3.4.24.11: neprilysin
This is an abbreviated version!
For detailed information about neprilysin, go to the full flat file.
Word Map on EC 3.4.24.11
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3.4.24.11
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angiotensin
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natriuretic
-
alzheimer
-
angiotensin-converting
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phosphoramidon
-
atrial
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amyloid
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thiorphan
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cardiovascular
-
hypertension
-
bradykinin
-
neuropeptides
-
aminopeptidase
-
ejection
-
airway
-
anp
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ventricular
-
blocker
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captopril
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endothelins
-
opioids
-
metallopeptidase
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tachykinins
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renin-angiotensin
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hf
-
valsartan
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enalapril
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renin-angiotensin-aldosterone
-
neurokinin
-
vasoactive
-
endothelin-converting
-
hfref
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naloxone
-
insulin-degrading
-
bestatin
-
kinin
-
diuretic
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3.4.15.1
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lily
-
aceis
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met-enkephalin
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bronchoconstriction
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angioedema
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amastatin
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angiotensin-1-7
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kininase
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lisinopril
-
nt-probnp
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medicine
-
bronchoconstrictors
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pharmacology
-
analysis
-
molecular biology
-
angiotensin-receptor
- 3.4.24.11
- angiotensin
-
natriuretic
- alzheimer
-
angiotensin-converting
- phosphoramidon
- atrial
-
amyloid
- thiorphan
- cardiovascular
- hypertension
- bradykinin
- neuropeptides
- aminopeptidase
-
ejection
- airway
- anp
- ventricular
-
blocker
- captopril
- endothelins
-
opioids
- metallopeptidase
- tachykinins
-
renin-angiotensin
- hf
- valsartan
- enalapril
-
renin-angiotensin-aldosterone
- neurokinin
-
vasoactive
-
endothelin-converting
-
hfref
- naloxone
-
insulin-degrading
- bestatin
- kinin
-
diuretic
-
3.4.15.1
-
lily
-
aceis
- met-enkephalin
-
bronchoconstriction
- angioedema
- amastatin
-
angiotensin-1-7
-
kininase
- lisinopril
-
nt-probnp
- medicine
-
bronchoconstrictors
- pharmacology
- analysis
- molecular biology
-
angiotensin-receptor
Reaction
preferential cleavage of polypeptides between hydrophobic residues, particularly with Phe or Tyr at P1' =
Synonyms
Abeta-degrading enzyme, acute lymphoblastic leukemia antigen, antigen, CALLA (common acute lymphoblastic leukemia-associated), atriopeptidase, CALLA, CALLA (common acute lymphoblastic leukemia-associated) antigens, CALLA antigen, CALLA glycoproteins, CD10, CD10/neutral endopeptidase, CD10/neutral endopeptidase 24.11, common acute lymphoblastic leukemia antigen, common acute lymphoblastic leukemia-associated antigens, Common acute lymphocytic leukemia antigen, endopeptidase CD10, Endopeptidase-2, endopeptidase-24.11, enkephalinase, EP24.11, glycoprotein, CALLA, kidney-brush-border neutral endopeptidase, kidney-brush-border neutral peptidase, kidney-brush-border neutral proteinase, membrane metallo-endopeptidase, membrane metalloendopeptidase, MME, NEP, NEP 24.11, NEP, enkephalinase, neutrophil cluster-differentiation antigen 10, common acute lymphoblastic leukemia antigen, NEP-1, NEP/CD10, NEP2, NEP4A, NEP4B, neprilypsin, neprilysin, neprilysin 4, neutral endopeptidase, neutral endopeptidase 24.11, neutral endopeptidase 24.11/CD10, neutral metallendopeptidase, NL-1, peptidase, endo-, peptidase, membrane metalloendo-, SEP, skin fibroblast elastase
ECTree
3.4.24.11 neprilysinAdvanced search results
results (
results (Substrates Products
Substrates Products on EC 3.4.24.11 - neprilysin
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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-Arg-Pro-Pro-Gly-Phe-Ser-Ala-Phe-Lys(2,4-dinitrophenyl) + H2O
?
a bradykinin-based peptide substrate QFS
-
-
?
(7-methoxycoumarin-4-yl)acetyl-Arg-Pro-Pro-Gly-Phe-Ser-Ala-Phe-Lys-(2,4-dinitrophenyl) + H2O
(7-methoxycoumarin-4-yl)acetyl-Arg-Pro-Pro-Gly-Phe-Ser-Ala + Phe-Lys-(2,4-dinitrophenyl)
bradykinin-based quenched fluorescent substrate assay
-
-
?
