3.4.24.86: ADAM 17 endopeptidase
This is an abbreviated version!
For detailed information about ADAM 17 endopeptidase, go to the full flat file.
Word Map on EC 3.4.24.86
-
3.4.24.86
-
adam10
-
ectodomains
-
sheddase
-
metalloproteinases
-
endothelial
-
phorbol
-
sirna
-
amyloid
-
egf
-
alzheimer
-
notch
-
angiotensin
-
membrane-anchored
-
arthritis
-
amphiregulin
-
ace2
-
hb-egf
-
hydroxamate
-
timp-3
-
heparin-binding
-
l-selectin
-
trans-signaling
-
angiotensin-converting
-
covid-19
-
alpha-secretase
-
mmp-2
-
sars-cov-2
-
egf-like
-
juxtamembrane
-
medicine
-
prodomains
-
furin
-
secretase
-
tgf-alpha
-
membrane-proximal
-
tmprss2
-
sil-6r
-
non-amyloidogenic
-
cxcl16
-
rhomboid
-
epiregulin
-
gamma-secretase
-
neuregulins
-
molecular biology
-
adamalysins
-
metzincins
-
membrane-tethered
-
fractalkine
-
betacellulin
-
marimastat
-
analysis
-
egfr-dependent
- 3.4.24.86
- adam10
- ectodomains
- sheddase
- metalloproteinases
- endothelial
-
phorbol
- sirna
-
amyloid
- egf
- alzheimer
- notch
- angiotensin
-
membrane-anchored
- arthritis
- amphiregulin
- ace2
- hb-egf
- hydroxamate
- timp-3
-
heparin-binding
- l-selectin
-
trans-signaling
-
angiotensin-converting
- covid-19
- alpha-secretase
- mmp-2
- sars-cov-2
-
egf-like
-
juxtamembrane
- medicine
- prodomains
- furin
-
secretase
- tgf-alpha
-
membrane-proximal
- tmprss2
-
sil-6r
-
non-amyloidogenic
- cxcl16
- rhomboid
- epiregulin
- gamma-secretase
- neuregulins
- molecular biology
- adamalysins
-
metzincins
-
membrane-tethered
- fractalkine
- betacellulin
- marimastat
- analysis
-
egfr-dependent
Reaction
Narrow endopeptidase specificity. Cleaves Pro-Leu-Ala-Gln-Ala-/-Val-Arg-Ser-Ser-Ser in the membrane-bound, 26-kDa form of tumor necrosis factor alpha (TNFalpha). Similarly cleaves other membrane-anchored, cell-surface proteins to "shed" the extracellular domains =
Synonyms
(TACE/ADAM17/CD156q), (TACE:ADAM17), a disintegrin and metallo protease domain 17, a disintegrin and metalloprotease 17, a disintegrin and metalloprotease-17, a disintegrin and metalloproteinase 17, a disintegrin and metalloproteinase-17, ADAM-17, ADAM17, ADAM17 proteinase, ADAM17/tumor necrosis factor-alpha (TNF-A)converting enzyme, ADAMTS-2, CD156, H-TACE, human TACE B, metalloprotease TACE, metalloprotease-disintegrin tumour necrosis factor alpha convertase, metalloproteinase ADAM17, pro tumor necrosis factor cleavage enzyme, pro-tumor necrosis factor-alpha-processing enzyme, proteinase, pro-tumor necrosis factor (9CI), sheddase, TACE, TACE proteinase, TACE/ADAM17, TNF converting enzyme, TNF-alpha convertase, TNF-alpha converting enzyme, TNF-alpha processing protease, TNFalpha converting enzyme, tumor necrosis factor alpha convertase, tumor necrosis factor alpha converting enzyme, tumor necrosis factor alpha-converting enzyme, tumor necrosis factor-alpha converting enzyme, tumor necrosis factor-alpha-converting enzyme, tumour necrosis factor alpha-converting enzyme, tumour necrosis factor-alpha converting enzyme
ECTree
3.4.24.86 ADAM 17 endopeptidaseAdvanced search results
results (
results (Substrates Products
Substrates Products on EC 3.4.24.86 - ADAM 17 endopeptidase
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SUBSTRATE 
PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
Reversibility
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
(7-methoxycoumarin-4-yl)-acetyl-KSPLAQA-VRSSSRK(2,4-dinitrophenyl)-NH2 + H2O
?
-
-
-
-
?
