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  4. Human Receptor-interacting serine/threonine-protein kinase 3(RIPK3) ELISA kit

Human Receptor-interacting serine/threonine-protein kinase 3(RIPK3) ELISA kit

  • 中文名稱：
    人受體相互作用絲氨酸/蘇氨酸激酶3(RIPK3)酶聯(lián)免疫試劑盒
  • 貨號(hào)：
    CSB-EL019737HU
  • 規(guī)格：
    96T/48T
  • 價(jià)格：
    ￥3600/￥2500
  • 其他：

產(chǎn)品詳情

  • 產(chǎn)品描述：
    人受體相互作用絲氨酸/蘇氨酸激酶3(RIPK3)酶聯(lián)免疫試劑盒（CSB-EL019737HU）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RIPK3含量。RIPK3是一種控制壞死性凋亡和細(xì)胞凋亡的激酶，由TNF-α和ZBP1激活，磷酸化MLKL導(dǎo)致膜損傷。在神經(jīng)元中，RIPK3不誘導(dǎo)細(xì)胞死亡，而是驅(qū)動(dòng)抗病毒基因轉(zhuǎn)錄，具有細(xì)胞環(huán)境依賴性。RIPK3的研究涉及其在壞死性凋亡、細(xì)胞凋亡和抗病毒炎癥轉(zhuǎn)錄中的作用。試劑盒檢測(cè)范圍為0.156 ng/ml-10 ng/ml，該產(chǎn)品可用于探索RIPK3在炎癥性疾病模型、神經(jīng)退行性病變或腫瘤微環(huán)境中的表達(dá)規(guī)律，支持體外實(shí)驗(yàn)或動(dòng)物模型中蛋白動(dòng)態(tài)變化的定量研究，為解析壞死性凋亡相關(guān)分子機(jī)制提供可靠工具。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)品說明書。
  • 別名：
    Receptor interacting protein 3 ELISA Kit; Receptor interacting serine threonine kinase 3 ELISA Kit; Receptor interacting serine/threonine protein kinase 3 ELISA Kit; Receptor-interacting protein 3 ELISA Kit; Receptor-interacting serine/threonine-protein kinase 3 ELISA Kit; RIP 3 ELISA Kit; RIP like protein kinase 3 ELISA Kit; RIP-3 ELISA Kit; RIP-like protein kinase 3 ELISA Kit; RIPK 3 ELISA Kit; RIPK3 ELISA Kit; RIPK3_HUMAN ELISA Kit
  • 縮寫：
  • Uniprot No.：
  • 種屬：
    Homo sapiens (Human)
  • 樣本類型：
    serum, plasma, tissue homogenates
  • 檢測(cè)范圍：
    0.156 ng/ml-10 ng/ml
  • 靈敏度：
    0.039 ng/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：
    Immunology
  • 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 human RIPK3 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 %

    98

    Range %

    94-103

    1:2

    Average %

    95

    Range %

    90-102

    1:4

    Average %

    89

    Range %

    84-94

    1:8

    Average %

    90

    Range %

    85-96

  • 回收率：

    The recovery of human RIPK3 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)

    93

    86-98

    EDTA plasma (n=4)

    87

    80-95

  • 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.

    ng/ml

    OD1

    OD2

    Average

    Corrected

    10

    2.512

    2.634

    2.573

    2.408

    5

    1.818

    1.767

    1.793

    1.627

    2.5

    1.305

    1.328

    1.317

    1.151

    1.25

    0.806

    0.829

    0.817

    0.652

    0.625

    0.524

    0.521

    0.522

    0.357

    0.312

    0.347

    0.353

    0.350

    0.185

    0.156

    0.263

    0.254

    0.258

    0.093

    0

    0.166

    0.165

    0.165

    　

  • 本試劑盒所含材料：
      • A micro ELISA plate --- The 96-well plate has been pre-coated with an anti-human RIPK3 antibody. This dismountable microplate can be divided into 12 x 8 strip plates.
      • Two vials lyophilized standard --- Dilute a bottle of the standard at dilution series, read the OD values, and then draw a standard curve.
      • Biotin-labeled RIPK3 antibody (100 x concentrate) 1 x 120 μl ---Act as the detection antibody.
      • HRP-avidin (100 x concentrate) 1 x 120 μl --- Bind to the detection antibody and react with the TMB substrate to make the solution chromogenic.
      • Biotin-antibody Diluent 1 x 15 ml ---Dilute the high concentration Biotin-antibody to an appropriate working solution.
      • HRP-avidin Diluent 1 x 15 ml ---Dilute the high concentration HRP-avidin solution to an appropriate solution.
      • Sample Diluent 1 x 50 ml---Dilute the sample to an appropriate concentration.
      • Wash Buffer (25 x concentrate) 1 x 20 ml --- Wash away unbound or free substances.
      • TMB Substrate 1 x 10 ml --- Act as the chromogenic agent. TMB interacts with HRP, eliciting the solution turns blue.
      • Stop Solution 1 x 10 ml --- Stop the color reaction. The solution color immediately turns from blue to yellow.
      • Four Adhesive Strips (For 96 wells) --- Cover the microplate when incubation.
      • An instruction manual

