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Rat superoxide dismutase 1, soluble (SOD1) ELISA kit

  • 中文名稱:
    大鼠超氧化物歧化酶1,可溶性(SOD1)酶聯免疫試劑盒
  • 貨號:
    CSB-EL022397RA
  • 規(guī)格:
    96T/48T
  • 價格:
    ¥3600/¥2500
  • 其他:

產品詳情

  • 產品描述:
    大鼠超氧化物歧化酶1,可溶性(SOD1)酶聯免疫試劑盒(CSB-EL022397RA)為雙抗夾心法ELISA試劑盒,定量檢測血清、血漿、組織培養(yǎng)上清液、組織勻漿樣本中的SOD1含量。SOD1(銅鋅超氧化物歧化酶1)是第一個被確定的家族性肌萎縮側索硬化癥(ALS)的遺傳基因,其突變會導致蛋白質異常聚集,引發(fā)神經元退行。SOD1在細胞內清除超氧自由基,突變后失去功能,導致氧化應激和神經元損傷。研究SOD1有助于理解ALS的發(fā)病機制,并開發(fā)新的治療策略。試劑盒檢測范圍為15.6 pg/mL-1000 pg/mL,適用于體外細胞模型、組織樣本或體液中的SOD1定量分析;為研究氧化應激相關疾病機制、藥物干預效果評估或生物標志物探索提供可靠工具。本品僅用于科研,不用于臨床診斷,產品具體參數及操作步驟詳見產品說明書。
  • 別名:
    Sod1 ELISA Kit; Superoxide dismutase [Cu-Zn] ELISA Kit; EC 1.15.1.1 ELISA Kit
  • 縮寫:
  • Uniprot No.:
  • 種屬:
    Rattus norvegicus (Rat)
  • 樣本類型:
    serum, plasma, cell culture supernates, tissue homogenates
  • 檢測范圍:
    15.6 pg/mL-1000 pg/mL
  • 靈敏度:
    3.9 pg/mL
  • 反應時間:
    1-5h
  • 樣本體積:
    50-100ul
  • 檢測波長:
    450 nm
  • 研究領域:
    Metabolism
  • 測定原理:
    quantitative
  • 測定方法:
    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 rat SOD1 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)  
    1:200 Average % 93  
    Range % 88-95  
    1:400 Average % 104  
    Range % 100-107  
    1:800 Average % 92  
    Range % 87-95  
    1:1600 Average % 97  
    Range % 92-100  
  • 回收率:
    The recovery of rat SOD1 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 89-95  
    EDTA plasma (n=4) 95 92-97  
                 
                 
  • 標準曲線:
    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  
    1000 2.774 2.767 2.771 2.638  
    500 2.226 2.305 2.266 2.133  
    250 1.737 1.624 1.681 1.548  
    125 1.108 1.088 1.098 0.965  
    62.5 0.636 0.628 0.632 0.499  
    31.2 0.339 0.321 0.330 0.197  
    15.6 0.231 0.224 0.228 0.095  
    0 0.130 0.136 0.133    
  • 數據處理:
  • 貨期:
    3-5 working days