2 KFRRQRPRLSHKGPMPF + 2 H2O
KFRRQRPR + LSHKGPMPF + KFRRQRPRL + SHKGPMPF
-
-
-
ir
2 LVQPRGSRNGPGPWQGGRRKFRRQRPRLSHKGPMPF + 2 H2O
LVQPRGSRNGPGPWQGGRRKFRRQRPRL + SHKGPMPF + LVQPRGSRNGPGPWQGGRRKFRRQRPR + LSHKGPMPF
-
-
-
ir
2 pGlu-RPRLSHKGPMPF + 2 H2O
pGlu-RPRL + pGlu-RPR + SHKGPMPF + LSHKGPMPF
-
-
-
ir
2-aminobenzoyl-ARFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-AR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-DRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-DR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-FRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-FR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-HRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-HR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-IRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-IR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-KRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-KR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-LRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-LR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-NRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-NR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-RAFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RA + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-RDFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RD + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-REFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RE + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-rGF-N-(2,4-dinitrophenyl)ethylenediamine + H2O
2-aminobenzoyl-D-Arg-Gly + Phe-N-(2,4-dinitrophenyl)ethylenediamine
-
-
-
-
ir
2-aminobenzoyl-RGFK(Dnp)-OH + H2O
2-aminobenzoyl-RG + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-RGFK-2,4-dinitrophenyl amide + H2O
2-aminobenzoyl-RG + FK-2,4-dinitrophenyl amide
-
-
-
-
ir
2-aminobenzoyl-RGFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RG + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-rGL-N-(2,4-dinitrophenyl)ethylenediamine + H2O
2-aminobenzoyl-D-Arg-Gly + Leu-N-(2,4dinitrophenyl)ethylenediamine
-
-
-
-
ir
2-aminobenzoyl-rGV-N-(2,4-dinitrophenyl)ethylenediamine + H2O
2-aminobenzoyl-D-Arg-Gly + Val-N-(2,4-dinitrophenyl)ethylenediamine
-
-
-
-
ir
2-aminobenzoyl-RHFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RH + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-RKFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RK + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-RNFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RN + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-RPFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RP + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-RQFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RQ + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-RRFK-2,4-dinitrophenyl amide + H2O
2-aminobenzoyl-RR + FK-2,4-dinitrophenyl amide
-
-
-
-
ir
2-aminobenzoyl-RRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-rRL-N-(2,4-dinitrophenyl)ethylenediamine + H2O
2-aminobenzoyl-D-Arg-L-Arg + Leu-N-(2,4-dinitrophenyl)ethylenediamine
-
-
-
-
ir
2-aminobenzoyl-RSFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RS + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-rSL-N-(2,4-dinitrophenyl)ethylenediamine + H2O
2-aminobenzoyl-D-Arg-L-Ser + Leu-N-(2,4-dinitrophenyl)ethylenediamine
-
-
-
-
ir
2-aminobenzoyl-RTFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RT + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-SRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-SR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-TRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-TR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-VRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-VR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-WRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-WR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-YRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-YR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
amyloid beta peptide Abeta42 + H2O
?
-
the peptide primarily undergoes degradation by NEP in vivo in the brain
-
-
?
amyloid beta peptide1-40 + H2O
amyloid beta peptide Asp1-Lys16 + amyloid beta peptide Asp1-Leu17 + amyloid beta peptide Asp1-Phe19
the wild-type enzyme cleaves Ab1-40 predominantly at Lys16-Leu17, Leu17-Val18 and Phe19-Phe20. The mutant G399V/G714K cleaves preferentially at Phe20-Ala21
main cleavage fragments after 60 min with the wild-type enzyme. After 360 min these fragments are degraded further, accompanied by the appearance of Val12-Leu17 and Tyr10-Leu17 fragments
-
?
amyloid beta(1-40) mutant A21G + H2O
?
