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Mouse Phosphotylinosital 3 kinase,PI3K ELISA Kit

  • 中文名稱:
    小鼠磷酸肌醇3激酶(PI3K)酶聯(lián)免疫試劑盒
  • 貨號(hào):
    CSB-E08419m
  • 規(guī)格:
    96T/48T
  • 價(jià)格:
    ¥3800/¥2500
  • 其他:

產(chǎn)品詳情

  • 產(chǎn)品描述:
    小鼠磷酸肌醇3激酶(PI3K)酶聯(lián)免疫試劑盒(CSB-E08419m)為雙抗夾心法ELISA試劑盒,定量檢測(cè)血清、血漿、組織勻漿樣本中的PIK3CA含量。PIK3CA是一種在多種癌癥中常見的癌基因,編碼的蛋白是PI3K/AKT信號(hào)通路的關(guān)鍵組分。該通路異常激活可促進(jìn)腫瘤細(xì)胞生長(zhǎng)、存活和增殖。PIK3CA突變與腫瘤的發(fā)生發(fā)展密切相關(guān),已成為癌癥研究和治療的重要靶點(diǎn)。試劑盒檢測(cè)范圍為23.5 pg/mL-1500 pg/mL,本產(chǎn)品選用高特異性配對(duì)抗體構(gòu)建檢測(cè)體系,適用于評(píng)估實(shí)驗(yàn)動(dòng)物模型中PI3K表達(dá)水平的變化,可廣泛應(yīng)用于腫瘤機(jī)制研究、代謝性疾病動(dòng)物模型分析以及藥物干預(yù)下信號(hào)通路活性檢測(cè)等科研場(chǎng)景。實(shí)驗(yàn)操作采用標(biāo)準(zhǔn)ELISA流程,支持多樣本類型并行檢測(cè),為探索PI3K相關(guān)分子機(jī)制提供可靠的定量工具,助力基礎(chǔ)研究與轉(zhuǎn)化醫(yī)學(xué)中的靶點(diǎn)驗(yàn)證工作。本品僅用于科研,不用于臨床診斷,產(chǎn)品具體參數(shù)及操作步驟詳見產(chǎn)品說(shuō)明書。
  • 別名:
    Pik3ca ELISA Kit; Phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit alpha isoform ELISA Kit; PI3-kinase subunit alpha ELISA Kit; PI3K-alpha ELISA Kit; PI3Kalpha ELISA Kit; PtdIns-3-kinase subunit alpha ELISA Kit; EC 2.7.1.153 ELISA Kit; Phosphatidylinositol 4,5-bisphosphate 3-kinase 110 kDa catalytic subunit alpha ELISA Kit; PtdIns-3-kinase subunit p110-alpha ELISA Kit; p110alpha ELISA Kit; Phosphoinositide-3-kinase catalytic alpha polypeptide ELISA Kit; Serine/threonine protein kinase PIK3CA ELISA Kit; EC 2.7.11.1 ELISA Kit
  • 縮寫:
  • Uniprot No.:
  • 種屬:
    Mus musculus (Mouse)
  • 樣本類型:
    serum, plasma, tissue homogenates
  • 檢測(cè)范圍:
    23.5 pg/mL-1500 pg/mL
  • 靈敏度:
    5.8 pg/mL
  • 反應(yīng)時(shí)間:
    1-5h
  • 樣本體積:
    50-100ul
  • 檢測(cè)波長(zhǎng):
    450 nm
  • 研究領(lǐng)域:
    Cancer
  • 測(cè)定原理:
    quantitative
  • 測(cè)定方法:
    Sandwich
  • 精密度:
    Intra-assay Precision (Precision within an assay): CV%<8%        
    Three samples of known concentration were tested twenty times on one plate to assess.    
    Inter-assay Precision (Precision between assays): CV%<10%        
    Three samples of known concentration were tested in twenty assays to assess.      
                   
