SAB3500126
Monoclonal Anti-ORAI1 antibody produced in mouse
clone 3F6H5, purified immunoglobulin, buffered aqueous solution
Sinónimos:
Anti-Calcium release-activated calcium channel protein 1, Anti-TMEM142A, Anti-Transmembrane protein 142A
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About This Item
Código UNSPSC:
12352203
NACRES:
NA.41
Productos recomendados
origen biológico
mouse
Nivel de calidad
conjugado
unconjugated
forma del anticuerpo
purified immunoglobulin
tipo de anticuerpo
primary antibodies
clon
3F6H5, monoclonal
Formulario
buffered aqueous solution
mol peso
predicted mol wt 33 kDa
reactividad de especies
human, rat, mouse
técnicas
immunofluorescence: suitable
immunohistochemistry: suitable
indirect ELISA: suitable
western blot: suitable
Nº de acceso UniProt
Condiciones de envío
dry ice
temp. de almacenamiento
−20°C
modificación del objetivo postraduccional
unmodified
Información sobre el gen
human ... ORAI1(84876)
Inmunógeno
raised against a 16 amino acid peptide from near the carboxy terminus of human ORAI1.
Características y beneficios
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.
Descripción de destino
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.
Forma física
Supplied at approx. 1 mg/mL in phosphate buffered saline containing 0.02% sodium azide.
Cláusula de descargo de responsabilidad
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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Código de clase de almacenamiento
10 - Combustible liquids
Clase de riesgo para el agua (WGK)
WGK 2
Punto de inflamabilidad (°F)
Not applicable
Punto de inflamabilidad (°C)
Not applicable
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Certificados de análisis (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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