| + |
ERK1/2 | up-regulates 
phosphorylation
|
ADAM17 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-89614 |
Thr735 |
KPFPAPQtPGRLQPA |
Homo sapiens |
|
| pmid |
sentence |
| 12058067 |
We report that the cytosolic tail of the tumor necrosis factor alpha-converting enzyme (tace) is phosphorylated by erk at threonine 735.These results demonstrate that secretases are able to discriminate between the different stimuli that trigger membrane protein ectodomain cleavage and indicate that phosphorylation by mapks may regulate the proteolytic function of membrane secretases. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAPK3 | up-regulates
phosphorylation
|
ADAM17 |
0.359 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-89625 |
Thr735 |
KPFPAPQtPGRLQPA |
Homo sapiens |
|
| pmid |
sentence |
| 12058067 |
Extracellular signal-regulated kinase phosphorylates tumor necrosis factor alpha-converting enzyme at threonine 735: a potential role in regulated sheddingwe show that extracellular signal-regulated kinase (erk) acts as an intermediate in protein kinase c-regulated trka cleavage. We report that the cytosolic tail of the tumor necrosis factor alpha-converting enzyme (tace) is phosphorylated by erk at threonine 735. In addition, we show that erk and tace associate. This association is favored by erk activation and by the presence of threonine 735. In contrast to the erk route, the p38 mapk was able to stimulate trka cleavage in cells devoid of tace activity, indicating that other proteases are also involved in trka shedding. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAPK14 | up-regulates activity
phosphorylation
|
ADAM17 |
0.402 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163970 |
Thr735 |
KPFPAPQtPGRLQPA |
Cricetulus griseus |
CHO Cell |
| pmid |
sentence |
| 20188673 |
We show that p38 MAP kinase, which is activated in response to inflammatory or stress signals, directly activates TACE, a membrane-associated metalloprotease that is also known as ADAM17 and effects shedding in response to growth factors and Erk MAP kinase activation. p38alpha MAP kinase interacts with the cytoplasmic domain of TACE and phosphorylates it on Thr(735), which is required for TACE-mediated ectodomain shedding |
|
| Publications: |
1 |
Organism: |
Cricetulus Griseus |
| Pathways: | NOTCH Signaling and Myogenesis, P38 Signaling and Myogenesis |
| + |
ADAM17 | down-regulates activity 
cleavage
|
GP1BA |
0.284 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261861 |
Val466 |
ATSPTILvSATSLIT |
Homo sapiens |
Blood Platelet |
| pmid |
sentence |
| 25297919 |
GPIbα is shed by metalloproteases such as ADAM17, a process that releases a soluble GPIbα fragment termed glycocalicin. ADAM17 cleaves within the GPIbα-based peptide (LRGV465LK) through a mechanism that is only partially understood [42]. GPIbα shedding has been shown to be constitutive but it can be increased by activation of protein kinases C (PKC) or inhibition of calmodulin [42, 43]. Shedding leads to decreased receptor density |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
hsa-mir-708-3p | down-regulates quantity by repression
post transcriptional regulation
|
ADAM17 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-279889 |
|
|
Homo sapiens |
MRC-5 Cell |
| pmid |
sentence |
| 29869625 |
MiR-708-3p directly regulates its target gene, a disintegrin and metalloproteinase 17 (ADAM17), through a binding site in the 3' untranslated region. MiR-708-3p blocked the expression of ADAM17 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
hsa-mir-224-5p | down-regulates quantity by repression
post transcriptional regulation
|
ADAM17 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-279890 |
|
|
Homo sapiens |
SCC-9 Cell |
| pmid |
sentence |
| 31207072 |
Luciferase and Western blot assays revealed that ADAM17 protein was a downstream target of miR-224. MiR-224 inhibits the growth and invasion of OSCC cells by regulating the expression of ADAM17. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ADAM17 | up-regulates quantity
cleavage
|
TNF |
0.702 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-46754 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 9034190 |
We have now purified and cloned a metalloproteinase that specifically cleaves precursor TNF-alpha. [...]This enzyme (called the tnf-alpha-converting enzyme, or tace) is a new member of the family of mammalian adamalysins (or adams), for which no physiological catalytic function has previously been identified. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | P38 Signaling and Myogenesis |
| + |
ADAM17 | up-regulates activity
cleavage
|
NOTCH |
0.738 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254334 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 10882063 |
... here we show that an additional processing event occurs in the extracellular part of the receptor, preceding cleavage by the gamma-secretase-like activity. Purification of the activity accounting for this cleavage in vitro shows that it is due to tace (tnfalpha-converting enzyme), a member of the adam (a disintegrin and metalloprotease domain) family of metalloproteases. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GPR50 | up-regulates activity
binding
|
ADAM17 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-278099 |
|
|
Homo sapiens |
Hep-G2 Cell |
| pmid |
sentence |
| 32405532 |
GPR50 and ADAM17 can directly interact with each other (as both are cell membrane proteins), which was confirmed via coimmunoprecipitation (coIP; Figure 6C), indicating that ligand-independent Notch signaling activation is mediated through the GPR50-ADAM17 interaction |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ADAM17 | up-regulates activity
cleavage
|
EREG |
0.561 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259843 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26284334 |
ADAM17 is involved in the release and activation of several growth factors and cytokine receptor ligands. Among the growth factors activated by ADAM17 are TGF-alpha, amphiregulin, epiregulin and HB-EGF |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ADAM17 | up-regulates activity
cleavage
|
NOTCH1 |
0.737 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-78903 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10882063 |