(7-methoxycoumarin-4-yl)-acetyl-Pro-Leu-Ala-Gln-Ala-Val-[N-3-[2,4-dinitrophenyl]-L-2,3-diaminopropionyl]-Arg-Ser-Ser-Ser-Arg-NH2 + H2O
?
-
-
-
-
?
(7-methoxycoumarin-4-yl)-acetyl-SPLAQAVRSSSRK-(2,4-dinitrophenyl)-NH2 + H2O
?
-
-
-
-
?
(7-methoxycoumarin-4-yl)acetyl-Ser-Pro-Leu-Ala-Gln-Ala-Val-Arg-Ser-Ser-Ser-Arg-Lys(Dnp)-NH2 + H2O
?
-
-
-
-
?
4',5'-dimethoxyfluoresceinyl-SPLAQAVRSSSR-cys(4-(3-succinimid-1-yl)fluorescein)-NH2 + H2O
?
-
-
-
-
?
7-methoxycoumarin-4-(yl)acetyl-Pro-Leu-Ala-Gln-Ala-Val-Arg-Ser-Ser-Ser-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl-Arg-NH2 + H2O
?
-
an internally quenched peptide substrate is used
-
-
?
7-methoxycoumarin-4-yl-acetyl-Lys-Pro-Leu-Gly-Pro-Leu-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl-Ala-Arg + H2O
?
-
-
-
-
?
amyloid precursor protein + H2O
soluble amyloid precursor protein alpha fragment + C83
-
-
-
?
CD16 + H2O
?
substrates CD16a and CD16b are IgG Fc receptors expressed by human natural killer cells and neutrophils, respectively. Substrates contain three separate cleavage sites in close proximity at P1/P1' positions Ala195/Val196, Val196/Ser197, and Thr198/Ile199, revealing a membrane proximal cleavage region in CD16. Mutation S197P effectively blocks CD16a and CD16b cleavage in cell-based assays. Mutant CD16a/S197P is resistant to cleavage when expressed in cells. The S197P mutation does not disrupt IgG binding by the receptor or its activation of NK92 cells by antibody-treated tumor cells
-
-
?
CD16b + H2O
?
human IgG Fc receptor CD16, i.e. FcgammaRIII. CD16b plasma levels are significantly decreased in patients administered a selective inhibitor targeting the metalloproteases ADAM10 and ADAM17. Inhibition of ADAM17 significantly blocks the cleavage of CD16b following neutrophil activation and apoptosis
-
-
?
cell surface VEGF receptor Flt + H2O
?
-
release of an N-terminal extracellular fragment which can antagonize the effects of vascular endothelial growth factor, substrate can be cleaved to release an N-terminal extracellular fragment. Overexpression of ADAM10, EC 3.4.24.81, and ADAM17 increase cleavage while knockdown of ADAM10 and ADAM17 reduce N-terminal cleavage
-
?
CSF-1 receptor + H2O
?
TACE cleaves the receptor between residues Gln503 and Ser504. Replacement of fourteen residues at the end of the CSF-1 extracellular domain blocks TACE cleavage
-
-
?
erbB4/HER4 + H2O
?
-
epidermal growth factor, essential function in heart and neural development, TACE is essential for regulated shedding of the HER4 JM-a receptor
-
-
?
Glu(EDANS)-Pro-Leu-Ala-Gln-Ala-Val-Arg-Ser-Ser(4O-(beta-D-Gal-(1->3)-alpha-D-GalNAc))-Ser-Lys(DABCYL) + H2O
Glu(EDANS)-Pro-Leu-Ala-Gln-Ala + Val-Arg-Ser-Ser(4O-(beta-D-Gal-(1->3)-alpha-D-GalNAc))-Ser-Lys(DABCYL)
-
-
-
?
Glu(EDANS)-Pro-Leu-Ala-Gln-Ala-Val-Arg-Ser-Ser-Ser-Lys(DABCYL) + H2O
Glu(EDANS)-Pro-Leu-Ala-Gln-Ala + Val-Arg-Ser-Ser-Ser-Lys(DABCYL)
-
-
-
?
growth hormone binding protein + H2O
?
-
shedding, TACE is critical for PMA-induced GH receptor proteolysis and GHBP generation
-
-
?
growth hormone receptor + H2O
?
-
growth hormone receptor/TACE interaction precedes proteolysis and is transient
-
-
?
intercellular adhesion molecule 1 + H2O
soluble intercellular adhesion molecule 1 + ?