  • 線性度:
    To assess the linearity of the assay, samples were spiked with high concentrations of mouse PI3K in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay.  
      Sample Serum(n=4)    
    1:1 Average % 102    
    Range % 95-106    
    1:2 Average % 102    
    Range % 96-107    
    1:4 Average % 87    
    Range % 83-92    
    1:8 Average % 95    
    Range % 89-99    
  • 回收率:
    The recovery of mouse PI3K spiked to levels throughout the range of the assay in various matrices was evaluated. Samples were diluted prior to assay as directed in the Sample Preparation section.  
     
    Sample Type Average % Recovery Range    
    Serum (n=5) 97 92-101    
    EDTA plasma (n=4) 102 93-105    
                   
                   
  • 標(biāo)準(zhǔn)曲線:
    These standard curves are provided for demonstration only. A standard curve should be generated for each set of samples assayed.  
     
    pg/ml OD1 OD2 Average Corrected    
    1500 2.725 2.812 2.769 2.625    
    750 2.020 2.165 2.093 1.949    
    375 1.514 1.565 1.540 1.396    
    187.5 1.014 1.023 1.019 0.875    
    94 0.614 0.665 0.640 0.496    
    47 0.384 0.392 0.388 0.244    
    23.5 0.271 0.277 0.274 0.130    
    0 0.143 0.144 0.144      
  • 數(shù)據(jù)處理:
  • 貨期:
    3-5 working days

產(chǎn)品評(píng)價(jià)