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  • 本試劑盒不含材料：
      • A microplate reader capable of measuring absorbance at 450 nm, with the correction wavelength set at 540 nm or 570 nm.
      • An incubator that can provide stable incubation conditions up to 37°C±5°C.
      • Centrifuge
      • Vortex
      • Squirt bottle, manifold dispenser, or automated microplate washer
      • Absorbent paper for blotting the microtiter plate
      • 50-300ul multi-channel micropipette
      • Pipette tips
      • Single-channel micropipette with different ranges
      • 100ml and 500ml graduated cylinders
      • Deionized or distilled water
      • Timer
      • Test tubes for dilution

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  • 數(shù)據(jù)處理：
  • 貨期：
    3-5 working days

引用文獻(xiàn)

產(chǎn)品評(píng)價(jià)

相關(guān)問答

■ 常見問題解答
Q:

Can I use this product CSB-EL019737HU to detece ripk3 in cell media?

A:
Thanks for your inquiry!
Sorry we usually test samples stated in the manual. We suggest you do a pretest if you want to test cell media

靶點(diǎn)詳情

  • 功能：
    Serine/threonine-protein kinase that activates necroptosis and apoptosis, two parallel forms of cell death. Necroptosis, a programmed cell death process in response to death-inducing TNF-alpha family members, is triggered by RIPK3 following activation by ZBP1. Activated RIPK3 forms a necrosis-inducing complex and mediates phosphorylation of MLKL, promoting MLKL localization to the plasma membrane and execution of programmed necrosis characterized by calcium influx and plasma membrane damage. In addition to TNF-induced necroptosis, necroptosis can also take place in the nucleus in response to orthomyxoviruses infection: following ZBP1 activation, which senses double-stranded Z-RNA structures, nuclear RIPK3 catalyzes phosphorylation and activation of MLKL, promoting disruption of the nuclear envelope and leakage of cellular DNA into the cytosol. Also regulates apoptosis: apoptosis depends on RIPK1, FADD and CASP8, and is independent of MLKL and RIPK3 kinase activity. Phosphorylates RIPK1: RIPK1 and RIPK3 undergo reciprocal auto- and trans-phosphorylation. In some cell types, also able to restrict viral replication by promoting cell death-independent responses. In response to Zika virus infection in neurons, promotes a cell death-independent pathway that restricts viral replication: together with ZBP1, promotes a death-independent transcriptional program that modifies the cellular metabolism via up-regulation expression of the enzyme ACOD1/IRG1 and production of the metabolite itaconate. Itaconate inhibits the activity of succinate dehydrogenase, generating a metabolic state in neurons that suppresses replication of viral genomes. RIPK3 binds to and enhances the activity of three metabolic enzymes: GLUL, GLUD1, and PYGL. These metabolic enzymes may eventually stimulate the tricarboxylic acid cycle and oxidative phosphorylation, which could result in enhanced ROS production.; (Microbial infection) In case of herpes simplex virus 1/HHV-1 infection, forms heteromeric amyloid structures with HHV-1 protein RIR1/ICP6 which may inhibit RIPK3-mediated necroptosis, thereby preventing host cell death pathway and allowing viral evasion.
  • 基因功能參考文獻(xiàn)：
    1. The major function of RIP1 kinase activity in TNF-induced necroptosis is to autophosphorylate serine 161. This specific phosphorylation then enables RIP1 to recruit RIP3 and form a functional necrosome, a central controller of necroptosis. PMID: 28176780
    2. RIPK3-dependent cell death and inflammasome activation in FLT3-internal-tandem-duplication-expressing leukemia-initiating cells PMID: 27517160
    3. The necroptosis-inducing kinase RIPK3 reduces adipose tissue inflammation and glucose intolerance. PMID: 27323669
    4. We showed that RIP3 spontaneously drives a necroptosis-induced inflammation in established intestinal cell lines and in ileal/colonic samples from IBD patients. PMID: 28844856
    5. These data demonstrate that caspase-8 functions in synovial antigen-presenting cells to regulate the response to inflammatory stimuli by controlling RIPK3 action, and this delicate balance maintains homeostasis within the joint. PMID: 28978351