-
Flemish variant of amyloid beta. Decreased degradation by neprilysin compared to either wild-type peptide or the other mutant peptides
-
-
?
amyloid-beta(1-7)AAC + H2O
?
a synthetic peptide, design and synthesis of a quenched fluorogenic peptide substrate qf-Abeta(1-7)AAC (with the sequence VHHQKAAC), which has a fluorophore, Alexa-350, linked to the side-chain of its C-terminal cysteine and a quencher, Dabcyl, linked to its N-terminus
-
-
?
amyloid-beta(12-16)AAC + H2O
?
a synthetic peptide, design and synthesis of a quenched fluorogenic peptide substrate qf-Abeta(12-16)AAC (with the sequence VHHQKAAC), which has a fluorophore, Alexa-350, linked to the side-chain of its C-terminal cysteine and a quencher, Dabcyl, linked to its N-terminus. This peptide emits strong fluorescence upon cleavage. qf-Abeta(12-16)AAC is more sensitive to NEP than the previously reported peptide substrates, so that concentrations of NEP as low as 0.03 nM can be detected at peptide concentration of 0.002 mM
-
-
?
benzoyl-Gly-Gly-Arg-Leu-2-naphthylamide + H2O
benzoyl-Gly-Gly-Arg + L-Leu-2-naphthylamide
-
-
-
-
?
glutaryl-Ala-Ala-Phe-2-naphthylamide + H2O
glutaryl-Ala-Ala + Phe-2-naphthylamide
-
-
-
?
glutaryl-Ala-Ala-Phe-4-methoxy-2-naphthylamide + H2O
glutaryl-Ala-Ala + Phe-4-methoxy-2-naphthylamide
glutaryl-Gly-Gly-Phe-2-naphthylamide + H2O
glutaryl-Gly-Gly + Phe-2-naphthylamide
-
-
-
?
glutaryl-Gly-Gly-Phe-2-naphthylamide + H2O
glutaryl-Gly-Gly-Phe + 2-naphthylamine
-
-
-
-
?
hippuryl-Arg-Arg-Ala-2-naphthylamide + H2O
hippuryl-Arg-Arg + Ala-2-naphthylamide
-
-
-
-
?
His-Lys-Thr-Asp-Ser-Phe-Val-Gly-Leu-Met-NH2 + H2O
His-Lys-Thr-Asp-Ser + Phe-Val-Gly + Leu-Met-NH2
leucine5-enkephalin + H2O
?
Tyr-Gly-Gly-Phe-Leu is cleaved at the Gly-Phe bond by the wild-type enzyme
-
-
?
N-(4-carboxy-1-oxobutyl)-L-alanyl-L-alanyl-N-(4-methoxy-2-naphthalenyl)-L-phenylalaninamide + H2O
N-(4-carboxy-1-oxobutyl)-L-alanyl-L-alanyl-L-phenylalanine + 4-methoxy-2-naphthylamine
-
-
-
?
N-benzyloxycarbonyl-Gly-Gly-Leu 2-naphthylamide + H2O
N-benzyloxycarbonyl-Gly-Gly + L-leucine 2-naphthylamide
-
-
-
?
N-benzyoxycarbonyl-Gly-Gly-Leu-2-naphthylamide + H2O
N-benzyoxycarbonyl-Gly-Gly + L-Leu-2-naphthylamide
-
-
-
-
?
N-formyl-L-Met-Leu-Phe + H2O
?
-
the enzyme may play an important role in modulating chemotactic response by cleavage of the chemotactic substance N-formyl-Met-Leu-Phe
-
-
?
Nalpha-benzoyl-Gly-Arg-Arg-Ala-2-naphthylamide + H2O
Nalpha-benzoyl-Gly-Arg-Arg + Ala-2-naphthylamide
-
-
-
?
Nalpha-benzoyl-Gly-Arg-Arg-Leu-2-naphthylamide + H2O
Nalpha-benzoyl-Gly-Arg-Arg + Leu-2-naphthylamide
-
-
-
?
Nalpha-benzoyl-Gly-Arg-Arg-Phe-2-naphthylamide + H2O
Nalpha-benzoyl-Gly-Arg-Arg + Phe-2-naphthylamide
-
-
-
?
Nalpha-benzoyl-Gly-Arg-Leu-2-naphthylamide + H2O
Nalpha-benzoyl-Gly-Arg + Leu-2-naphthylamide
-
-
-
?
Nalpha-benzoyl-Gly-Gly-Arg-Leu-2-naphthylamide + H2O
Nalpha-benzoyl-Gly-Gly-Arg + Leu-2-naphthylamide
-
-
-
?
Nalpha-benzoyl-Gly-Lys-Arg-Arg-Leu-2-naphthylamide + H2O
Nalpha-benzoyl-Gly-Lys-Arg-Arg + Leu-2-naphthylamide
-
-
-
?