引用文獻

產品評價

靶點詳情

  • 最新研究進展:
    SOD1即超氧化物歧化酶1(Superoxide dismutase 1),是重要的抗氧化酶之一。研究表明,SOD1的突變與家族性漸凍人癥(Familial Amyotrophic Lateral Sclerosis,FALS)相關。最新研究發(fā)現,SOD1與白血病干細胞的維持和耐藥性密切相關。此外,SOD1在肺部疾病、心臟病、肝臟疾病和癌癥等多種疾病中也具有重要作用。
  • 功能:
    Destroys radicals which are normally produced within the cells and which are toxic to biological systems.
  • 基因功能參考文獻:
    1. Results provide evidence that ALS mutant SOD1 inhibits axonal transport of mitochondria by inducing PINK1/Parkin-dependent Miro1 degradation. PMID: 28973175
    2. SOD1 protein expression is upregulated and associated with greater oxidant production in skeletal muscle from Ts65Dn mice. PMID: 28697486
    3. These results suggest that the superoxide anion may be the cause of the observed oxidative damage to SOD1(G93A) rat neural tissues and that the iron-sulfur clusters may be the source of poorly liganded redox active iron implicated in ALS pathogenesis. Low temperature EPR spectroscopy appears to be a valuable tool in assessing the role of metals in neurodegenerative diseases PMID: 27130034
    4. SOD1 and zinc have roles in methotrexate-induced germ cell toxicity PMID: 28011267
    5. A motility defect in SOD1-G93A was highly correlated with mitochondrial movement. PMID: 27464601
    6. Diabetic testes showed decreased Nrf2, HO-1, SOD1, PCNA, and Bcl-2 expressions whereas increased COX-2, NF-kappaB, MT, IL-6, and p-ERK levels. SOD1 and GPX5 were decreased in the epididymis of diabetic rat, whereas Zn supplementation attenuated these changes. PMID: 27025721
    7. These findings suggest that diabetes increases lipid peroxidation and decreases SOD1 levels, and treadmill exercise can mitigate diabetes-induced oxidative damage in the hippocampus. PMID: 25293488
    8. The found of this study suggest that, from a histological standpoint, the SOD1-G93A rat is a valid model of ALS bulbar symptoms. PMID: 25825172
    9. SOD1 has sequence homology to an antihypertensive snake bradykinin-potentiating peptide. PMID: 26047849
    10. the knockdown of mutant SOD1 in only the motor cortex resulted in a significant delay of disease onset, expansion of lifespan, enhanced survival of spinal motor neurons,and maintenance of neuromuscular junctions PMID: 25411487
    11. These data extend clinical findings of a more rapid disease progression in individuals with bulbar symptoms to the SOD1-G93A rat model of ALS. PMID: 24291387
    12. Data suggest that expression of CuZnSOD/Sod1 (and mitochondrial MnSOD/Sod2) is down-regulated as retinal neurons undergo apoptosis following onset of diabetes/diabetic retinopathy. PMID: 24527463
    13. Results highlight misfolded SOD1 as common to two Amyotrophic lateral sclerosis (ALS) rodent animal models and familial ALS patient lymphoblasts with four different SOD1 mutations. PMID: 23736301
    14. SOD1, constitutively produced and released by microglia, is identified as an essential component of neuroprotection mediated by microglia. PMID: 22572742
    15. both SIRT3 and PGC-1alpha protect against mitochondrial fragmentation and neuronal cell death by mutant SOD1 PMID: 22819776
    16. Xanthine/xanthine oxidase treatment increases SOD1 and SOD2 protein and activity levels in cardiac progenitor cells. PMID: 22758933
    17. CuZn-SOD levels were increased in the hippocampus in OLETF rats. PMID: 22981416
    18. Data indicate that Cu-ZnSod expression decreased upon long reperfusion and trxr1 expression did not vary. PMID: 22377061
    19. Data show that aging is associated with reduction in superoxide dismutase (SOD) Cu/Zn-SOD protein expression and total SOD enzymatic activity in mesenteric lymphatic vessel (MLV). PMID: 22540739
    20. Cu/Zn-SOD activity was not significantly changed in response to vitamin E administration at any time points, whereas Cu/Zn-SOD mRNA levels were significantly increased after longer time points with high doses (30 and 100 mg/kg) of vitamin E. PMID: 22732938
    21. The increased expression of antioxidant SOD1, specifically in hippocampal neurons, will provide protection from age-related cognitive decline. PMID: 21942371
    22. dehydroepiandrosterone treatment did not alter disease progression or survival in SOD1-G93A rats PMID: 22409357
    23. Using gastrocnemius muscles of mice overexpressing human mutant SOD1 (mutSOD1) at different disease stages. PMID: 22178654
    24. expression of Cu,Zn-superoxide dismutase decreased significantly in the dorsal hippocampus (CA1 and CA2) and tended to decrease in ventral regions (CA3 and dentate gyrus) by the 24th hour after 3-fold exposure to hypoxia. PMID: 22451871
