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Human growth differentiation factor 2,GDF2 ELISA Kit

  • 中文名称:
    人生长分化因子2(GDF2)酶联免疫试剂盒
  • 货号:
    CSB-E11769h
  • 规格:
    96T/48T
  • 价格:
    ¥3200/¥2500
  • 其他:

产品详情

  • 产品描述:
        生长分化因子2(Growth differentiation factor 2,GDF2),也称为骨形态发生蛋白4(Bone morphogenetic protein 4,BMP4),是一种TGF-β超家族的成员。GDF2参与胚胎发育、组织再生、骨形成和细胞增殖等生物学过程。在肿瘤的发生和发展中,GDF2的含量通常下调,但在某些肿瘤中可能升高,因此GDF2也被认为是一个潜在的肿瘤生物标志物。
        j9九游会登录入口首页生物所提供的Human growth differentiation factor 2,GDF2 ELISA Kit属于ELISA检测试剂盒,采用双抗夹心法定量检测人血清、血浆,组织匀浆样本中的GDF2,其灵敏度为0.98 pg/mL,检测范围为3.9 pg/mL-250 pg/mL。
     
  • 别名:
    GDF2 ELISA Kit; BMP9Growth/differentiation factor 2 ELISA Kit; GDF-2 ELISA Kit; Bone morphogenetic protein 9 ELISA Kit; BMP-9 ELISA Kit
  • 缩写:
    GDF2
  • Uniprot No.:
  • 种属:
    Homo sapiens (Human)
  • 样本类型:
    serum, plasma,tissue homogenates
  • 检测范围:
    3.9 pg/mL-250 pg/mL
  • 灵敏度:
    0.98 pg/mL
  • 反应时间:
    1-5h
  • 样本体积:
    50-100ul
  • 检测波长:
    450 nm
  • 研究领域:
    Others
  • 测定原理:
    quantitative
  • 测定方法:
    Sandwich
  • 数据处理:
  • 货期:
    3-5 working days