    6. The induced expression of RIP3 by UHRF1 RNAi depends on the presence of Sp1. Remarkably, the ectopic expression of RIP3 in RIP3-null cancer cells results in a decrease in tumor growth in mice. Therefore, our findings offer insights into RIP3 expression control in cancer cells and suggest an inhibitory effect of RIP3 on tumorigenesis. PMID: 28981102
    7. 2-hydroxyglutarate bound to DNMT1 and stimulated its association with the RIP3 promoter, inducing hypermethylation that reduces RIP3 protein and consequently impaired RIP3-dependent necroptosis. PMID: 28564603
    8. the in vivo effects were diametrically reversed with RIP3 deletion or RIP1 blockade, resulting in marked tumor protection. The dichotomy between the in vivo and in vitro results suggests that the microenvironmental milieu resulting from RIP1/RIP3 signaling is likely responsible for its protumorigenic effects PMID: 27932417
    9. Shikonin induces glioma cell necroptosis in vitro by reactive oxygen species overproduction and promoting RIP1/RIP3 necrosome formation. PMID: 28816233
    10. In critically ill trauma patients, plasma levels of the necroptosis mediator RIP3 at 48 h were associated with AKI stage and RBC transfusions. PMID: 26925809
    11. our results reveal that the necroptosis adaptor RIPK3 has key anti-inflammatory and anti-tumoral functions in the intestine, and define RIPK3 as a novel colon tumor suppressor PMID: 27344176
    12. adhesion-induced eosinophil cytolysis takes place through RIPK3-MLKL-dependent necroptosis, which can be counterregulated by autophagy PMID: 28412393
    13. Renal clear cell carcinoma cells cells express increased amounts of RIPK1 and RIPK3 and are poised to undergo necroptosis in response to TNFR1 signaling. PMID: 27362805
    14. The results highlight a new role of TSC2 in protecting glioblastoma against photodynamic therapy-induced cell death, and TSC2 and YWHAZ as new RIP3 partners. PMID: 27984090
    15. inactivation of RIP1/RIP3 resulted in reduction of SOCS1 protein levels and partial differentiation of AML cells. AML cells with inactivated RIP1/RIP3 signaling show increased sensitivity to IFN-gamma-induced differentiation. PMID: 27748372
    16. results reveal a pathway for MLKL-dependent programmed necrosis that is executed in the absence of RIPK3 and potentially drives the pathogenesis of severe liver diseases. PMID: 27756058
    17. Necroptosis signaling is modulated by the kinase RIPK1 and requires the kinase RIPK3 and the pseudokinase MLKL. (Review) PMID: 26865533
    18. Results demonstrate that RIPK3 restricts malignant myeloproliferation by activating the inflammasome, which promotes differentiation and cell death, and that loss of RIPK3 increases leukemic burden in mice. Reduced RIPK3 expression is observed across several human acute myeloid leukemia subtypes. PMID: 27411587
    19. Data identify RIPK3 and the inflammasome as key tumor suppressors in acute myeloid leukemia (AML). PMID: 27411587
    20. The main route of cell death induced by shikonin is RIP1K-RIP3K-mediated necroptosis. PMID: 26496737
    21. Results suggest that impaired hepatic proteasome function by alcohol exposure may contribute to hepatic accumulation of RIP3 resulting in necroptosis and steatosis while RIP1 kinase activity is important for alcohol-induced inflammation. PMID: 26769846
    22. The expression level of RIP3K was significantly lower in the malignant tumors. PMID: 26749282
    23. CNOT3 suppression promotes necroptosis by stabilizing mRNAs for cell death-inducing proteins, Ripk1 and Ripk3. PMID: 26437789
    24. RIPK3 expression may allow unmasking the necroptotic signalling machinery in melanoma and points to reactivation of this pathway as a treatment option for metastatic melanoma. PMID: 26355347
    25. Additionally, later in infection, RIP3 is cleaved by the coxsackievirus B3-encoded cysteine protease 3C(pro), which serves to abrogate RIP3-mediated necrotic signaling and induce a nonnecrotic form of cell death. PMID: 26269957
    26. although JNK activation and RIP3 expression are induced by FS, neither contributes to the liver injury. PMID: 25423287
    27. The RIP3 expression is reduced in tumors compared to normal tissue in 85% of breast cancer patients, suggesting that RIP3 deficiency is positively selected during tumor growth/development. PMID: 25952668
    28. Data implicate the infiltrating macrophages as a source of damaging inflammasomes after photoreceptor detachment in a RIP3-dependent manner and suggest a novel therapeutic target for treatment of retinal diseases. PMID: 25906154