    25. The present results suggested that inhibition of Shh signaling pathway exacerbated rat ischemic damage caused by pMCAO, which may be correlated with down-regulated expression of Gli1, Ptch1 and SOD1. PMID: 22133807
    26. Data have shown that different stressors have diverse effect on hepatic CuZnSOD and MnSOD activity as well as on serum CORT level. PMID: 21625958
    27. Thus mitochondrial dysfunction is a key early element in pathogenesis of motor neuron degeneration in transgenic SOD1 rats PMID: 21745570
    28. rat Cu/Zn SOD can be nitrated, a modification that could lead to the depressed activity of this enzyme found in placentas from diabetic rats PMID: 20815790
    29. Results describe changes in SOD1 immunoreactivity associated with lipid peroxidation and inflammatory responses in the hippocampi of STZ-induced type I diabetic rats. PMID: 20924670
    30. most, but not all, properties of SOD1 remain the same with a GFP tag PMID: 20221404
    31. Cu,Zn-superoxide dismutase increases toxicity of mutant and zinc-deficient superoxide dismutase by enhancing protein stability PMID: 20663894
    32. Data indicate that acute and/or chronic stress models have different degrees of influence on serum corticosterone and copper-zinc/manganese superoxide dismutase subcellular protein levels. PMID: 20020182
    33. A significant reduction of Cu,Zn-Sod-1 activity level is observed during fast speed running in the crural diaphragm muscle. PMID: 20134035
    34. results suggest that mutant SOD1 and defective mitochondria create localized dysfunctional domains in motor axons, which may lead to progressive axonopathy in ALS PMID: 19344250
    35. Transcriptional regulation and environmental induction of gene encoding copper- and zinc-containing superoxide dismutase. PMID: 11912919
    36. Levels of Sod1 mRNA were significantly reduced in congestive heart failure following myocardial infarction. PMID: 14575298
    37. Associated with copper deficiency were consistent reductions in immunoreactive SOD in erythrocytes. PMID: 15337829
    38. Medroxyprogesterone acetate inhibits the effect of idarubicin on blood levels of this enzyme. PMID: 15372991
    39. the role of PPARgamma is specific to events occurring during reperfusion, in which to CuZn-SOD is a mediator of neuroprotection PMID: 15618443
    40. respiratory motor neuron loss results in significant electrophysiologic changes and diaphragmatic atrophy in SOD1 G93A rats PMID: 16084734
    41. mutant superoxide dismutase has a role in experimental amyotrophic lateral sclerosis PMID: 16195234
    42. Overexpression of SOD1 in whole lens prevents H2O2-induced oxidative damage (cataract formation) to the lens and subsequent control of gap junctions by protein kinase Cgamma. PMID: 16254550
    43. Levels are not significantly altered in the rat prostate during aging and thus is unlikely to be an important factor in the evolution of epithelial cell hyperplasia. PMID: 16372329
    44. These findings show a heterogeneous expression of Cu/Zn SOD in restricted cell types in the germinative zones and suggest a role for antioxidant Cu/Zn SOD in progenitor cells of the immature rat brain. PMID: 16567040
    45. We hypothesized that LA might induce dissociation of p56(Lck) from CD4, thus leading to its downmodulation. PMID: 16631605
    46. In conclusion, this study demonstrates an age-related decline in Cu/Zn-SOD and IDO activities, the two enzymes responsible for scavenging O2*-. PMID: 16688932
    47. acute and rapid endothelial cell endocytosis of CuZn-SOD, possibly via activation of a receptor-mediated pathway PMID: 17077646
    48. EcSOD, CuZnSOD, catalase, and MMP-2 mRNA expression did not statistically vary between aortic aneurysm and normal tissue PMID: 17196988
    49. Ischemic attack causes a rapid response in hippocampal tissue as well as in the cerebrospinal fluid, represented by an increase in the activity of endogenous antioxidant enzymes SOD and CAT. PMID: 17215005
    50. Data show that activation of brain calcineurin (Cn) by Cu-Zn superoxide dismutase (SOD1) depends on direct SOD1-Cn protein interactions occurring in vitro and in vivo. PMID: 17324120

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  • 亞細胞定位:
    Cytoplasm. Nucleus.
  • 蛋白家族:
    Cu-Zn superoxide dismutase family
  • 數據庫鏈接:

    KEGG: rno:24786

    STRING: 10116.ENSRNOP00000002885

    UniGene: Rn.6059