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  4. Recombinant Human Programmed cell death protein 10 (PDCD10)

Recombinant Human Programmed cell death protein 10 (PDCD10)

  • 中文名稱：
    人PDCD10重組蛋白
  • 貨號(hào)：
    CSB-YP861141HU
  • 規(guī)格：
  • 來(lái)源：
    Yeast
  • 其他：
  • 中文名稱：
    人PDCD10重組蛋白
  • 貨號(hào)：
    CSB-EP861141HU-B
  • 規(guī)格：
  • 來(lái)源：
    E.coli
  • 共軛：
    Avi-tag Biotinylated

    E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.

  • 其他：
  • 中文名稱：
    人PDCD10重組蛋白
  • 貨號(hào)：
    CSB-BP861141HU
  • 規(guī)格：
  • 來(lái)源：
    Baculovirus
  • 其他：
  • 中文名稱：
    人PDCD10重組蛋白
  • 貨號(hào)：
    CSB-MP861141HU
  • 規(guī)格：
  • 來(lái)源：
    Mammalian cell
  • 其他：

產(chǎn)品詳情

  • 純度：
    >85% (SDS-PAGE)
  • 基因名：
    PDCD10
  • Uniprot No.：
  • 別名：
    Apoptosis related protein 15; CCM3; Cerebral cavernous malformations 3 protein; MGC1212; MGC24477; PDC10_HUMAN; PDCD 10; PDCD10; Programmed cell death 10; Programmed cell death protein 10; TF 1 cell apoptosis related protein 15; TF-1 cell apoptosis-related protein 15; TFAR15
  • 種屬：
    Homo sapiens (Human)
  • 蛋白長(zhǎng)度：
    full length protein
  • 表達(dá)區(qū)域：
    1-212
  • 氨基酸序列
    MRMTMEEMKN EAETTSMVSM PLYAVMYPVF NELERVNLSA AQTLRAAFIK AEKENPGLTQ DIIMKILEKK SVEVNFTESL LRMAADDVEE YMIERPEPEF QDLNEKARAL KQILSKIPDE INDRVRFLQT IKDIASAIKE LLDTVNNVFK KYQYQNRRAL EHQKKEFVKY SKSFSDTLKT YFKDGKAINV FVSANRLIHQ TNLILQTFKT VA
  • 蛋白標(biāo)簽：
    Tag?type?will?be?determined?during?the?manufacturing?process.
    The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
  • 產(chǎn)品提供形式：
    Lyophilized powder
    Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
  • 復(fù)溶：
    We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
  • 儲(chǔ)存條件：
    Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
  • 保質(zhì)期：
    The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
    Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
  • 貨期：
    Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
    Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
  • 注意事項(xiàng)：
    Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
  • Datasheet ：
    Please contact us to get it.

產(chǎn)品評(píng)價(jià)

靶點(diǎn)詳情

  • 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.
  • 基因功能參考文獻(xiàn)：
    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 authors 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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  • 相關(guān)疾?。?/div>
    Cerebral cavernous malformations 3 (CCM3)
  • 亞細(xì)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
  • 組織特異性：
    Ubiquitous.
  • 數(shù)據(jù)庫(kù)鏈接：

    HGNC: 8761

    OMIM: 603285

    KEGG: hsa:11235

    STRING: 9606.ENSP00000376506

    UniGene: Hs.478150