靶點(diǎn)詳情

  • 功能:
    Phosphoinositide-3-kinase (PI3K) phosphorylates phosphatidylinositol (PI) and its phosphorylated derivatives at position 3 of the inositol ring to produce 3-phosphoinositides. Uses ATP and PtdIns(4,5)P2 (phosphatidylinositol 4,5-bisphosphate) to generate phosphatidylinositol 3,4,5-trisphosphate (PIP3). PIP3 plays a key role by recruiting PH domain-containing proteins to the membrane, including AKT1 and PDPK1, activating signaling cascades involved in cell growth, survival, proliferation, motility and morphology. Participates in cellular signaling in response to various growth factors. Involved in the activation of AKT1 upon stimulation by receptor tyrosine kinases ligands such as EGF, insulin, IGF1, VEGFA and PDGF. Involved in signaling via insulin-receptor substrate (IRS) proteins. Essential in endothelial cell migration during vascular development through VEGFA signaling, possibly by regulating RhoA activity. Required for lymphatic vasculature development, possibly by binding to RAS and by activation by EGF and FGF2, but not by PDGF. Regulates invadopodia formation through the PDPK1-AKT1 pathway. Participates in cardiomyogenesis in embryonic stem cells through a AKT1 pathway. Participates in vasculogenesis in embryonic stem cells through PDK1 and protein kinase C pathway. Also has serine-protein kinase activity: phosphorylates PIK3R1 (p85alpha regulatory subunit), EIF4EBP1 and HRAS. Plays a role in the positive regulation of phagocytosis and pinocytosis.
  • 基因功能參考文獻(xiàn):
    1. miR152 may have an important role in pancreatic beta cell function, and established an association between miR152 and the PI3Kalpha axis. PMID: 30106118
    2. H1047R mutation of Pik3ca induces centrosome amplification in cultured mouse cells. PMID: 29170395
    3. The crucial role of p110beta and the more subtle role of p110alpha in the production of PIP3 molecular species following platelet stimulation has been demonstrated. PMID: 29902570
    4. Here, we describe a role for PI3K/AKT in the regulation of TRF1, an essential component of the shelterin complex. PI3K and AKT chemical inhibitors reduce TRF1 telomeric foci and lead to increased telomeric DNA damage and fragility. We identify the PI3Kalpha isoform as responsible for this TRF1 inhibition. PMID: 29097657
    5. The data establish oncogenic PIK3CA mutations as a cause of glutamine dependency in colorectal cancer. PMID: 27321283
    6. High PI3k expression is associated with gastrointestinal stromal tumor. PMID: 28923937
    7. High PI3K expression is sensitive to initial injury intensity induced by freeze damage. PMID: 27647425
    8. excessive proliferation of endometrial epithelial cells was observed in Pik3cad/d mice. Our studies suggest that Pik3ca has a critical role in uterine gland development and female fertility PMID: 29346447
    9. Long latency DMBA induced mouse mammary tumors reproduce the molecular profile of human luminal breast carcinomas, displaying a high incidence of activating Pik3caH1047 and loss of function Pten mutations. PMID: 27588403
    10. Data show that the phosphoinositide 3-kinase (PI3K) inhibitor BKM120 led to a precipitous drop in DNA synthesis within 8 h of drug treatment, whereas DNA synthesis in normal tissues was less affected. PMID: 27402769
    11. Using genetic inactivation of the growth and metabolism regulator, Pik3ca (encoding PIK3CA also known as p110alpha, alpha/+), the interplay between the maternal genome and the fetal genome on placental phenotype, was examined. PMID: 27621448
    12. Data suggest a critical role for KDM3A in the PI3K/AP-1 oncogenic axis and propose a novel strategy for inhibition of KDM3A against liver tumor development under PI3K pathway activation. PMID: 28692045
    13. Data show that tumors lacking PSMA had less than half the abundance of type 1 insulin-like growth factor receptor (IGF-1R), less activity in the survival pathway mediated by PI3K-AKT signaling, and more activity in the proliferative pathway mediated by MAPK-ERK1/2 signaling. PMID: 28292957
    14. Both PIK3CA mutants H1047R and E545K are able to activate the AKT/mTOR pathway. An intact AKT2/mTOR complex 1 cascade is required for tumourigenesis induced by H1047R/c-Met or E545K/c-Met in the liver in mice. PMID: 26716908
    15. We further demonstrate that loss of one allele of PTEN is sufficient to shift isoform dependency from p110alpha to p110beta in vivo. These results provide insight into the molecular mechanism by which ErbB2-positive breast cancer escapes p110alpha inhibition. PMID: 28783168
    16. Studies indicate that the Pten+/- genotype displayed neoplasia in multiple organs, including the endometrium and that the Pten is a key regulatory player in the PI3K/PTEN/AKT pathway. PMID: 27910071
    17. Data show that docetaxel, rapamycin and tanespimycin multi-drug loaded micelles targeted against HSP90 and the PI3K/AKT/mTOR pathway in prostate cancer. PMID: 28350865
    18. Data show that macrophage M2 polarization was mediated through PTEN/PI3k/AKT pathway activation. PMID: 28273403
    19. Constitutive Activation of PI3K is associated with Ovarian Granulosa Cell Tumors. PMID: 27197196
    20. Together with recent identification of somatic mutations in p110a (encoded by PIK3CA), our data establish a potential mechanistic link between AGGF1 and PIK3CA, the two genes identified for Klippel-Trenaunay syndrome (KTS) PMID: 27522498