Nalpha-benzoyl-Gly-Lys-Lys-Arg-Arg-Leu-2-naphthylamide + H2O
Nalpha-benzoyl-Gly-Lys-Lys-Arg-Arg + Leu-2-naphthylamide
-
-
-
?
neuropeptide Y + H2O
truncated neuropeptide Y + C-terminal fragments of neuropeptide Y
-
-
neuropeptide Y 21-36 and 31-36 are the most abundant fragments generated in vivo
-
?
pulmonary vasodilative vasoactive intestinal peptide + H2O
?
rapid inactivation
-
-
?
pyroglutamyl-Leu-Asn-Phe-Thr-Pro-Asn-Trp-Gly-Thr-NH2 + H2O
pyroglutamyl-Leu-Asn + Phe-Thr-Pro-ASn-Trp-Gly-Thr-NH2
succinyl-Ala-Ala-Phe-4-methylcoumarin 7-amide + H2O
succinyl-Ala-Ala + Phe-4-methylcoumarin 7-amide
succinyl-Ala-Ala-Phe-7-amido-4-methylcoumarin + H2O
succinyl-Ala-Ala-Phe + 7-amino-4-methylcoumarin
succinyl-Arg-Arg-Leu-2-naphthylamide + H2O
succinyl-Arg-Arg + Leu-2-naphthylamide
-
-
-
?
succinyl-Arg-Pro-Phe-His-Leu-Leu-Val-Tyr-7-amido-4-methylcoumarin + H2O
?
-
-
-
-
?
Z-Ala-Ala-Leu-4-nitroanilide + H2O
Z-Ala-Ala-Leu + 4-nitroaniline
-
-
-
?
amyloid beta peptide1-40 + H2O
?
multiple cleavage sites, product peaks corresponding to Abeta1-16, Abeta1-17, Abeta10-17, Abeta20-28, Abeta20-29, and Abeta20-30. The C-terminal products result from the cleavages at K28-G29, G29-A30, and A30-I31. These products are derived from the trans-membrane region of the amyloid precursor protein (APP) from which Abeta is formed and are rather hydrophobic
-
-
?
Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Met-NH2 + H2O
?
-
-
-
-
?
Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Met-NH2 + H2O
?
-
-
-
-
?
Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Met-NH2 + H2O
?
-
i.e. substance P, seven peptides are produced
-
-
?
Asp-Tyr(SO3H)-Met-Gly-Trp-Met-Asp-PheNH2 + H2O
?
-
i.e. cholecystokinin-8, two distinct cleavage sites: Asp-Tyr(SO3H)-Met-Gly-/-Trp-Met-Asp-/-PheNH2, the splitting of the Asp7-Phe8NH2 bond proceeds 4-times more rapidly than the Gly4-Trp5 bond
-
-
?
Atrial natriuretic factor + H2O
?
-
human alpha atrial natriuretic peptide/cardiodilatin shows a single major cleavage site within the disulfide-linked loop between Cys and Phe in position 7 and 8
-
-
?
Atrial natriuretic factor + H2O
?
-
seven sites of hydrolysis: Arg4-Ser5, Cys7-Phe8, Arg11-Met12, Arg14-Ile15, Gly16-Ala17, Gly-20-Leu21, Ser25-Phe26. The initial attack takes place at a bond within the disulfide-linked loop and produces a peptide having the same amino acid composition as intact atrial natriuretic factor
-
-
?
Atrial natriuretic factor + H2O
?
-
dominant enzyme in the hydrolysis of atrial natriuretic factor
-
-
?
atrial natriuretic peptide + H2O
?
-
no activity with brain natriuretic peptide
-
-
?
D-Ala2-Leu5-enkephalin + H2O
Tyr-D-Ala-Gly + Phe-Leu
-
i.e. Tyr-D-Ala-Gly-Phe-Leu
-
?
D-Ala2-Leu5-enkephalin + H2O
Tyr-D-Ala-Gly + Phe-Leu
-
i.e. Tyr-D-Ala-Gly-Phe-Leu
-
-
?
D-Ala2-Leu5-enkephalin + H2O
Tyr-D-Ala-Gly + Phe-Leu
-
i.e. Tyr-D-Ala-Gly-Phe-Leu
-
-
?
D-Ala2-Leu5-enkephalin + H2O
Tyr-D-Ala-Gly + Phe-Leu
-
i.e. Tyr-D-Ala-Gly-Phe-Leu
-
-
?