-
-
-
?
interleukin (IL)-6R + H2O
?
exclusively the extracellular domains of ADAM17 are needed for interaction with substrate, whereas the transmembrane- and cytoplasmic-region are dispensable for this process. In the extracellular part solely the membrane-proximal domain of ADAM17 is mandatory for recognition
-
-
?
LAQAVRSSSR + H2O
?
-
fluorimetric assay for TACE, fluorogenic substrate, a 10-amino-acid peptide capped with an o-aminobenzoyl group on the N-terminal end and with a 3-(2,4-dinitrophenyl)-L-2,3-diaminopropionic amide group on the C-terminal end, enzymatic conversion of the substrate results in a fluorescence enhancement of 11fold
-
-
?
lipoprotein-related protein I + H2O
?
-
lipoprotein-related protein I shedding is significantly decreased in embryonic fibroblast cells lacking ADAM10 and/or ADAM17
-
-
?
Mca-PLAQAV-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl amide-RSSSR-NH2 + H2O
?
-
-
-
-
?
MHC class I polypeptide-related sequence A + H2O
soluble MHC class I polypeptide-related sequence A + ?
-
-
-
?
MHC class I-related chain + H2O
?
-
i.e. transmembrane protein expressed in pathological conditions, ligands for the activating receptor NKG2D found on cytotoxic lymphocytes. The recruitment of both enzyme and substrate to detergent-resistant membrane microdomains is crucial for efficient proteolysis
-
-
?
NH2-LAQAVRSSSR-OH + H2O
?
-
uncapped counterpart of the fluorogenic substrate
-
-
?
Notch 1 + H2O
?
-
ADAM17 is required for Notch1 receptor proteolysis in NSCLC cells in vitro and in vivo
-
-
?
o-aminobenzoyl-LAQAFRSSSR-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl amide + H2O
o-aminobenzoyl-LAQA + FRSSSR-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl amide
-
enzymatic cleavage 22%
-
-
?
o-aminobenzoyl-LAQAIRSSSR-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl amide + H2O
o-aminobenzoyl-LAQA + IRSSSR-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl amide
-
enzymatic cleavage 66%
-
-
?
o-aminobenzoyl-LAQALRSSSR-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl amide + H2O
o-aminobenzoyl-LAQA + LRSSSR-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl amide
-
enzymatic cleavage 92%
-
-
?
o-aminobenzoyl-LAQAVRSSSR-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl amide + H2O
o-aminobenzoyl-LAQA + VRSSSR-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl amide
-
enzymatic cleavage 90%
-
-
?
o-aminobenzoyl-LAQFVRSSSR-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl amide + H2O
o-aminobenzoyl-LAQF + RSSSR-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl amide
-
enzymatic cleavage 39%
-
-
?
o-aminobenzoyl-LAQGVRSSSR-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl amide + H2O
o-aminobenzoyl-LAQG + VRSSSR-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl amide
-
enzymatic cleavage 11%
-
-
?
o-aminobenzoyl-LAQLVRSSSR-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl amide + H2O
o-aminobenzoyl-LAQL + VRSSSR-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl amide
-
enzymatic cleavage 34%
-
-
?
o-aminobenzoyl-LAQVARSSSR-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl amide + H2O
o-aminobenzoyl-LAQVA + RSSSR-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl amide
-
enzymatic cleavage 19%
-
-
?
PLAAAVFSS + H2O
PLAAA + VFSS
mutant peptide derived from TNF-alpha, very poor substrate
-
-
?
PLAMAVMSS + H2O
PLAMA + VMSS
mutant peptide derived from TNF-alpha, very poor substrate
-
-
?
pro amphiregulin + H2O
?
-
TACE is capable of cleaving both N- and C-terminal sites in the pro-amphiregulin ectodomain
-
-
?
pro heparin-binding epidermal growth factor + H2O
?
-
purified soluble TACE cleaves a single site in the juxtamembrane stalk of pro heparin-binding epidermal growth factor
-
-
?
