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Merck

SAB3500126

Sigma-Aldrich

Monoclonal Anti-ORAI1 antibody produced in mouse

clone 3F6H5, purified immunoglobulin, buffered aqueous solution

Synonym(e):

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

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About This Item

UNSPSC-Code:
12352203
NACRES:
NA.41

Biologische Quelle

mouse

Konjugat

unconjugated

Antikörperform

purified immunoglobulin

Antikörper-Produkttyp

primary antibodies

Klon

3F6H5, monoclonal

Form

buffered aqueous solution

Mol-Gew.

predicted mol wt 33 kDa

Speziesreaktivität

human, rat, mouse

Methode(n)

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

UniProt-Hinterlegungsnummer

Versandbedingung

dry ice

Lagertemp.

−20°C

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

human ... ORAI1(84876)

Immunogen

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

Leistungsmerkmale und Vorteile

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.

Zielbeschreibung

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.

Physikalische Form

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

Haftungsausschluss

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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Lagerklassenschlüssel

10 - Combustible liquids

WGK

WGK 2

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


Analysenzertifikate (COA)

Suchen Sie nach Analysenzertifikate (COA), indem Sie die Lot-/Chargennummer des Produkts eingeben. Lot- und Chargennummern sind auf dem Produktetikett hinter den Wörtern ‘Lot’ oder ‘Batch’ (Lot oder Charge) zu finden.

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Die Dokumentenbibliothek aufrufen

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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