ADAM9 Antibody

Code CSB-PA618774ESR1HU
Size US$166
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  • Western blot
    All lanes: Disintegrin and metalloproteinase domain-containing protein 9 antibody at 2μg/ml
    Lane 1: Mouse liver tissue
    Lane 2: Mouse heart tissue
    Secondary
    Goat polyclonal to rabbit IgG at 1/10000 dilution
    Predicted band size: 91, 73 kDa
    Observed band size: 91 kDa

  • Immunohistochemistry of paraffin-embedded human liver cancer using CSB-PA618774ESR1HU at dilution of 1:100

  • Immunohistochemistry of paraffin-embedded human placenta tissue using CSB-PA618774ESR1HU at dilution of 1:100

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Product Details

Full Product Name
Rabbit anti-Homo sapiens (Human) ADAM9 Polyclonal antibody
Uniprot No.
Target Names
Alternative Names
ADAM 9 antibody; ADAM metallopeptidase domain 9 antibody; Adam9 antibody; ADAM9_HUMAN antibody; Cellular disintegrin-related protein antibody; Cone rod dystrophy 9 antibody; CORD9 antibody; Disintegrin and metalloproteinase domain-containing protein 9 antibody; MCMP antibody; MDC9 antibody; Meltrin-gamma antibody; Metalloprotease/disintegrin/cysteine-rich protein 9 antibody; Mltng antibody; Myeloma cell metalloproteinase antibody
Raised in
Rabbit
Species Reactivity
Human, Mouse
Immunogen
Recombinant Human Disintegrin and metalloproteinase domain-containing protein 9 protein (475-685AA)
Immunogen Species
Homo sapiens (Human)
Conjugate
Non-conjugated
Clonality
Polyclonal
Isotype
IgG
Purification Method
Antigen Affinity Purified
Concentration
It differs from different batches. Please contact us to confirm it.
Buffer
PBS with 0.02% sodium azide, 50% glycerol, pH7.3.
Form
Liquid
Tested Applications
ELISA, WB, IHC
Recommended Dilution
Application Recommended Dilution
WB 1:500-1:2000
IHC 1:20-1:200
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
Cleaves and releases a number of molecules with important roles in tumorigenesis and angiogenesis, such as TEK, KDR, EPHB4, CD40, VCAM1 and CDH5. May mediate cell-cell, cell-matrix interactions and regulate the motility of cells via interactions with integrins.; May act as alpha-secretase for amyloid precursor protein (APP).
Gene References into Functions
  1. miR-129-5p suppressed cell proliferation and invasion ability through regulating ADAM9. PMID: 29879625
  2. Studies indicate that a disintegrin and a metalloprotease 9 (ADAM9) is involved in solid cancers with the different mechanisms which it employ to drive tumor progression [Review]. PMID: 29550974
  3. Collective results suggested that galangin may act as an effective chemotherapeutic agent for glioma cancer depending on its ability to bring about ADAM9 and Erk1/2 activation. PMID: 29115634
  4. miR-543 serves as a tumor suppressor in glioblastoma multiforme through ADAM9 regulation. PMID: 28849046
  5. Study demonstrates that diabetes-mediated decrease in miR-126 leads to a corresponding increase in its target, ADAM9, which in turn cleaves MERTK (inactivates downstream engulfment signaling), thus resulting in defective macrophage efferocytosis of apoptotic cardiomyocytes. PMID: 27827458
  6. These results revealed that ADAM9 down-regulates miR-1 via activating EGFR signaling pathways, which in turn enhances CDCP1 expression to promote lung cancer progression. PMID: 28537886
  7. These findings suggested that miR302a inhibited osteosarcoma cell growth and metastasis by targeting ADAM9. PMID: 28713950
  8. Data show that ADAM9 is over-expressed in an activated form in human ovarian clear cell carcinomas, and suggest that it plays a key role in cisplatin resistance. PMID: 29247567
  9. Mechanistic investigations found that quercetin suppressed Snail-dependent Akt activation by upregulating maspin and Snail-independent a disintegrin and metalloproteinase (ADAM) 9 expression pathways to modulate the invasive ability of NSCLC cells PMID: 28648644
