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Merck
CN

SAB3500126

ORAI1单克隆抗体 小鼠抗

clone 3F6H5, purified immunoglobulin, buffered aqueous solution

别名:

抗TMEM142A, 抗跨膜蛋白142A, 抗钙释放激活钙通道蛋白1

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关于此项目

NACRES:
NA.41
UNSPSC Code:
12352203
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产品名称

ORAI1单克隆抗体 小鼠抗, clone 3F6H5, purified immunoglobulin, buffered aqueous solution

biological source

mouse

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

3F6H5, monoclonal

form

buffered aqueous solution

mol wt

predicted mol wt 33 kDa

species reactivity

human, rat, mouse

technique(s)

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

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Quality Level

Gene Information

human ... ORAI1(84876)

Disclaimer

除非我们的产品目录或产品附带的其他公司文档另有说明,否则我们的产品仅供研究使用,不得用于任何其他目的,包括但不限于未经授权的商业用途、体外诊断用途、离体或体内治疗用途或任何类型的消费或应用于人类或动物。

Features and Benefits

请完全放心地评估我们的抗体。如果抗体在您的研究中无效,我们将全额退款或换货。了解更多。

General description

免疫细胞的抗原刺激通过Ca++释放激活的Ca++(CRAC)通道触发Ca++流入。ORAI1是最近发现的一种四跨膜蛋白,它是CRAC的重要组成部分。人体中这种蛋白质的错义突变会引起遗传性严重联合免疫缺陷(SCID),从而导致消融的T细胞Ca++流入。已有研究提出,ORAI1可作为高选择性Ca++质膜通道,通过与STIM1(即存储激活的内质网Ca+传感器)相互作用进行门控。ORAI1在SDS-PAGE中通常以高于预期的分子量迁移。预计该抗体与ORAI2或ORAI3无交叉反应性。

Immunogen

由人ORAI1羧基末端附近的16个氨基酸组成的肽。

Physical form

溶剂为含有0.02%叠氮化钠的1 mg/mL磷酸盐缓冲盐水。

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存储类别

10 - Combustible liquids

wgk

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable

法规信息

常规特殊物品
此项目有

历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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访问文档库

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.
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
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
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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