... here we show that an additional processing event occurs in the extracellular part of the receptor, preceding cleavage by the gamma-secretase-like activity. Purification of the activity accounting for this cleavage in vitro shows that it is due to tace (tnfalpha-converting enzyme), a member of the adam (a disintegrin and metalloprotease domain) family of metalloproteases. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | NOTCH Signaling, NOTCH Signaling and Myogenesis |
| + |
ADAM17 | up-regulates activity
cleavage
|
APP |
0.539 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262829 |
|
|
in vitro |
|
| pmid |
sentence |
| 9774383 |
By the use of gene disruption (knockout), we now demonstrate that TACE (tumor necrosis factor alpha converting enzyme), a member of the ADAM family (a disintegrin and metalloprotease-family) of proteases, plays a central role in regulated alpha-cleavage of APP. Our data suggest that TACE may be the alpha-secretase responsible for the majority of regulated alpha-cleavage in cultured cells. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
ADAM17 | up-regulates
cleavage
|
NOTCH |
0.738 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255371 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 23729744 |
Receptor–ligand engagement triggers a second NECD cleavage (S2 cleavage) by a metalloproteinase ADAM (known as Kuzbanian in Drosophila melanogaster) |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255370 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 18344021 |
Two ADAMs have been implicated in the S2 cleavage of Notch. In Drosophila, ADAM10 ortholog Kuzbanian is the main protease mediating Notch processing [35–38]. In mouse cells in vitro, ADAM17, and not ADAM10, appears to be a protease responsible for Notch cleavage |
|
| Publications: |
2 |
Organism: |
Mus Musculus |
| + |
ADAM17 | up-regulates activity
cleavage
|
TGFA |
0.49 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259841 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26284334 |
ADAM17 is involved in the release and activation of several growth factors and cytokine receptor ligands. Among the growth factors activated by ADAM17 are TGF-alpha, amphiregulin, epiregulin and HB-EGF |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
hsa-mir-145-5p | down-regulates quantity by repression
post transcriptional regulation
|
ADAM17 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-279885 |
|
|
Homo sapiens |
U-251SP Cell |
| pmid |
sentence |
| 23076445 |
Ectopic expression of miR-145 in U87 and U251n glioma cells caused decreased proliferation, migration and invasion with accompanying low protein expression of ADAM17. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ADAM17 | up-regulates 
|
EGFR |
0.455 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-166568 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20626350 |
Such phosphorylation is required for tace mediated ectodomain shedding of tgfalfa family ligands, which results in the activation of egfr and cell proliferation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ADAM17 | up-regulates activity
cleavage
|
HBEGF |
0.587 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259844 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26284334 |
ADAM17 is involved in the release and activation of several growth factors and cytokine receptor ligands. Among the growth factors activated by ADAM17 are TGF-alpha, amphiregulin, epiregulin and HB-EGF |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ADAM17 | down-regulates
cleavage
|
MUC1 |
0.307 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-95630 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12441351 |
These characteristics along with studies conducted with cell lines genetically deficient in various adams (for a disintegrin and metalloprotease) identified tumor necrosis factor-alpha converting enzyme (tace)/adam 17 as a muc1 sheddase. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SRC | up-regulates activity
phosphorylation
|
ADAM17 |
0.458 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-279115 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25371038 |
These data suggests that Src mediates TACE activation in mechanically stressed cardiomyocytes and this mechanism could be exploited for specific blockade of TNFalpha secretion and its detrimental effects in congestive heart failure.|We found that the non receptor tyrosine kinase Src mediates TACE activation in mechanically stretched rat cardiomyocytes by phosphorylating the Tyr 702 residue within the intracellular tail of TACE. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ADAM17 | up-regulates activity
cleavage
|
AREG |
0.444 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259842 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26284334 |
ADAM17 is involved in the release and activation of several growth factors and cytokine receptor ligands. Among the growth factors activated by ADAM17 are TGF-alpha, amphiregulin, epiregulin and HB-EGF |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
hsa-miR-148a-3p | down-regulates quantity by repression
post transcriptional regulation
|
ADAM17 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-279886 |
|
|
Homo sapiens |
HCT-116 Cell |
| pmid |
sentence |
| 33356812 |
Transfection of HCT116 with miR-148a inhibited ADAM17 expression and luciferase activity. MiR-148a directly suppresses ADAM17 in colonocytes and is downregulated in colon cancer. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
hsa-miR-338-3p | down-regulates quantity by repression
post transcriptional regulation
|
ADAM17 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-279888 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 26617808 |
MiR-338-3p is significantly reduced in gastric cancer and inhibits cell proliferation, migration and invasion through downregulation of ADAM17, therefore, miR-338-3p may represent a potential therapeutic target for gastric cancer intervention. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
hsa-mir-152-3p | down-regulates quantity by repression
post transcriptional regulation
|
ADAM17 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-279887 |
|
|
Homo sapiens |
HCT-116 Cell |
| pmid |
sentence |
| 33356812 |
Transfection of HCT116 with miR-152-3p inhibited ADAM17 expression and luciferase activity.MiR-152 directly suppresses ADAM17 in colonocytes and is downregulated in colon cancer. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
4.0
ADAM17
- 
- 