  10. ADAM9 is a component of cell-cell junctions. ADAM9 must be expressed by both adjacent cells for cell junction localisation. ADAM9 can self-associate via its ectodomain. The soluble ADAM9 ectodomain inhibits monocyte-endothelial transmigration. PMID: 28928095
  11. hese results emphasize the critical influence of ADAM9 on lung cancer progression and aggressiveness. ADAM9 should at least be a marker of cancer aggressiveness and a potential therapeutic target for cancer treatment. PMID: 28675123
  12. MiR-126-ADAM9 pathway-based therapeutic targeting may represent a novel approach for the inhibition of hepatitis B virus-related hepatocellular carcinoma metastases. PMID: 28639884
  13. miR-520f inhibited tumor cell invasion by directly targeting ADAM9 and the TGFbeta receptor TGFBR2. PMID: 28209612
  14. The results suggest that ADAM9 mRNA expression is associated with tumor grade and histological type in gliomas and can serve as an independent prognostic factor, specifically in LGG patients. PMID: 27571068
  15. ADAM9 could possibly be regarded as a biomarker for GC diagnosis and prevention. Moreover, as directly targeted by miR-126 in GC, ADAM9 may be a potential target for GC therapeutic treatment which warrants intensive study PMID: 28260063
  16. ADAM9 is a direct target of miR-20b and that miR-20b decreased the 5-FU resistance of HCT116-R cells. PMID: 27878272
  17. the present study demonstrated the expression and clinical roles of miR-140 in glioma and suggested that miR-140 inhibited proliferation, migration and invasion of glioma cells, partially at least via suppressing ADAM9 expression. Therefore, miR-140 may be a novel candidate target for the development of therapeutic strategies for patients with glioma PMID: 27498787
  18. Increased ADAM9 mRNA expression is associated with esophageal adenocarcinoma. PMID: 27026568
  19. data reveal miR-590 as a tumor suppressor in NSCLC, which is at least partially mediated through targeting of ADAM9. Restoration of miR-590 may provide a promising therapeutic strategy for NSCLC. PMID: 27770372
  20. results suggested that miR-203 played tumor suppressive roles by downregulating ADAM9 and HULC and indicated its potential application in cancer treatment PMID: 26179263
  21. ADAM9 enhances CDCP1 protein expression by suppressing miR-218 for lung tumor metastasis PMID: 26553452
  22. ADAM9 and ROS1 are direct downstream targets of miR-33a PMID: 26507842
  23. Activation of ERalpha but not ERbeta increases ADAM9 expression in cultured human neuronal cells. PMID: 26592768
  24. miR-126 may act as a tumor suppressor via inhibition of cell invasion by downregulating ADAM9 in breast cancer development. PMID: 26261534
  25. This study has identified tenascin-C as a promoter of the invasiveness of brain tumor-initiating cells through a mechanism involving ADAM-9 proteolysis via the c-Jun NH2-terminal kinase pathway. PMID: 25646025
  26. Whole exome sequencing was performed, which identified a novel, homozygous mutation in ADAM9, c.967delT; p.Ser323Glnfs*33. PMID: 25546566
  27. ADAM9 silencing inhibits the tumor growth of non-small lung cancer in vitro and in vivo. PMID: 25778452
  28. ADAM9 plays an important role in gastric cancer proliferation and invasion, and that while expressed at high levels in some cancer cells that are responsive to functional inhibition and antitumor activity of a catalytic site-directed antibody. PMID: 25344581
  29. Given the significant correlation between tumor ADAM9 expression and serum RCAS1 concentration in both cervical and endometrial cancer as well as the role for ADAM9 in RCAS1 shedding. PMID: 25177692