Pro-BTC + H2O
?
the cleavage site by ADAM17 is CVVA31-/-DGNS, N-linked glycosylation site is Asn34
-
-
?
pro-EPR + H2O
?
the cleavage site by ADAM17 is DNPR59-/-VAQV, N-linked glycosylation site is Asn47
-
-
?
pro-HB-EGF + H2O
?
the cleavage site by ADAM17 is RKVR62-/-DLQE, O-linked glycosylation sites are Thr75 and Thr85
-
-
?
pro-TGFalpha + H2O
?
the cleavage site by ADAM17 is VAAA39-/-VVSH, N-linked glycosylation site is Asn25
-
-
?
pro-tumor necrosis factor alpha + H2O
?
with and without a glycan moiety attached, glycosylation increases the enzyme activity. The cleavage site of TNFalpha by ADAM17 is only four residues away from a glycosylated residues, whereas glycosylation occurs 14 residues away from the TGFalpha cleavage site. Cleavage site for ADAM-17 is LAQA76-/-VRSS, O-linked glycosylation site is Ser80
-
-
?
proheparin-binding EGF-like growth factor + H2O
?
-
cleavage occurs between residues RKVR62-DLQE. Substrate shows O-linked glycosylation 13 residues apart from scissile bond
-
?
proTNF-alpha + H2O
soluble TNF-alpha + 9000 Da membrane-bound fragment of TNF-alpha
-
-
-
-
?
protransforming growth factor alpha + H2O
?
-
cleavage occurs between residues AAA39-VVSH. Substrate shows N-linked glycosylation 14 residues apart from scissile bond
-
?
RA175/SynCAM1 + H2O
?
-
neuronal RA175/SynCAM1 isoforms, members of the immunoglobulin family 4, are processed by TACE
-
-
?
S80-glycosylated (EDANS)-ELAQAVRSSSRK-(DABCYL) + H2O
?
TNF-alpha derived substrate
-
-
?
S80-glycosylated (EDANS)-EPLAQAVRSSSK-(DABCYL) + H2O
?
TNF-alpha derived substrate
-
-
?
sorCS1c + H2O
?
-
member of the vacuolar protein sorting 10p domain family of neuronal type-I receptors
-
-
?
sorCS2 + H2O
?
-
member of the vacuolar protein sorting 10p domain family of neuronal type-I receptors, minor shedding
-
-
?
sorLA + H2O
?
-
member of the vacuolar protein sorting 10p domain family of neuronal type-I receptors
-
-
?
sortilin + H2O
?
-
member of the vacuolar protein sorting 10p domain family of neuronal type-I receptors, minor shedding
-
-
?
TGF-alpha + H2O
?
ADAM17, but not related ADAM10, is required for amphiregulin, TGF-alpha, and TNFR1 shedding
-
-
?
transferrin receptor protein 1 + H2O
?
-
cleavage occurs between residues ECER100-LAGT. Substrate shows O-linked glycosylation 4 residues apart from scissile bond
-
?
TRP1 + H2O
?
the cleavage site by ADAM17 is ECER100-/-LAGT, O-linked glycosylation sites are: Thr104, Asn251, Asn317, Asn727
-
-
?
tumor necrosis factor receptor 1 + H2O
?
ADAM17, but not related ADAM10, is required for amphiregulin, TGF-alpha, and TNFR1 shedding
-
-
?
Alzheimer's disease amyloid precursor protein + H2O
?
-
TACE is involved in shedding of Alzheimer's disease amyloid precursor protein
-
-
?
amphiregulin + H2O
?
ADAM17, but not related ADAM10, is required for amphiregulin, TGF-alpha, and TNFR1 shedding
-
-
?
angiotensin-converting enzyme-2 + H2O
?
-
ADAM-17 is responsible for the ACE2 shedding
-
-
?
beta-amyloid precursor protein + H2O
?
-
Alzheimer amyloid precursor protein
-
-
?
CD30 + H2O
?
-
shedding of CD30 upon inhibition of the proteasome is catalyzed by ADAM17
-
-
?
glycoprotein Ibalpha + H2O
?
-
ADAM17 is the key enzyme mediating shedding of glycoprotein Ibalpha
-
-
?
glycoprotein Ibalpha + H2O
?
-
ADAM17 is the key enzyme mediating shedding of glycoprotein Ibalpha
-
-
?
heparin-binding EGF-like growth factor + H2O
?
-
ADAM17 may be involved in heparin-binding EGF-like growth factor cleavage in response to injury
-
-
?
intercellular adhesion molecule-1 + H2O
?