D-Ala2-Leu5-enkephalin + H2O
Tyr-D-Ala-Gly + Phe-Leu
-
i.e. Tyr-D-Ala-Gly-Phe-Leu
-
-
?
D-Ala2-Leu5-enkephalin + H2O
Tyr-D-Ala-Gly + Phe-Leu
-
i.e. Tyr-D-Ala-Gly-Phe-Leu
-
-
?
fibrinogen + H2O
fibrin + ?
inactivation, mechanism of NEP-mediated inactivation of fibrinogen through cleavage of the N-termini of the Aalpha- and Bbeta-chains of fibrinogen thereby significantly impairing initiation of fibrin formation by thrombin, overview
-
-
?
fibrinogen + H2O
fibrin + ?
fibrinogen from human and rat blood plasma, inactivation
-
-
?
gastrin G-17 + H2O
?
-
cleavage at four sites, Trp4-Leu5, Ala11-Tyr12, Gly13-Trp14 and Asp16-Phe17
-
-
?
gastrin G-17 + H2O
?
-
sulfated and unsulfated gastrin, cleavage is faster with the sulfated peptide
-
-
?
Glucagon + H2O
?
-
NEP24.11 is an important mediator of the degradation of both endogenous and exogenous glucagon in vivo
-
-
?
glutaryl-Ala-Ala-Phe-4-methoxy-2-naphthylamide + H2O
glutaryl-Ala-Ala + Phe-4-methoxy-2-naphthylamide
-
-
-
?
glutaryl-Ala-Ala-Phe-4-methoxy-2-naphthylamide + H2O
glutaryl-Ala-Ala + Phe-4-methoxy-2-naphthylamide
-
-
-
?
glutaryl-Ala-Ala-Phe-4-methoxy-2-naphthylamide + H2O
glutaryl-Ala-Ala + Phe-4-methoxy-2-naphthylamide
-
-
-
-
?
glutaryl-Ala-Ala-Phe-4-methoxy-2-naphthylamide + H2O
glutaryl-Ala-Ala + Phe-4-methoxy-2-naphthylamide
-
-
-
?
glutaryl-Ala-Ala-Phe-4-methoxy-2-naphthylamide + H2O
glutaryl-Ala-Ala + Phe-4-methoxy-2-naphthylamide
-
-
-
?
hippuryl-Arg-Arg-Leu-2-naphthylamide + H2O
hippuryl-Arg-Arg + Leu-2-naphthylamide
-
-
-
-
?
hippuryl-Arg-Arg-Leu-2-naphthylamide + H2O
hippuryl-Arg-Arg + Leu-2-naphthylamide
-
-
-
-
?
His-Lys-Thr-Asp-Ser-Phe-Val-Gly-Leu-Met-NH2 + H2O
His-Lys-Thr-Asp-Ser + Phe-Val-Gly + Leu-Met-NH2
-
-
-
-
?
His-Lys-Thr-Asp-Ser-Phe-Val-Gly-Leu-Met-NH2 + H2O
His-Lys-Thr-Asp-Ser + Phe-Val-Gly + Leu-Met-NH2
-
-
-
-
?
His-Lys-Thr-Asp-Ser-Phe-Val-Gly-Leu-Met-NH2 + H2O
His-Lys-Thr-Asp-Ser + Phe-Val-Gly + Leu-Met-NH2
-
-
-
-
?
His-Lys-Thr-Asp-Ser-Phe-Val-Gly-Leu-Met-NH2 + H2O
His-Lys-Thr-Asp-Ser + Phe-Val-Gly + Leu-Met-NH2
-
-
-
-
?
His-Lys-Thr-Asp-Ser-Phe-Val-Gly-Leu-Met-NH2 + H2O
His-Lys-Thr-Asp-Ser + Phe-Val-Gly + Leu-Met-NH2
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i.e. neurokinin A, hydrolysis at two sites: Ser5-Phe6 and Gly8-Leu9
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insulin B chain + H2O
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multiple cleavage sites, product analysis and cleavage sites preferences of wild-type and mutant neprilysins, cleavage sites, overview
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pyroglutamyl-Leu-Asn-Phe-Thr-Pro-Asn-Trp-Gly-Thr-NH2 + H2O
pyroglutamyl-Leu-Asn + Phe-Thr-Pro-ASn-Trp-Gly-Thr-NH2
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-
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?