    29. PolyIC stimulation of cervical cancer cells induced necroptotic cell death, which was strictly dependent on the expression of the receptor-interacting protein kinase RIPK3. PMID: 25888634
    30. Data suggest that neoalbaconol-induced necroptosis include receptor interacting serine/threonine kinase 1-dependent expression of tumor necrosis factor alpha and receptor interacting serine/threonine kinase 3-dependent generation of reactive oxygen species. PMID: 25575821
    31. Herpes simplex virus 1- and 2 ICP6 and ICP10 proteins prevent necroptosis in human cells by inhibiting the interaction between receptor-interacting protein kinase 1 (RIP1) and RIP3, a key step in tumor necrosis factor (TNF)-induced necroptosis. PMID: 25674983
    32. High expression of RIP3 in keratinocytes from toxic epidermal necrolysis patients potentiates MLKL phosphorylation/activation and necrotic cell death. PMID: 25748555
    33. RIP3 silencing in leukemia cells results in suppression of the complex regulation of the apoptosis/necroptosis switch and NF-kappaB activity. PMID: 25144719
    34. Suppression of RIP3-dependent necroptosis by human cytomegalovirus PMID: 25778401
    35. RIP3 activation following the induction of necroptosis requires the activity of an HSP90 and CDC37 cochaperone complex. PMID: 25852146
    36. The results of this study showed that cerebral ischemia activates transcriptional changes that lead to an increase in the endogenous RIP3 protein level. PMID: 24746856
    37. Enhanced RIP3 signaling in aneurysmal tissues contributes to abdominal aortic aneursym progression by causing smooth muscle cell necroptosis, as well as stimulating vascular inflammation. PMID: 25563840
    38. RIP3-dependent necroptosis mediates non-alcoholic steatohepatitis-induced liver fibrosis via activation of JNK, MCP-1-mediated recruitment of monocytes, and an expansion of intrahepatic biliary/progenitor cells. PMID: 24963148
    39. RIPK3 serves as a negative regulator of selective autophagy by regulating regulates p62-LC3 complex formation via the caspase-8-dependent cleavage of p62 PMID: 25450619
    40. RIP3 holds both necroptosis and apoptosis in balance through a Ripoptosome-like platform. PMID: 25459880
    41. an alanine residue substitution for Ser(89) enhanced RIP1 kinase activity and TNF-induced programmed necrosis without affecting RIP1-RIP3 necrosome formation. PMID: 24059293
    42. targeting the RIP kinase signalling pathway could be an effective therapeutic intervention in retinal degeneration patients. PMID: 24413151
    43. RIP3-mediated MLKL phosphorylation, though important for downstream signaling, is dispensable for stable complex formation between RIP3 and MLKL. PMID: 24095729
    44. Report role of MLKL/RIP3 pathway in necrotic membrane disruption. PMID: 24703947
    45. RIP3 protein expression is significantly increased in the inflamed tissue of inflammatory boowel disease pediatric patients. PMID: 24322838
    46. The protein levels of crucial modulators of necroptosis, RIP1 and RIP3, are increased by shikonin treatment in primary tumor tissues. PMID: 24314238
    47. the importance of the RIP3-MLKL interaction in the formation of functional necrosomes and suggest that translocation of necrosomes to mitochondria-associated membranes is essential for necroptosis signaling. PMID: 23612963
    48. procaspase-8 activity is essential for cell survival by inhibiting both apoptotic and nonapoptotic cell death dependent on receptor-interacting protein kinase 1 (RIP1) and RIP3 PMID: 23071110
    49. Study shows that RIP1 and RIP3 form an amyloid structure through their RIP homotypic interaction motifs and that this heterodimeric amyloid structure is a functional signaling complex that mediates programmed necrosis. PMID: 22817896
    50. study suggests that MLKL is a key RIP3 downstream component of TNF-induced necrotic cell death PMID: 22421439

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  • 亞細(xì)胞定位：
    Cytoplasm, cytosol. Nucleus.
  • 蛋白家族：
    Protein kinase superfamily, TKL Ser/Thr protein kinase family
  • 組織特異性：
    Highly expressed in the pancreas. Detected at lower levels in heart, placenta, lung and kidney.; [Isoform 3]: Expression is significantly increased in colon and lung cancers.
  • 數(shù)據(jù)庫(kù)鏈接：

    HGNC: 10021

    OMIM: 605817

    KEGG: hsa:11035

    STRING: 9606.ENSP00000216274

    UniGene: Hs.268551