-
ADAM-17 mediates shedding of intercellular adhesion molecule-1. The shedding of intercellular adhesion molecule-1 reduces the adhesive capacity of the cells. the cleavage site in the intercellular adhesion molecule-1 is not sequence-specific, but appears to be nonselective
-
-
?
interleukin (IL)-1R-II + H2O
?
exclusively the extracellular domains of ADAM17 are needed for interaction with substrate, whereas the transmembrane- and cytoplasmic-region are dispensable for this process. In the extracellular part solely the membrane-proximal domain of ADAM17 is mandatory for recognition
-
-
?
interleukin-6 receptor + H2O
?
the cleavage site by ADAM17 is LPVQ357-/-DSSV, N-linked glycosylation sites are: Asn55, Asn93, Asn221, Asn350
-
-
?
L-selectin + H2O
?
-
regulates plasma membrane composition and releases soluble signaling molecules and receptors from cells
-
-
?
L-selectin + H2O
?
-
during early events of death receptor-mediated neutrophil apoptosis, L-selectin downregulation occurs primarily by ADAM17-mediated shedding. During later stages of induced leukocyte apoptosis, soluble L-selectin production occurs independent of ADAM17
-
-
?
L-selectin + H2O
?
-
TACE is involved in cantharidin-induced shedding of L-selectin. Cantharidin induces sustained surface expression and cytoplasmic tail phosphorylation of TACE via p38 MAPK, while L-selectin is involved in promoting protein kinase C-dependent shedding
-
-
?
L-selectin + H2O
?
-
ADAM17 is the main sheddase of the adhesion protein L-selectin
-
-
?
p75 neurotrophin receptor + H2O
?
-
critical role of TACE in ectodomain shedding of the p75 neurotrophin receptor
-
-
?
p75 neurotrophin receptor + H2O
?
-
critical role of TACE in ectodomain shedding of the p75 neurotrophin receptor
-
-
?
p75 tumour necrosis factor receptor + H2O
?
-
-
-
-
?
preadipocyte factor 1 + H2O
?
-
TACE is the major protease responsible for conversion of membrane-bound Pref-1 to the biologically active diffusible form
-
-
?
proTGF-alpha + H2O
soluble TGF-alpha
the membrane-proximal domain in the extracellular part of ADAM17 is mandatory for recognition of the type-I transmembrane proteins, but not for the interaction with the type-II transmembrane molecule TNF-alpha
-
-
?
proTNF-alpha + H2O
soluble TNF-alpha
-
-
-
-
?
proTNF-alpha + H2O
soluble TNF-alpha
-
-
638993, 638994, 638995, 638996, 638997, 638998, 638999, 639000, 639001, 639002, 639003, 639004, 639005, 639006, 639007, 639008, 639009, 639010, 639011, 639012, 639013, 677450, 679641, 681665, 682211, 682570, 682629, 719165
-
-
?
proTNF-alpha + H2O
soluble TNF-alpha
-
-
release of proTNFalpha from cellular membranes
?
proTNF-alpha + H2O
soluble TNF-alpha
-
-
release of membrane-bound TNF-alpha
?
proTNF-alpha + H2O
soluble TNF-alpha
-
cleavage occurs between residues LAQA76-VRSS. Substrate shows O-linked glycosylation 4 residues apart from scissile bond
-
?
proTNF-alpha + H2O
soluble TNF-alpha
-
membrane-bound tumor necrosis factor alpha undergoes proteolysis
-
-
?
proTNF-alpha + H2O
soluble TNF-alpha
-
-
638979, 638980, 638981, 638983, 638984, 638987, 638988, 638991, 638992, 638994, 638995, 639000, 639001, 639002, 639003, 639004, 639006, 639010, 639011, 639012, 639013, 679671, 681016
-
-
?
receptor tyrosine kinase c-Kit + H2O
?
-
ADAM-17 controls mast cell survival by regulating shedding and surface expression of c-Kit
-
-
?
sorCS3 + H2O
?
-
member of the vacuolar protein sorting 10p domain family of neuronal type-I receptors
-
-
?
syndecan-1 + H2O
?
both ADAM10 and ADAM17 contribute to SDC1 shedding
-
-
?
TNF-alpha + H2O
?
-
ranitidine enhances TNF-alpha production after lipopolysaccharide treatment through augmented p38 activation, and this seems to occur through TACE
-
-
?
TNF-alpha + H2O
soluble TNF-alpha
-
membrane-bound tumor necrosis factor alpha undergoes proteolysis
-
-
?
transforming growth factor alpha + H2O
?
-
-
-
-
?
transforming growth factor alpha + H2O
?