pyroglutamyl-Leu-Asn-Phe-Thr-Pro-Asn-Trp-Gly-Thr-NH2 + H2O
pyroglutamyl-Leu-Asn + Phe-Thr-Pro-ASn-Trp-Gly-Thr-NH2
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-
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?
pyroglutamyl-Leu-Asn-Phe-Thr-Pro-Asn-Trp-Gly-Thr-NH2 + H2O
pyroglutamyl-Leu-Asn + Phe-Thr-Pro-ASn-Trp-Gly-Thr-NH2
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-
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?
succinyl-Ala-Ala-Phe-4-methylcoumarin 7-amide + H2O
succinyl-Ala-Ala + Phe-4-methylcoumarin 7-amide
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?
succinyl-Ala-Ala-Phe-4-methylcoumarin 7-amide + H2O
succinyl-Ala-Ala + Phe-4-methylcoumarin 7-amide
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succinyl-Ala-Ala-Phe-4-methylcoumarin 7-amide + H2O
succinyl-Ala-Ala + Phe-4-methylcoumarin 7-amide
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?
succinyl-Ala-Ala-Phe-4-methylcoumarin 7-amide + H2O
succinyl-Ala-Ala + Phe-4-methylcoumarin 7-amide
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?
succinyl-Ala-Ala-Phe-4-methylcoumarin 7-amide + H2O
succinyl-Ala-Ala + Phe-4-methylcoumarin 7-amide
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?
succinyl-Ala-Ala-Phe-7-amido-4-methylcoumarin + H2O
succinyl-Ala-Ala-Phe + 7-amino-4-methylcoumarin
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succinyl-Ala-Ala-Phe-7-amido-4-methylcoumarin + H2O
succinyl-Ala-Ala-Phe + 7-amino-4-methylcoumarin
Rattus norvegicus Wistar-Hannover
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?
Tyr-Gly-Gly-Phe-Met + H2O
Tyr-Gly-Gly + Phe-Met
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i.e. methionine enkephalin
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?
Tyr-Gly-Gly-Phe-Met + H2O
Tyr-Gly-Gly + Phe-Met
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i.e. methionine enkephalin
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?
Tyr-Gly-Gly-Phe-Met + H2O
Tyr-Gly-Gly + Phe-Met
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i.e. methionine enkephalin
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?
additional information
?
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NEP-1 plays an important role in the regulation of nematode locomation. NEP-1 is a central component that controls the neuronal innervation of pharyngeal pumping in Caenorhabditis elegans
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additional information
?
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the enzyme may play an important role as regulator of plasma-derived peptides in the nephron
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additional information
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elevation of the enzyme activity in serum from underground coal miners exposed to chronic inhalation of coal mine dust particles. The enzyme reflects the chronic pulmonary inflammatory state induced by coalmine dust exposure, and so may be a marker of lung injury
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additional information
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the enzyme is involved in the processing of other peptide hormones
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additional information
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the enzyme is responsible for the difference in metabolism of sulfated and unsulfated gastrin in human circulation
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?
additional information
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the enzyme is the major inactivator of enkephalin in brain
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additional information
?
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the enzyme may participate in the regulation of blood pressure and water and sodium excretion through inactivation of kinins
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?
additional information
?
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induction of neutral endopeptidase (NEP) activity of SK-N-SH cells by natural compounds from green tea. Caffeine leads to an increase in specific cellular neutral endopeptidase activity more than theophylline, theobromine or theanine. The combination of epigallocatechin and epigallocatechingallate with caffeine, theobromine or theophylline induces cellular neutral endopeptidase activity. The enhancement of cellular neutral endopeptidase activity by green tea extract and its natural products might be correlated with an elevated level of intracellular cyclic adenosine monophosphate
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?
additional information
?
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neutral endopeptidase 24.11/CD10 suppresses the progression of ovarian carcinomas
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?
additional information
?
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hydrolysis of polypeptides between hydrophobic residues
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?
additional information
?
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a quenched fluorogenic peptide substrate containing the first seven residues of the Abeta peptide plus a C-terminal Cysteine residue is synthesized to detect neprilysin activity. A fluorophore is attached to the C-terminal Cysteine and its fluorescence is quenched by a quencher linked to the N-terminus of the peptide
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?
additional information
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the enzyme degrades a wide range of peptide substrates, physiologically relevant peptides are such as enkephalins, tachykinins, and natriuretic peptides
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?
additional information
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the enzyme directly interacts with phosphatidylserine and cardiolipin but not with cholesterol
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?
additional information
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the enzyme has broader substrate specificity and is a peptidase capable of cleaving a variety of physiological peptides
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?
additional information
?
