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1 Citations 17 Q&As
Facts about Disintegrin and metalloproteinase domain-containing protein 17.
Responsible for the proteolytic release of several other cell-surface proteins, such as p75 TNF-receptor, interleukin 1 receptor type II, p55 TNF-receptor, transforming growth factor-alpha, L-selectin, growth hormone receptor, MUC1 and the amyloid precursor protein. Acts as an activator of Notch pathway by mediating cleavage of Notch, generating the membrane-associated intermediate fragment called Notch extracellular truncation (NEXT).
Human | |
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Gene Name: | ADAM17 |
Uniprot: | P78536 |
Entrez: | 6868 |
Belongs to: |
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No superfamily |
ADAM 17; ADAM metallopeptidase domain 17; ADAM metallopeptidase domain 18; ADAM17; ADAM18; CD156b antigen; CD156b; CSVP; disintegrin and metalloproteinase domain-containing protein 17; EC 3.4.24.86; MGC71942; Snake venom-like protease; TACE; TACEcSVP; TNF-alpha convertase; TNF-alpha converting enzyme; TNF-alpha-converting enzyme; tumor necrosis factor, alpha, converting enzyme
Mass (kDA):
93.021 kDA
Human | |
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Location: | 2p25.1 |
Sequence: | 2; NC_000002.12 (9488486..9555830, complement) |
Ubiquitously expressed. Expressed at highest levels in adult heart, placenta, skeletal muscle, pancreas, spleen, thymus, prostate, testes, ovary and small intestine, and in fetal brain, lung, liver and kidney.
Membrane; Single-pass type I membrane protein.
This article will provide an explanation of what Adam17 is and how it can be targeted by siRNA. Adam17 is a sheddase that is involved in regulating the stability of the gene FoxM1. This protein plays a crucial role in tumorigenicity in glioma cell lines. It is also a target of siRNA. It has been implicated in different types of tumors, including gliomas.
TACE is also called ADAM17. It is a processor of many receptors that include the TNFa receptor and p75 neurotrophin (NTR). It also processes ligands belonging to the EGFR family. While ADAM17 is vital for normal brain function, its roles during trauma to the CNS are not clear. ADAM17 is also vital for brain cell survival and development.
Scientists examined the effects of ADAM17 on Ace2 expression and production on cell surfaces to determine if ADAM17 is responsible for SARS virus infection. They found that blocking ADAM17's enzymatic function prevented the virus from reproducing, and decreased sACE2 levels dampened the virus's ability to infect. ADAM17 could play a role as a mediator in COVID-19 pathogenesis.
TAAD is an important health risk in patients with mutations in TGFb signaling pathway. ADAM17 hypoactivity was neutralized by genetic reduction of TGFb1 or pharmacological inhibition of TbRI signaling. Furthermore, ADAM17 may be regulated by TGFbRI. This suggests that ADAM17 may affect the heat shock response in patients suffering from SARS-CoV-2.
The ADAM17 marker triggers the EGFR/AKT/GSK3b signaling pathway, which increases the stability of FoxM1 in Glioma cells. The ability to regulate FoxM1 stability could increase the longevity of therapy against GBM. However, the exact mechanism that activates FoxM1 in glioma cells is unsolved.
We know little about the mechanism of FOXM1 regulation, however the ADAM17 gene is involved in a myriad of processes such as self-renewal and cell proliferation and tumorigenesis. It is also linked to multiple human cancers, suggesting that dysregulation could be a contributing factor in the development of tumors and the progression. As a result, our understanding of the role of FOXM1 in cancer remains a little naive however a thorough understanding of its regulation will offer novel insights on disease mechanisms and therapeutic strategies.
The role of FOXM1 in human glioma cell development is undefined This study provides new information on its regulation in a murine model. FOXM1 is a regulator gene in hematopoietic stem cells . It is involved in the transition from B-cells into T-cells. It is vital in cell proliferation and plays a significant role in the infiltration of immune cells by tumors.
SUMO-like proteins (SUMO) are small proteins that covalently attach and alter the function of proteins. There are four SUMO forms in mammals. Each regulates distinct aspects of FOXM1 stability and activity. FOXM1 activity is also affected by SUMO-mediated degradation. These findings offer more insight into how the ADAM17 marker regulates FoxM1 stability via activating GSK3b.
Serglycin is a key molecule that regulates the cellular behaviour of glioma LN-18 cells and regulates their proliferative and invasive potential. Serglycin also associates with glioma-stem cells. Consequently, it regulates the expression of important tumor-promoting markers, including Snail. In this article, we review the effects of serglycin on glioma cell lines and review some of the mechanisms that regulate the gene expression of serglycin.
The expression of RTVP-1 has been linked with poor clinical outcomes in patients with gliomas. The gene's promoter connects to STAT3 (C/EBPb). In addition, IL-6 stimulates RTVP-1 within the glioma cells. This promotes mesenchymal and migration. These findings suggest that this transcription factor could play a significant role in the progression and development of glioma.
PSAP is expressed in glioma tumors and stem cells. qPCR and ELISA confirmed PSAP overexpression. MTS tests also revealed that PSAP overexpression increased the proliferation rate of GSC-21 glioma cell. Neurosphere formation rate was significantly higher in cells overexpressing PSAP compared to the control group. Additionally, PSAP synthesis was increased.
It is a key regulator of the development of the glioma. It is regulated by STAT3 and C/EBPb. The overexpression of RTVP-1 in glioma cells results in a mesenchymal-like morphology. Eliminating RTVP-1 results in a decrease of cell migration and a reduction in tumorigenic power.
Boster Bio's ADAM17 Marker is a nucleotide-rich Oligo Duplex that is specifically designed to destroy ADAM17. When synthesis is taking place, every base is monitored with trityl analysis. After synthesis, RNA duplexes can be purified through affinity-solid phase extraction. Mass spectrometry is performed on the annealed duplex to verify its composition. Each lot is then compared with the previous lot to ensure the best consistency.
We have shown that this vector inhibits the ADAM17-induced production of sTNF in U937 cells by using this lentiviral vector. Transfection efficiency was also greater than 90%, which indicates that shRNA lentivirus has entered the host cell successfully. In addition, ADAM17-shRNA lentivirus inhibits ADAM17's biological activity.
MAPK14 activates ADAM17 in BMECs. ADAM17 is a key factor in the growth and migration of HCC cells. To confirm further that ADAM17 is an important target for siRNA, the researchers transfected BMECs using si-ADAM17 or overexpression plasmids. Secreted CX3CL1 from BMECs was identified using an ELISA.
The ADAM17 gene is the cause of numerous diseases including cancer. Therefore, it is crucial to employ an ADAM17 marker gene to determine the disease. Boster Bio offers this product to researchers to assess the levels of ADAM17 in patients. A Western Blot was created using blood samples. You can also perform the test with different types of cells.
RS773 cells expressed ADAM10 in CM as an extracellular protein. After prodomain removal and the protein is now one molecule with a 68kDa. The ExoV is positive for the specific exosomal marker CD81 and the ADAM10 substrate MICA/B. Both cells were utilized in TEM analysis. These results show that ADAM10 is present in both MSC cells and HL cells.
PMID: 9034191 by Moss M.L., et al. Cloning of a disintegrin metalloproteinase that processes precursor tumour-necrosis factor-alpha.
PMID: 9034190 by Black R.A., et al. A metalloproteinase disintegrin that releases tumour-necrosis factor- alpha from cells.
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