产品评价

靶点详情

  • 最新研究进展:
    GDF2,也称为骨形态发生蛋白2,是一种成员,属于TGF-β超家族。最近的研究表明,GDF2在心血管疾病和肿瘤中发挥着重要的作用。例如,研究表明,GDF2具有促进血管新生的作用,并且在冠心病和动脉硬化等疾病的发病过程中可能发挥着保护作用。
  • 功能:
    Potent circulating inhibitor of angiogenesis. Signals through the type I activin receptor ACVRL1 but not other Alks. Signaling through SMAD1 in endothelial cells requires TGF-beta coreceptor endoglin/ENG.
  • 基因功能参考文献:
    1. Case-control analyses reveal significant overrepresentation of rare variants in ATP13A3, AQP1 and SOX17, and provide independent validation of a critical role for GDF2 in heritable pulmonary arterial hypertension. PMID: 29650961
    2. Low BMP9 expression is associated with breast cancer. PMID: 30015950
    3. BMP-9 was found the most effective to induce osteogenic transdifferentiation of fat tissue in vitro PMID: 28054585
    4. Epigenetic Regulation of GDF2 Suppresses Anoikis in Ovarian and Breast Epithelia. PMID: 26678910
    5. BMP9 is highly expressed in bladder cancer cells. BMP9 promotes bladder cancer cell proliferation and migration through up-regulation of lncRNA UCA1. PMID: 29642505
    6. Bone morphogenetic protein 9 (BMP9) was identified as a target of miR-149 in MG63 cells, and BMP9 expression was negatively correlated with miR149 level in osteosarcoma clinical samples. miR-149 promotes osteosarcoma progression via targeting BMP9. PMID: 28956179
    7. The binding free energies indicate that ALK-3 preferably binds to BMP-2 instead of BMP-9. The structural analysis shows that ALK-3 binding with BMP-2 occurs in a perfectly symmetry pathway, whereas this symmetry is lost for possible ALK-3 interactions with BMP-9 PMID: 28869862
    8. The BMP9-induced phosphorylation of Smad1/5/8 was increased with the overexpression of RUNX3, and yet was decreased with the knockdown of RUNX3. Collectively, our findings suggest that RUNX3 is an essential modulator of the BMP9-induced osteoblast lineage differentiation of mesenchymal stem cells (MSCs). PMID: 29039519
    9. BMP9 is overexpressed in hepatic stellate cells in a cohort of liver fibrosis patients. PMID: 29223735
    10. our study indicates that BMP9 can inhibit the growth and metastasis of breast cancer cells, which may be related to interaction between pre-adipocytes/adipocytes and MDA-MB-231 cells via leptin signaling pathway. PMID: 28415788
    11. BMP9 interacts with a hydrophobic surface of the N-terminal orphan domain of ENG, which adopts a new duplicated fold generated by circular permutation. PMID: 28564608
    12. this is the first study that accurately identifies BMP9 as a profibrotic factor in fibroblasts. PMID: 27208502
    13. the combination of BMP-9 and MC-GAG stimulates chondrocytic and osteogenic differentiation of hMSCs. PMID: 27275929
    14. The results from this study demonstrate that the use of rhBMP9 significantly and markedly induced osteoblast differentiation when compared to rhBMP2 and PMID: 27699987
    15. The results demonstrate that although BMP9 alone does not influence leukocyte recruitment, it primes the vascular endothelium to mount a more intense response when challenged with LPS through an increase in TLR4, E-selectin, and VCAM-1 and ultimately through enhanced leukocyte recruitment. PMID: 27647829
    16. Data suggest BMP9/GDF2 and BMP10 synergize with TNFA to increase monocyte recruitment to vascular endothelial cells; process appears to be mediated mainly via ALK2/ACVR1 (which exhibits protein kinase activity). These studies used in vitro flow monocyte adhesion assay. (BMP9 = growth differentiation factor 2; BMP10 = bone morphogenetic protein 10; TNFA = tumor necrosis factor alpha; ALK2/ACVR1 = activin A receptor type 1) PMID: 28646109
    17. These results suggest that BMP9-transduced calvarial mesenchymal progenitor cells seeded in a PPCN-g thermoresponsive scaffold is capable of inducing bone formation in vivo and is an effective means of creating tissue engineered bone for critical sized defects. PMID: 28249039
    18. circulating levels significantly decreased in type 2 diabetes mellitus patients and associated with glucose homoeostasis and insulin sensitivity PMID: 27940998
    19. the data identify MxA as a novel stimulator of BMP4 and BMP9 transcriptional signaling, and suggest it to be a candidate IFN-alpha-inducible mechanism that might have a protective role against development of pulmonary arterial hypertension and other vascular diseases. PMID: 27875556
    20. BMP9 inhibited the proliferation and migration of the A549 cells. PMID: 27177272
    21. his study shows that BMP9 inhibition is associated with Osteosarcoma (OS) development and that enhanced expression of BMP9 may be a potential treatment method for OS PMID: 27706722
    22. IGF1 can enhance BMP9-induced osteogenic differentiation in mesenchymal stem cells. PMID: 26645636
    23. In ovarian and breast epithelial cells, epigenetic regulation of GDF2 suppresses anoikis. PMID: 26678910
    24. BMP9 also influenced the expression of PPARgamma. PMID: 26609524