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human neprilysin-2 has a more restricted substrate specificity compared to human neprilysin with less activity against several vasoactive peptides
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?
additional information
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activity measurement optimization using the synthetic fluorogenic peptide substrates, evaluation and kinetics, overview
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additional information
?
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activity measurement optimization using the synthetic fluorogenic peptide substrates, evaluation and kinetics, overview
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additional information
?
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analysis of intact amyloid-beta peptides and their NEP cleavage products by mass spectrometry. 73% of amyloid-beta4-40, 31% of amyloid-beta4-42, 45% of amyloid-beta1-40, and 18% of amyloid-beta1-42 degradation resulting from NEP catalyzed hydrolysis. Amyloid-beta4-9/amyloid-beta1-9, amyloid-beta10-17, and amyloid-beta20-30 are the major enzymatic products
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additional information
?
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analysis of intact amyloid-beta peptides and their NEP cleavage products by mass spectrometry. 73% of amyloid-beta4-40, 31% of amyloid-beta4-42, 45% of amyloid-beta1-40, and 18% of amyloid-beta1-42 degradation resulting from NEP catalyzed hydrolysis. Amyloid-beta4-9/amyloid-beta1-9, amyloid-beta10-17, and amyloid-beta20-30 are the major enzymatic products
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?
additional information
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in vitro NEP proteolysis generates fragments that lack the ability to bind to the apelin receptor, NEP fully inactivates apelin
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additional information
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in vitro NEP proteolysis generates fragments that lack the ability to bind to the apelin receptor, NEP fully inactivates apelin
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?
additional information
?
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murine amyloid-beta has a far lower propensity to aggregate than human amyloid-beta. Amyloid-beta degradation products formed during NEP incubation are identified by mass spectrometry, analysis of predominant NEP cleavage sites detected by mass spectrometry for human and murine amyloid-beta1-42 and amyloid-beta.4-15. In addition to the amyloid-beta4-9 fragment, di- and tetra-peptides amyloid-beta18-19 and amyloid-beta39-42 are also observed
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additional information
?
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murine amyloid-beta has a far lower propensity to aggregate than human amyloid-beta. Amyloid-beta degradation products formed during NEP incubation are identified by mass spectrometry, analysis of predominant NEP cleavage sites detected by mass spectrometry for human and murine amyloid-beta1-42 and amyloid-beta.4-15. In addition to the amyloid-beta4-9 fragment, di- and tetra-peptides amyloid-beta18-19 and amyloid-beta39-42 are also observed
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additional information
?
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murine amyloid-beta has a far lower propensity to aggregate than human amyloid-beta. Amyloid-beta degradation products formed during NEP incubation are identified by mass spectrometry, analysis of predominant NEP cleavage sites detected by mass spectrometry for human and murine amyloid-beta1-42 and amyloid-beta.4-15. In addition to the amyloid-beta4-9 fragment, di- and tetra-peptides amyloid-beta18-19 and amyloid-beta39-42 are also observed
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?
additional information
?
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murine amyloid-beta has a far lower propensity to aggregate than human amyloid-beta. Amyloid-beta degradation products formed during NEP incubation are identified by mass spectrometry, analysis of predominant NEP cleavage sites detected by mass spectrometry for human and murine amyloid-beta1-42 and amyloid-beta.4-15. In addition to the amyloid-beta4-9 fragment, di- and tetra-peptides amyloid-beta18-19 and amyloid-beta39-42 are also observed
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?
additional information
?
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catabolism of atrial and brain natriuretic peptide is independent of neutral endopeptidase. One or more other peptidase degrade atrial natriuretic peptide or brain natriuretic peptide in the heart, lungs and kidney
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?
additional information
?
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nicastrin controls neprilysin at a transcriptional level by contributing to the production of the beta-amyloid precursor protein intracellular domain with the gamma-secretase complex
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?
additional information
?
