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  4. PDCD10 Antibody

PDCD10 Antibody

  • 货号：
    CSB-PA017665GA01HU
  • 规格：
    ￥3,900
  • 其他：

产品详情

  • Uniprot No.：
    Q9BUL8
  • 基因名：
    PDCD10
  • 别名：
    Apoptosis related protein 15 antibody; CCM3 antibody; Cerebral cavernous malformations 3 protein antibody; MGC1212 antibody; MGC24477 antibody; PDC10_HUMAN antibody; PDCD 10 antibody; PDCD10 antibody; Programmed cell death 10 antibody; Programmed cell death protein 10 antibody; TF 1 cell apoptosis related protein 15 antibody; TF-1 cell apoptosis-related protein 15 antibody; TFAR15 antibody
  • 宿主：
    Rabbit
  • 反应种属：
    Human,Mouse,Rat
  • 免疫原：
    Human PDCD10
  • 免疫原种属：
    Homo sapiens (Human)
  • 抗体亚型：
    IgG
  • 纯化方式：
    Antigen Affinity Purified
  • 浓度：
    It differs from different batches. Please contact us to confirm it.
  • 保存缓冲液：
    PBS with 0.1% Sodium Azide, 50% Glycerol, pH 7.3. -20°C, Avoid freeze / thaw cycles.
  • 产品提供形式：
    Liquid
  • 应用范围：
    ELISA,WB,IHC
  • Protocols：
  • 储存条件：
    Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
  • 货期：
    Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.

