產(chǎn)品編號 | bs-6847R-Cy5 |
英文名稱 | Rabbit Anti-PDCD10/Cy5 Conjugated antibody |
中文名稱 | Cy5標記的凋亡相關(guān)蛋白10抗體 |
別 名 | Apoptosis related protein 15; CCM3; Cerebral cavernous malformations 3 protein; MGC1212; MGC24477; PDC10_HUMAN; PDCD 10; PDCD10; Programmed cell death 10; Programmed cell death protein 10; TF 1 cell apoptosis related protein 15; TF-1 cell apoptosis-related protein 15; TFAR15. |
規(guī)格價格 | 100ul/2980元 購買 大包裝/詢價 |
說 明 書 | 100ul |
研究領(lǐng)域 | 細胞生物 發(fā)育生物學 神經(jīng)生物學 細胞凋亡 激酶和磷酸酶 |
抗體來源 | Rabbit |
克隆類型 | Polyclonal |
交叉反應 | Rat, (predicted: Human, Mouse, Chicken, Pig, Horse, Rabbit, ) |
產(chǎn)品應用 | IF=1:50-200
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
分 子 量 | 22kDa |
性 狀 | Lyophilized or Liquid |
濃 度 | 1mg/ml |
免 疫 原 | KLH conjugated synthetic peptide derived from humna PDCD10 |
亞 型 | IgG |
純化方法 | affinity purified by Protein A |
儲 存 液 | 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
保存條件 | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
產(chǎn)品介紹 |
background: This gene encodes an evolutionarily conserved protein associated with cell apoptosis. The protein interacts with the serine/threonine protein kinase MST4 to modulate the extracellular signal-regulated kinase (ERK) pathway. It also interacts with and is phosphoryated by serine/threonine kinase 25, and is thought to function in a signaling pathway essential for vascular developent. Mutations in this gene are one cause of cerebral cavernous malformations, which are vascular malformations that cause seizures and cerebral hemorrhages. Multiple alternatively spliced variants, encoding the same protein, have been identified. [provided by RefSeq, Jul 2008]. Function: Promotes cell proliferation. Modulates apoptotic pathways. Increases mitogen-activated protein kinase activity and MST4 activity. Important for cell migration, and for normal structure and assembly of the Golgi complex. Important for KDR/VEGFR2 signaling. Increases the stability of KDR/VEGFR2 and prevents its breakdown. Required for normal cardiovascular development. Required for normal angiogenesis, vasculogenesis and hematopoiesis during embryonic development. Subunit: Homodimer. Interacts (via C-terminus) with CCM2 and PXN. Interacts (via N-terminus) with MST4, STK24 and STK25. Interacts with GOLGA2. Identified in a complex with CCM1 and CCM2. Interacts with KDR/VEGFR2. Interaction with KDR/VEGFR2 is enhanced by stimulation with VEGFA. Subcellular Location: Cytoplasm. Golgi apparatus membrane; Peripheral membrane protein; Cytoplasmic side. Cell membrane; Peripheral membrane protein; Cytoplasmic side. Note=Partially co-localizes with endogenous PXN at the leading edges of migrating cells. Tissue Specificity: Ubiquitous. DISEASE: Defects in PDCD10 are the cause of cerebral cavernous malformations type 3 (CCM3) [MIM:603285]. Cerebral cavernous malformations (CCMs) are congenital vascular anomalies of the central nervous system that can result in hemorrhagic stroke, seizures, recurrent headaches, and focal neurologic deficits. CCMs have an incidence of 0.1%-0.5% in the general population and usually present clinically during the 3rd to 5th decade of life. The lesions are characterized by grossly enlarged blood vessels consisting of a single layer of endothelium and without any intervening neural tissue, ranging in diameter from a few millimeters to several centimeters. Similarity: Belongs to the PDCD10 family. Database links:
Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
1、抗體溶解方法 | |
2、抗體修復方式 | |
3、常用試劑的配制 | |
4、免疫組化操作步驟 | |
5、免疫組化問題解答 | |
6、Western Blotting 操作步驟 | |
7、Western Blotting 問題解答 | |
8、關(guān)于肽鏈的設(shè)計 | |
9、多肽的溶解與保存 | |
10、酶標抗體效價測定程序 | |
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