  30. our data indicated that miR-126 inhibits cell growth, invasion, and migration of OS cells by downregulating ADAM-9. PMID: 25213697
  31. We identified a novel autosomal recessive ADAM9 mutation causing autosomal recessive cone-rod dystrophy (arCRD), anterior polar and posterior subcapsular cataract in a consanguineous Egyptian family. PMID: 25091951
  32. Results show how ADAM9 regulates lung cancer metastasis to the brain by facilitating the tPA-mediated cleavage of CDCP1. PMID: 25060522
  33. ADAM9 is expressed in an inducible fashion on PMN surfaces where it degrades some ECM proteins, and it promotes alveolar-capillary barrier injury during ALI PMID: 25063875
  34. ADAM9 up-regulates N-cadherin via miR-218 suppression in lung adenocarcinoma cells. PMID: 24705471
  35. this study describes the role of miR-126 in bladder cancer progression, identifying miR-126 and ADAM9 as potential clinical biomarkers of disease aggressiveness PMID: 24823697
  36. ADAM9 high expression is correlated positively and significantly with HDGF high expression in non-small cell lung cancer. PMID: 24770635
  37. The expression of circulating ADAM9 is down-regulated in pulmonary sarcoidosis. PMID: 23857158
  38. ADAM9 is an important molecule in the processes of invasion and metastasis. PMID: 23499592
  39. The over-expression of MGAM was confirmed with a 6.6 fold increase in expression at the mRNA level whereas the fold change in ADAM9 demonstrated a 1.6 fold increase. PMID: 23405089
  40. ADAM9 expression was low in castration resistant prostate cancer (CRPC), correlated with poor prognosis and might be involved in the succession from hormonal sensitive prostate cancer (HSPC) to CRPC by various functions. PMID: 23106877
  41. miR-126&126* restored expressions play a tumor suppressor role by directly regulating ADAM9 and MMP7 in melanoma. PMID: 23437250
  42. a novel molecular mechanism of ADAM9 in the regulation of prostate cancer cell proliferation. PMID: 23342005
  43. ADAM9 plays a crucial role in UV-induced EGFR activation and is overexpressed in skin cancer cell lines PMID: 19003995
  44. Transient transfection of ADAM9 and ACE cDNAs into HEK293 cells demonstrated that ADAM9 requires both membrane anchorage and its catalytic domain to shed ACE. PMID: 22480688
  45. The miR-126/ADAM9 axis plays essential role in the inhibition of invasive growth of pancreatic cancer cells. PMID: 22064652
  46. ADAM10 activity is regulated by inhibition of ADAM9, and this regulation may be used to control shedding of amyloid precursor protein by enhancing alpha-secretase activity, a key regulatory step in the etiology of Alzheimer disease PMID: 21956108
  47. ADAM-9 expression plays an important role in mediating cell-cell contacts between fibroblasts and melanoma cells and that these interactions contribute to proteolytic activities required during invasion of melanoma cells. PMID: 21135106
  48. The data of this suggested that promoter polymorphisms which regulate ADAM9 transcription are protective against SAD. PMID: 19237226
  49. ADAM9 plays a crucial role in prostate cancer progression and therapeutic resistance in part by altering E-cadherin and integrin expression. PMID: 20672324
  50. Secreted variants of ADAM9 are a key determinant in manifestation of aggressive migratory phenotypes associated with breast cancer progression. PMID: 20736367

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Involvement in disease
Cone-rod dystrophy 9 (CORD9)
Subcellular Location
[Isoform 1]: Cell membrane; Single-pass type I membrane protein.; [Isoform 2]: Secreted.
Tissue Specificity
Widely expressed. Expressed in chondrocytes. Isoform 2 is highly expressed in liver and heart.
Database Links

HGNC: 216

OMIM: 602713

KEGG: hsa:8754

STRING: 9606.ENSP00000419446

UniGene: Hs.591852

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