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Merck
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Key Documents

SAB3500126

Sigma-Aldrich

Monoclonal Anti-ORAI1 antibody produced in mouse

clone 3F6H5, purified immunoglobulin, buffered aqueous solution

Sinonimo/i:

Anti-Calcium release-activated calcium channel protein 1, Anti-TMEM142A, Anti-Transmembrane protein 142A

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About This Item

Codice UNSPSC:
12352203
NACRES:
NA.41

Origine biologica

mouse

Coniugato

unconjugated

Forma dell’anticorpo

purified immunoglobulin

Tipo di anticorpo

primary antibodies

Clone

3F6H5, monoclonal

Forma fisica

buffered aqueous solution

PM

predicted mol wt 33 kDa

Reattività contro le specie

human, rat, mouse

tecniche

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

N° accesso UniProt

Q96D31

Condizioni di spedizione

dry ice

Temperatura di conservazione

−20°C

modifica post-traduzionali bersaglio

unmodified

Informazioni sul gene

human ... ORAI1(84876)

Immunogeno

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

Caratteristiche e vantaggi

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.

Descrizione del bersaglio

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.

Stato fisico

Supplied at approx. 1 mg/mL in phosphate buffered saline containing 0.02% sodium azide.

Esclusione di responsabilità

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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Codice della classe di stoccaggio

10 - Combustible liquids

Classe di pericolosità dell'acqua (WGK)

WGK 2

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable

Certificati d'analisi (COA)

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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
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
Filip Maciąg et al.
Biochimica et biophysica acta. Molecular cell research, 1866(7), 1137-1150 (2019-01-20)
Orai proteins form highly selective Ca2+ release-activated channels (CRACs). They play a critical role in store-operated Ca2+ entry (SOCE; i.e., the influx of external Ca2+ that is induced by the depletion of endoplasmic reticulum Ca2+ stores). Of the three Orai
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