-
-
638993, 638994, 638995, 638996, 638997, 638998, 638999, 639000, 639001, 639002, 639003, 639004, 639005, 639006, 639007, 639008, 639009, 639010, 639011, 639012, 639013
-
-
?
transforming growth factor alpha + H2O
?
-
-
638979, 638980, 638981, 638983, 638984, 638987, 638988, 638991, 638992, 638994, 638995, 639000, 639001, 639002, 639003, 639004, 639006, 639010, 639011, 639012, 639013
-
-
?
additional information
?
-
-
TACE is a multidomain, type I transmembrane protein, contains a pro-domain which is removed by proteolysis to generate the active enzyme and a zinc-dependent metalloprotease catalytic domain, TACE cleaves peptides containing the sequence of the processing site at the physiolocically relevant peptide bond
-
-
?
additional information
?
-
TACE is a multidomain, type I transmembrane protein, contains a pro-domain which is removed by proteolysis to generate the active enzyme and a zinc-dependent metalloprotease catalytic domain, TACE cleaves peptides containing the sequence of the processing site at the physiolocically relevant peptide bond
-
-
?
additional information
?
-
-
o-aminobenzoyl-LAQVARSSSR-N-3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl diaminopropionic amide is no substrate
-
-
?
additional information
?
-
-
4-dinitrophenyl)-L-2,3-diaminopropionyl diaminopropionic amide-PChaGC(Me)HK(NMA)-NH2 is not cleaved at all by TACE
-
-
?
additional information
?
-
-
TACE is the only enzyme confirmed to process TNF-alpha in vitro and in vivo
-
-
?
additional information
?
-
-
ectodomain shedding of the hypoxia-induced carbonic anhydrase IX is a metalloprotease-dependent process regulated by TACE/ADAM17
-
-
?
additional information
?
-
-
TACE is not involved in shedding of angiotensin converting enzyme
-
-
?
additional information
?
-
-
TACE may have a role in phorbol myristate acetate-induced shedding of epiregulin
-
-
?
additional information
?
-
-
a comparison of the binding sites of matrix metalloproteinases and tumor necrosis factor-alpha converting enzyme
-
-
?
additional information
?
-
-
protein in the absence of salt or inhibitor shows a rapid and specific autocleavage between residues Y352-V353 which resides within the surrounding sequence TLGLAYVGSPRN
-
-
?
additional information
?
-
affinity for TACE is measured by an internally quenched peptide substrate with its sequence derived from the pro-TNF-alpha cleavage site using a catalytic domain of recombinant human TACE enzyme
-
-
?
additional information
?
-
analysis of ADAM cognate substrates reveals that glycosylation is often present in the vicinity of the scissile bond
-
-
?
additional information
?
-
high throughput screening assays are developed using glycosylated and non-glycosylated substrate, and positional scanning, substrate specificity, overview
-
-
?
additional information
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mutations at the P2 site and the P2' site of the substrate peptide largely affect the peptide cleavage efficiency in the enzymaticassay. The P2/P2'sites may affect the efficiency of the conformation search for the correct peptide orientation, which in turn affects the substrate cleavage efficiency. Peptide PRYEA?YKMG is not a substrate
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noncatalytic domains of ADAM17 do not directly bind to TNF-alpha derived substrates used but affect the binding nevertheless, most likely because of steric hindrance. Noncatalytic domains of ADAM17 affect the size/shape of the carbohydrate-binding pocket contained within the catalytic domain of ADAM17. Protease shows significantly decreased activity when the TNF-alpha-derived sequence is induced into alpha-helical conformation
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additional information
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angiotensin converting enzyme is not cleaved by TACE
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additional information
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in mice, the interleukin-6 receptor is not a target of ADAM17
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TACE-mediated ectodomain shedding of erbB ligands, epitomized by TGFalpha is a key component of the neuron-to-glia signaling mechanism used by excitatory amino acids to facilitate the advent of female puberty
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additional information
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compounds are assessed in two cellular assays, the human peripheral blood mononuclear cell assay (PBMC) and the human whole blood assay (WBA), for their ability to suppress the formation of TNF-alpha brought about by lipopolysaccharide (LPS) stimulation. Success in the PBMC assay relies on the ability of the inhibitor to penetrate into the cells, thus enabling it to inhibit TACE and thereby to suppress the release of intracellular, soluble TNF-alpha. In the WBA, compounds must also have the ability to penetrate cells
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