    21. p110beta has a role in mediating skeletal muscle metabolic signaling by regulating expression of AMP-activated protein kinase PMID: 27965101
    22. The mRNA levels of leptin and of 17-beta-dehydrogenase 3, and enzyme important for testosterone production, were significantly higher in the testis of adult alpha-/- males( PI3K catalytic subunit p110alpha deletion). PMID: 28357399
    23. PI3K signaling plays a modulatory role in the regulation of the transcriptional rhythm of the Dbp gene by targeting BMAL1 and CLOCK. PMID: 27022680
    24. Analysis of 18 signalling signatures revealed that PI3K signalling is significantly induced whereas EGFR signalling is significantly reduced in Pten() versus PIK3CA(H1047R) tumors. Thus, Pten() and PIK3CA(H1047R) tumors exhibit discernable differences that may impact tumorigenesis and response to therapy. PMID: 26814435
    25. activating PIK3CA mutations gives rise to sporadic venous malformations in mice, which closely resemble the histology of the human disease. PMID: 27030594
    26. These data demonstrate a causal relationship between activating Pik3ca mutations and the genesis of vascular malformations. PMID: 27030595
    27. data demonstrate that the PI3K p110alpha-Akt/Rac1 and NOX1 signalling pathways play a pivotal role in VEGF-induced vascular differentiation and cell migration. PMID: 26553657
    28. miR-490-5p functions as a tumour suppressor in renal carcinoma by targeting PIK3CA PMID: 26559013
    29. Reelin thus plays a role in restraining RAS and PI3-kinase promotion of cell motility and potentially tumour metastasis. PMID: 27071537
    30. Chronic CoQ(10) supplementation attenuates aspects of diabetic cardiomyopathy, even in a setting of reduced cardiac PI3K(p110alpha) protective signaling PMID: 25937176
    31. A subgroup of colon cancers might arise in the setting of activated PI3K, as seen in a PIK3CA mutant mouse model. PMID: 26863299
    32. p110a as well as p110d Class IA PI3Ks are important to immune regulation; inhibition of both subunits may be an effective therapeutic approach in inflammatory autoimmune diseases like rheumatoid arthritis. PMID: 26883061
    33. Interestingly, we observed that IRGM1 enhanced F-actin polymerization and triggers epithelial mesenchymal transition (EMT) through a mechanism involved in PIK3CA mediated Rac1 activation. PMID: 26202910
    34. Study demonstrates the oncogenic cooperation between PI3K and Yap pathways along liver carcinogenesis. The PIK3CA/Yap mouse represents an important preclinical liver tumor model. PMID: 25826091
    35. Data show that the RNA-binding protein lin28a/microRNA let-7a axis regulated glucose metabolism in part through the insulin-PI3K-mTOR pathway. PMID: 25688987
    36. ARID1A and PIK3CA mutations cooperate to promote tumour growth through sustained IL-6 overproduction. PMID: 25625625
    37. Cone-specific deletion of p110alpha resulted in cone degeneration. PMID: 25742742
    38. Pten and Pik3ca have distinct consequences on the activation of the phosphatidylinositol 3-kinase pathway in endometrial epithelium. PMID: 25698082
    39. Hepatic expression of p110alpha containing hot spot mutations results in rapid hepatic steatosis, paradoxically accompanied by increased glucose tolerance, and marked glycogen accumulation. PMID: 26169833
    40. Results show that PI3Kalpha does not directly regulate myocardial contractility, but is required for recovery from tamoxifen/Cre toxicity. PMID: 25618408
    41. Data indicate that the effects of irisin were abolished by the inhibition of phosphoinositide 3-kinase (PI3K) p110alpha subunit and the phosphorylation of Akt/protein kinase B. PMID: 26201094
    42. miR-378 inhibits hepatic insulin signalling through targeting Pik3ca. PMID: 25471065
    43. oncogenic Pik3ca(H1047R) activates a multipotent genetic program in normally lineage-restricted populations at the early stage of tumour initiation, setting the stage for future intratumoural heterogeneity PMID: 26266985
    44. Study shows that both ubiquitous and endothelial cell-specific expression of the Pik3caH1047R mutation during embryonic development lead to severe vascular malformations that result in lethality prior to E10.5. PMID: 25958091
    45. expression of the Pik3ca(H1047R) mutation throughout the body resulted in a dramatic increase in body weight within 3 weeks of induction, which was associated with increased organ size rather than adiposity PMID: 25550458
    46. 2 PDX models showed gained mutations such as PIK3CA or FBWX7 mutation. Ten patient-derived advanced colon cancer xenograft models were established. PMID: 25526474
    47. functional interaction of RAS with p110alpha in host tissue was required for efficient establishment and growth of metastatic tumors PMID: 25003191
    48. Data indicate cellular repressor of E1A-stimulated gene (CREG) as a factor in regulating endothelial differentiation and vasculogenesis via VEGF/PI3K/Akt pathway. PMID: 24896346
    49. Pancreas-specific disruption of Pik3ca or Rac1, but not Pik3cb, prevented the development of pancreatic tumors in Kras(G12D/+);Ptf1a(Cre/+) mice. PMID: 25311989
    50. Prostate tumor driven by polyomaviruses MT depends on p110alpha but not p110beta. PMID: 24991009

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  • 蛋白家族:
    PI3/PI4-kinase family
  • 數(shù)據(jù)庫(kù)鏈接: