PDCD10 Antibody

Code CSB-PA469157
Size US$166
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Image
  • The image on the left is immunohistochemistry of paraffin-embedded Human tonsil tissue using CSB-PA469157(PDCD10 Antibody) at dilution 1/20, on the right is treated with fusion protein. (Original magnification: ×200)
  • The image on the left is immunohistochemistry of paraffin-embedded Human renal cancer tissue using CSB-PA469157(PDCD10 Antibody) at dilution 1/20, on the right is treated with fusion protein. (Original magnification: ×200)
  • Gel: 12%SDS-PAGE, Lysate: 50 μg, Lane 1-3: Hela cells, Jurkat cells, 231 cells, Primary antibody: CSB-PA469157(PDCD10 Antibody) at dilution 1/200, Secondary antibody: Goat anti rabbit IgG at 1/8000 dilution, Exposure time: 10 seconds
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Product Details

Uniprot No.
Target Names
PDCD10
Alternative Names
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
Raised in
Rabbit
Species Reactivity
Human,Mouse,Rat
Immunogen
Fusion protein of Human PDCD10
Immunogen Species
Homo sapiens (Human)
Conjugate
Non-conjugated
Isotype
IgG
Purification Method
Antigen affinity purification
Concentration
It differs from different batches. Please contact us to confirm it.
Buffer
-20°C, pH7.4 PBS, 0.05% NaN3, 40% Glycerol
Form
Liquid
Tested Applications
ELISA,WB,IHC
Recommended Dilution
Application Recommended Dilution
ELISA 1:1000-1:5000
WB 1:200-1:1000
IHC 1:25-1:100
Troubleshooting and FAQs
Storage
Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
Lead Time
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.

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Target Background

Function
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.
Gene References into Functions
  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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Involvement in disease
Cerebral cavernous malformations 3 (CCM3)
Subcellular Location
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.
Protein Families
PDCD10 family
Tissue Specificity
Ubiquitous.
Database Links

HGNC: 8761

OMIM: 603285

KEGG: hsa:11235

STRING: 9606.ENSP00000376506

UniGene: Hs.478150

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