    25. Data suggest ALK1 and ACVR2A/ACVR2B, acting as BMP9 co-receptors, rearrange pro-domains of BMP9--pro-domain dimer complex leading to displacement of pro-domains after receptor binding, release of mature non-dimer BPM9, and activation of signaling. PMID: 26677222
    26. DLL4/Notch1 and BMP9 interdependent signaling induces endothelial cell quiescence via P27KIP1/thrombospondin pathway. PMID: 26471266
    27. BMP9 Crosstalk with the Hippo Pathway Regulates Endothelial Cell Matricellular and Chemokine Responses PMID: 25909848
    28. BMP-9 induces vascular smooth muscle cell osteogenic differentiation and calcification via ALK1, Smad and ALP dependent mechanisms. PMID: 25297851
    29. This review summarizes the indirect connection between BMP9 and liver fibrosis, with a focus on the BMP9 signaling pathway members ALK1, endoglin, Id1, hepcidin and Snail. [review] PMID: 25393508
    30. Data show that bone morphogenetic protein 9 (BMP9) can inhibit the migration and invasion of MDA-MB-231 breast cancer cells and promote osteogenesis and proliferation of HS-5 bone marrow-derived mesenchymal stem cells in the co-culture system. PMID: 25209393
    31. structural analysis of the bone morphogenetic protein 9 procomplex PMID: 25751889
    32. These findings suggest that BMP9 can inhibit the proliferation and metastasis of SK-BR-3 cells via inactivating ERK1/2 and PI3K/AKT signaling pathways PMID: 24805814
    33. BMP9 is regulated by redox-dependent proteolysis PMID: 25237187
    34. in primary, non-malignant cells BMP-9 stabilizes the epithelial phenotype and inhibits proliferation, in hepatocellular carcinoma cells it induces cell growth and the acquisition of a migratory phenotype. PMID: 24670474
    35. these observations indicate that BMP9 is an important mediator of breast cancer bone metastasis and a potential therapeutic target for treating this deadly disease. PMID: 24413988
    36. BMP9 can regulate tumor growth of osteosarcoma cells through the Wnt/beta-catenin pathway. PMID: 24337584
    37. results strongly suggest that Creld2 may be directly regulated by BMP9 and ER stress response may play an important role in regulating osteogenic differentiation PMID: 24019898
    38. the cross-talk between EGF and BMP9 signalling pathways in mesenchymal stem cells may underline their important roles in regulating osteogenic differentiation. PMID: 23844832
    39. ResultS suggest that BMP9 may inhibit the migration and invasiveness of Osteosarcoma cells through a Smad-dependent pathway by downregulating the expression and activity of MMP9. PMID: 23807047
    40. BMP9 signaling may be relevant during hepatocarcinogenesis in vivo. PMID: 23936038
    41. We demonstrate a cross-talk between BMPs and CRYAB and a major effect of this regulatory interaction on resistance to apoptosis. PMID: 24072698
    42. Mutations in BMP9 (also known as GDF2) were identified in three probands with hereditary hemorrhagic telangiectasia. PMID: 23972370
    43. BMP-9 was able to induce the phosphorylation of Smad-1/5/8 and ERK 1/2 proteins, but did not induce p38 phosphorylation. PMID: 23313128
    44. the enhanced expression of BMP-9 in osteosarcoma cells by adBMP-9 exerted inhibitory effects on growth and migration of osteosarcoma cells possibly via blockade of the PI3K/AKT signaling pathway. PMID: 22948234
    45. BMP9 regulates the SDF1/CXCR4 axis in endothelial cells. BMP9 signaling via endoglin switches cells from an SDF1-responsive autocrine state to an SDF1-nonresponsive paracrine state repressing endothelial cell migration & promoting vessel maturation. PMID: 23018639
    46. SNPs in the BMP9 gene appear to contribute to the risk of OPLL in association with certain clinical and demographic characteristics. PMID: 22829878
    47. platelets regulate blood/lymphatic vessel separation by inhibiting the proliferation, migration, and tube formation of LECs, mainly because of the release of BMP-9 upon activation by CLEC-2/podoplanin in PMID: 22556408
    48. data suggest that both the VEGF/VEGF receptor and the BMP9/ALK1 pathways are essential for stimulating angiogenesis, and targeting both pathways simultaneously may be an attractive strategy to overcome resistance to antiangiogenesis therapy PMID: 22493445
    49. Mutual regulation by BMP-9 and CV2 is essential in regulating the development of the vascular endothelium. PMID: 22474252
    50. Increased ET-1 production by endothelial cells as a consequence of BMPR II dysfunction may be clinically relevant in the pathogenesis of pulmonary arterial hypertension. PMID: 22299030

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  • 相关疾病:
    Telangiectasia, hereditary hemorrhagic, 5 (HHT5)
  • 亚细胞定位:
    Secreted.
  • 蛋白家族:
    TGF-beta family
  • 组织特异性:
    Detected in blood plasma (at protein level).
  • 数据库链接:

    HGNC: 4217

    OMIM: 605120

    KEGG: hsa:2658

    STRING: 9606.ENSP00000249598

    UniGene: Hs.279463