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NEP degrades murine amyloid-beta faster than human amyloid-beta, observed with full-length amyloid-beta containing 40 or 42 amino acids (Abeta1-40 and Abeta1-42) and a truncated form (Abeta4-15), which contains one of the main NEP cleavage sites for amyloid-beta (between positions 9 and 10), harbours all three amino acid differences between murine and human amyloid-beta sequences, and is less prone to aggregation and thus might be a simpler model to investigate amyloid-beta biochemistry. Murine amyloid-beta has a far lower propensity to aggregate than human amyloid-beta. Amyloid-beta degradation products formed during NEP incubation are identified by mass spectrometry, analysis of predominant NEP cleavage sites detected by mass spectrometry for human and murine amyloid-beta1-42 and amyloid-beta.4-15. In addition to the amyloid-beta4-9 fragment, di- and tetra-peptides amyloid-beta18-19 and amyloid-beta39-42 are also observed
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additional information
?
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NEP degrades murine amyloid-beta faster than human amyloid-beta, observed with full-length amyloid-beta containing 40 or 42 amino acids (Abeta1-40 and Abeta1-42) and a truncated form (Abeta4-15), which contains one of the main NEP cleavage sites for amyloid-beta (between positions 9 and 10), harbours all three amino acid differences between murine and human amyloid-beta sequences, and is less prone to aggregation and thus might be a simpler model to investigate amyloid-beta biochemistry. Murine amyloid-beta has a far lower propensity to aggregate than human amyloid-beta. Amyloid-beta degradation products formed during NEP incubation are identified by mass spectrometry, analysis of predominant NEP cleavage sites detected by mass spectrometry for human and murine amyloid-beta1-42 and amyloid-beta.4-15. In addition to the amyloid-beta4-9 fragment, di- and tetra-peptides amyloid-beta18-19 and amyloid-beta39-42 are also observed
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-
additional information
?
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NEP degrades murine amyloid-beta faster than human amyloid-beta, observed with full-length amyloid-beta containing 40 or 42 amino acids (Abeta1-40 and Abeta1-42) and a truncated form (Abeta4-15), which contains one of the main NEP cleavage sites for amyloid-beta (between positions 9 and 10), harbours all three amino acid differences between murine and human amyloid-beta sequences, and is less prone to aggregation and thus might be a simpler model to investigate amyloid-beta biochemistry. Murine amyloid-beta has a far lower propensity to aggregate than human amyloid-beta. Amyloid-beta degradation products formed during NEP incubation are identified by mass spectrometry, analysis of predominant NEP cleavage sites detected by mass spectrometry for human and murine amyloid-beta1-42 and amyloid-beta.4-15. In addition to the amyloid-beta4-9 fragment, di- and tetra-peptides amyloid-beta18-19 and amyloid-beta39-42 are also observed
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?
additional information
?
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NEP degrades murine amyloid-beta faster than human amyloid-beta, observed with full-length amyloid-beta containing 40 or 42 amino acids (Abeta1-40 and Abeta1-42) and a truncated form (Abeta4-15), which contains one of the main NEP cleavage sites for amyloid-beta (between positions 9 and 10), harbours all three amino acid differences between murine and human amyloid-beta sequences, and is less prone to aggregation and thus might be a simpler model to investigate amyloid-beta biochemistry. Murine amyloid-beta has a far lower propensity to aggregate than human amyloid-beta. Amyloid-beta degradation products formed during NEP incubation are identified by mass spectrometry, analysis of predominant NEP cleavage sites detected by mass spectrometry for human and murine amyloid-beta1-42 and amyloid-beta.4-15. In addition to the amyloid-beta4-9 fragment, di- and tetra-peptides amyloid-beta18-19 and amyloid-beta39-42 are also observed
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?
additional information
?
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the enzyme is the major inactivator of enkephalin in brain
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?
additional information
?
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the enzyme may participate in the regulation of blood pressure and water and sodium excretion through inactivation of kinins
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?
additional information
?
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the enzyme is the major inactivator of enkephalin in brain
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?
additional information
?
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the enzyme may participate in the regulation of blood pressure and water and sodium excretion through inactivation of kinins
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?
additional information
?
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in sepsis, the local concentration and action of adrenomedullin in tissue may be differentially regulated by NEP
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?
additional information
?
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neutral endopeptidase inhibition has natriuretic and aquaretic actions in cirrhosis without any effect on blood pressure and kidney perfusion due to a significant overexpression of thgis enzyme in renal cortex
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?
additional information
?
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physiological role in metabolism of insect peptides at the synapse
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?
additional information
?
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could play an important role in the hydrolysis of neuropeptides
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?
additional information
?
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the enzyme may participate in the regulation of blood pressure and water and sodium excretion through inactivation of kinins
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?
