check Cart for Availability

由来生物

mouse

品質水準

結合体

unconjugated

抗体製品の状態

purified immunoglobulin

抗体製品タイプ

primary antibodies

クローン

3F6H5, monoclonal

フォーム

buffered aqueous solution

分子量

predicted mol wt 33 kDa

交差性

human, rat, mouse

テクニック

immunofluorescence: suitable
immunohistochemistry: suitable
indirect ELISA: suitable
western blot: suitable

UniProtアクセッション番号

輸送温度

dry ice

保管温度

−20°C

ターゲットの翻訳後修飾

unmodified

遺伝子情報

human ... ORAI1(84876)

免疫原

raised against a 16 amino acid peptide from near the carboxy terminus of human ORAI1.

特徴および利点

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.

ターゲットの説明

Antigen stimulation of immune cells triggers Ca++ entry through Ca++ release-activated Ca++ (CRAC) channels. ORAI1 is a recently identified four-transmembrane spanning protein that is an essential component of CRAC. A missense mutation in this protein in humans is the cause of one fo rm of hereditary severe combined immune deficiency (SCID) which results in ablated T-cell Ca++ entry. It has been suggested that ORAI1 functions as a highly selective Ca++ plasma membrane channel that is gated through interactions with STIM1, the store-activated endoplasmic reticulum Ca++ sensor. ORAI1 often migrates at a higher than expected molecular weight in SDS-PAGE. This antibody is predicted to have no cross-reactivity to ORAI2 or ORAI3.

物理的形状

約1 mg/mLのPBS (0.02% アジ化ナトリウム含有)

免責事項

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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保管分類コード

10 - Combustible liquids

WGK

WGK 2

引火点(°F)

Not applicable

引火点(℃)

Not applicable


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文書ライブラリにアクセスする

Agnese Secondo et al.
Stroke, 50(5), 1240-1249 (2019-04-23)
Background and Purpose- Disturbance of endoplasmic reticulum (ER) Ca2+ homeostasis causes neuronal cell injury in stroke. By contrast, ischemic preconditioning (IPC)-a brief sublethal ischemic episode affording tolerance to a subsequent ischemic insult-restores ER Ca2+ homeostasis. Under physiological conditions, ER calcium
Momin Mohis et al.
American journal of physiology. Heart and circulatory physiology, 315(1), H83-H91 (2018-07-10)
Senescence-related fibrosis contributes to cardiac dysfunction. Profibrotic processes are Ca2+ dependent. The effect of aging on the Ca2+ mobilization processes of human ventricular fibroblasts (hVFs) is unclear. Therefore, we tested whether aging altered intracellular Ca2+ release and store-operated Ca2+ entry
Guangyu Cheng et al.
Frontiers in molecular neuroscience, 17, 1391189-1391189 (2024-07-04)
This investigation aims to elucidate the novel role of Stromal Interaction Molecule 1 (STIM1) in modulating store-operated calcium entry (SOCE) and its subsequent impact on inflammatory cytokine release in T lymphocytes, thereby advancing our understanding of trigeminal neuralgia (TN) pathogenesis.
Gracious R Ross et al.
Biology open, 6(3), 326-332 (2017-01-28)
Excessive cardiac fibrosis, characterized by increased collagen-rich extracellular matrix (ECM) deposition, is a major predisposing factor for mechanical and electrical dysfunction in heart failure (HF). The human ventricular fibroblast (hVF) remodeling mechanisms that cause excessive collagen deposition in HF are
Ana Paula Arruda et al.
eLife, 6 (2017-12-16)
Defective Ca2+ handling is a key mechanism underlying hepatic endoplasmic reticulum (ER) dysfunction in obesity. ER Ca2+ level is in part monitored by the store-operated Ca2+ entry (SOCE) system, an adaptive mechanism that senses ER luminal Ca2+ concentrations through the

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