SAB3500126
ORAI1单克隆抗体 小鼠抗
clone 3F6H5, purified immunoglobulin, buffered aqueous solution
同義詞:
抗TMEM142A, 抗跨膜蛋白142A, 抗钙释放激活钙通道蛋白1
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About This Item
分類程式碼代碼:
12352203
NACRES:
NA.41
共軛:
unconjugated
application:
ELISA (i)
IF
IHC
WB
IF
IHC
WB
無性繁殖:
3F6H5, monoclonal
物種活性:
human, rat, mouse
citations:
8
技術:
immunofluorescence: suitable
immunohistochemistry: suitable
indirect ELISA: suitable
western blot: suitable
immunohistochemistry: suitable
indirect ELISA: suitable
western blot: suitable
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推薦產品
生物源
mouse
品質等級
共軛
unconjugated
抗體表格
purified immunoglobulin
抗體產品種類
primary antibodies
無性繁殖
3F6H5, monoclonal
形狀
buffered aqueous solution
分子量
predicted mol wt 33 kDa
物種活性
human, rat, mouse
技術
immunofluorescence: suitable
immunohistochemistry: suitable
indirect ELISA: suitable
western blot: suitable
UniProt登錄號
運輸包裝
dry ice
儲存溫度
−20°C
目標翻譯後修改
unmodified
基因資訊
human ... ORAI1(84876)
免疫原
由人ORAI1羧基末端附近的16个氨基酸组成的肽。
特點和優勢
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。
標靶描述
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。
外觀
溶剂为含有0.02％叠氮化钠的1 mg/mL磷酸盐缓冲盐水。
免責聲明
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。
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儲存類別代碼
10 - Combustible liquids
水污染物質分類（WGK）
WGK 2
閃點（°F）
Not applicable
閃點（°C）
Not applicable
從最近期的版本中選擇一個：
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
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
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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