产品评价

靶点详情

  • 功能：
    Promotes cell proliferation. Modulates apoptotic pathways. Increases mitogen-activated protein kinase activity and STK26 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.
  • 基因功能参考文献：
    1. We showed that overexpression of PDCD10 significantly inhibited miR-103-induced inhibition of cell proliferation, increased apoptosis, and decreased invasion and migration in A549 cells. PMID: 28734041
    2. Data show that PDCD10 expression levels are high in bladder cancer (BC) tissues and seems to correlate with worse prognosis. PDCD10 is directly modulated by miR26a/miR26b as a target in BC cells. PDCD10 promotes BC cell proliferation in vitro and growth and progression of BC in vivo. PMID: 30272373
    3. Over-expression of PDCD10 in HeLa cells increased the resistance to doxorubicin. PMID: 29482058
    4. The identified endothelial signalling pathway of CCM3-DLL4/Notch-EphB4-Erk1/2 may provide an insight into mechanism of CCM3-ablation-mediated angiogenesis. PMID: 28371279
    5. Case-control study to investigate the possible association of others polymorphisms (c.485+65 C/G, c.989+63 C/G, c.1980 A/G in CCM1 gene, c.472+127 C/T in CCM2 and c.150 G/A in CCM3) with cerebral cavernous malformations. The five polymorphisms were characterized in 64 sporadic patients and in 90 healthy controls by ASO-PCR. Results suggest that some polymorphisms in CCM genes could play an important role in the disease. PMID: 28870584
    6. CCM3 restrains ANGPT2 release from endothelial cells and maintains endothelial junctions. CCM3 depletion leads to increased ANGPT2 release. PMID: 27548575
    7. Data indicated that rs9853967 and rs11714980 polymorphisms in CCM3 and SERPINI1respectively could be associated with a protective role in cerebral cavernous malformations disease. PMID: 27737651
    8. Inhibition of Notch and activation of VEGF/p38 signaling were involved in miR-425-5p/CCM3 mediated inhibition of angiogenesis by sodium arsenite. PMID: 27132035
    9. Loss of endothelial programmed cell death 10 activates glioblastoma cells and promotes tumor growth. PMID: 26254477
    10. Studies suggest that the 3 proteins of the Cerebral Cavernous Malformations (CCM) complex KRIT1/CCM1, CCM2/malcavernin and CCM3/PDCD10 not only require one another for reciprocal stabilization, but also act as a platform for signal transduction. PMID: 26356566
    11. Study highlights the potential role of CCM3 in regulating tight junction complex organization and brain endothelial barrier permeability through CCM3-ERK1/2-cortactin cross-talk PMID: 26385474
    12. A novel CCM3 missense mutation (c.422T>G) detected in 2 Greek brothers with cerebral cavernous malformations causes a loss of function in Pdcd10 protein due to its localization in the 8th helix. It affects Leu141. It may play a role in angiogenesis. PMID: 26115622
    13. The proto-oncogene PDCD10 is direct target of miR-103 that can suppress Prostate cancer proliferation and migration by down-regulating the PDCD10. PMID: 26771762
    14. We report for the first time that PDCD10 expression is downregulated in GBM, which is associated with the activation of Akt signaling protein PMID: 26490252
    15. miR-181b was upregulated by hypoxia in retinoblastoma in an HIF-1a-independent manner. Additionally, miR-181b exerts its angiogenic function, at least in part, by inhibiting PDCD10 and GATA6. PMID: 25872572
    16. Results broaden our knowledge on the mechanisms by which CCM3 deficiency results in disease and open new avenues of research into both CCM3 and senescence biology. PMID: 25655101
    17. Study shows that PDCD10 mutations result in vascular permeability mediated by ROCK activity and a particularly severe clinical phenotype of patients and mouse model for cerebral cavernous malformation disease. PMID: 25122144
    18. A causative mutation in the PDCD10 gene (p.Gln112PhefsX13) was identified in an Italian family with cerebral cavernous malformations associated with meningioma. PMID: 26246098
    19. DNA mutational analysis in 87 Italian affected individuals with Cerebral cavernous malformations identified mutations in over 97.7% of cases, and PDCD10/CCM3 mutations account for 13.1% four of which already known and four novel ones. PMID: 25354366
    20. both CCM2 and CCM3 are required for normal endothelial cell network formation. PMID: 25825518
    21. Identification of genetic variants in the CCM3/PDCD10 gene which are critical indicators of cerebral cavernous malformations in humans. PMID: 25451273
    22. Prevalence, frequency and characterization of CCM1, CCM2 and CCM3 variants in cerebral cavernous malformation Spanish patients. PMID: 24466005
    23. DNA sequencing and deletion/duplication testing of the CCM1, CCM2, and CCM3 genes in the proband revealed a CCM1 c.601CNG mutation. PMID: 24007869
    24. The identification of other four new mutations in 40 sporadic patients with either single or multiple cerebral cavernous malformations, is reported. PMID: 24058906
    25. CCM3 mutations are associated with cerebral cavernous malformation in some Japanese patients. PMID: 23485406
    26. Loss of CCM3 impairs DLL4-Notch signalling and is associated with impaired endothelial angiogenesis and inherited cerebral cavernous malformations. PMID: 23388056
    27. CCM3 forms a stable complex with MST4 in vivo to promote cell proliferation and migration synergistically in a manner dependent on MST4 kinase activity. PMID: 23541896
    28. crystal of the CCM3-MST4 C-terminal domain complex belonged to space group P4(1)2(1)2 or P4(3)2(1)2, with unit-cell parameters a = 69.10, b = 69.10, c = 117.57 A PMID: 22750858
    29. role of CCM3 and ezrin/radixin/moesin family of proteins in cell's response to oxidative stress PMID: 22291017
    30. A novel large CCM3 deletion is identified with typical magnetic resonance imaging in a patient and her daughter. PMID: 20623299
    31. the crystal structures of CCM3 in complex with three different leucine-aspartate repeat (LD) motifs (LD1, LD2, and LD4) from the scaffolding protein paxillin PMID: 21632544
    32. adenoviral CCM3 expression inhibits endothelial cell migration, proliferation, and tube formation while downregulation of endogenous CCM3 results in increased formation of tube-like structures PMID: 20862502
    33. Among familial cases of Cerebral cavernous malformations 67% had a mutation in CCM1, 5.5% in CCM2, and 5.5% in CCM3 PMID: 21029238
    34. Genetic variations could interfere with the proper CCM1/CCM2/CCM3 protein complex, thus explaining the observed clinical variability in cerebral cavernous malformations in a large family. PMID: 20419355
    35. PDCD10/CCM3 acts as a critical regulator of neuronal survival during development PMID: 21041308
    36. Study propose that the Cerebral cavernous malformations protein complex functions in the PI3K signaling pathway through the interaction between PDCD10 and PtdIns(3,4,5)P3. PMID: 20668527
    37. The crystal structure of human PDCD10 complexed with inositol-(1,3,4,5)-tetrakisphosphate has been determined at 2.3A resolution. PMID: 20682288
    38. PDCD10 can form complexes with other members of the CCM family, including CCM2, a key mediator of receptor tyrosine kinase-dependent cell death in neuroblastic tumors. PMID: 20854465
    39. CCM3 is a cerebral cavernous malformation protein critical for vascular integrity PMID: 20489202
    40. CCM3 is located on the Golgi apparatus, forming a complex with proteins of the germinal center kinase III (GCKIII) family and GM130, a Golgi-resident protein. PMID: 20332113
    41. We report herein the identification of PDCD10 (programmed cell death 10) as the CCM3 gene. PMID: 15543491
    42. KRIT1, Malcavernin, and PDCD10 are differentially expressed in cerebral venous malformations and cerebral cavernous malformations PMID: 16239636
    43. Mutations in apoptosis-related gene, PDCD10, cause cerebral cavernous malformation 3. PMID: 16284570
    44. Sequence analysis of PDCD10 in a panel of 29 probands lacking Krit1 and MGC4607 mutations revealed only three mutations. PMID: 16329096
    45. The s screened the PCDC10 gene in 15 families that did not have a CCM1 or CCM2 mutation. Only two novel mutations were found, suggesting that mutations in this gene may only account for a small percentage of CCM familial cases. PMID: 16380626
    46. Five percent of patients with familial cerebral cavernomas have retinal cavernomas. These lesions are clinically asymptomatic. They can be associated with any of the 3 cerebral cavernous malformation genes. PMID: 16769843
    47. intergenic region of the head-to-head PDCD10-SERPINI1 gene pair provides an interesting and informative example of a complex regulatory system PMID: 17212813
    48. Results show that PDCD10 modulation of ERK signaling is mediated by MST4, and that PDCD10 may be a regulatory adaptor necessary for MST4 function, suggesting a link between cerebral cavernous malformation and the ERK-MAPK cascade via PDCD10/MST4. PMID: 17360971
    49. CCM3 (PDCD10) coprecipitates and colocalizes with CCM2. CCM3 directly binds to serine/threonine kinase 25 (STK25, YSK1, SOK1) and the phosphatase domain of Fas-associated phosphatase-1 (FAP-1, PTPN13, PTP-Bas, PTP-BL). PMID: 17657516
    50. To the best of our knowledge, this is the first report of an association between a mutation in the PDCD10 gene and spinal cavernous malformations. PMID: 18035376

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  • 相关疾病：
    Cerebral cavernous malformations 3 (CCM3)
  • 亚细胞定位：
    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.
  • 蛋白家族：
    PDCD10 family
  • 组织特异性：
    Ubiquitous.
  • 数据库链接：

    HGNC: 8761

    OMIM: 603285

    KEGG: hsa:11235

    STRING: 9606.ENSP00000376506

    UniGene: Hs.478150