Human A Disintegrin And Metalloprotease 9,ADAM9 ELISA Kit

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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HGNC: 216

UNIGENE: Hs.591852

KEGG: hsa:8754

STRING: 9606.ENSP00000419446

OMIM: 602713