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3.4.17.23: angiotensin-converting enzyme 2

This is an abbreviated version!
For detailed information about angiotensin-converting enzyme 2, go to the full flat file.

Word Map on EC 3.4.17.23

Reaction

angiotensin II
+
H2O
=
angiotensin-(1-7)
 +
L-phenylalanine

Synonyms

ACE, ACE 2, ACE-2, ACE-related carboxypeptidase, ACE2, ACE2 homologue, ACEH, ACEII, Ang converting enzyme 2, angiotensin converting enzyme 2, angiotensin converting enzyme II, angiotensin converting enzyme-2, angiotensin II converting enzyme 2, angiotensin-converting enzyme, angiotensin-converting enzyme 2, angiotensin-converting enzyme homolog, angiotensin-converting enzyme homologue, angiotensin-converting enzyme type 2, angiotensin-converting enzyme-2, angiotensin-converting enzyme-like protein, angiotensin-converting enzyme-related carboxypeptidase, angiotensinase, hACE2, sACE2, soluble angiotensin converting enzyme 2, TMPRSS2

ECTree

     3 Hydrolases
         3.4 Acting on peptide bonds (peptidases)
             3.4.17 Metallocarboxypeptidases
                3.4.17.23 angiotensin-converting enzyme 2

Engineering

Engineering on EC 3.4.17.23 - angiotensin-converting enzyme 2

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PROTEIN VARIANTS
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
L79I
E2RR65
mutation increases binding of SARS-CoV-2 spike protein
Q42L
E2RR65
mutation increases binding of SARS-CoV-2 spike protein
L79I
mutation increases binding of SARS-CoV-2 spike protein
Q42L
mutation increases binding of SARS-CoV-2 spike protein
analysis
receptor binding domain-ACE2 binding assay based on time-resolved FRET, which reliably monitors the interaction in a physiologically relevant and cellular context. The modular assay can monitor the impact of different cellular components, such as heparan sulfate, lipids, and membrane proteins on the receptor binding domain-ACE2 interaction and it can be extended to the full-length spike protein. The assay is high throughput compatible and can detect small-molecule competitive and allosteric modulators of the receptor binding domain-ACE2 interaction
D206G
deleterious missense variant
D355N
variant exhibits lower binding to SARS-CoV-2 S protein
D38V
variant exhibits lower binding to SARS-CoV-2 S protein
D509Yr
variant exhibits lower binding to SARS-CoV-2 S protein
E23K
the variant in the binding region increases disease susceptibility towards SARS-CoV-2
E329G
variant shows a strong binding affinity with SARS-CoV-2 spike protein variants with very strong E329G-V483A, E329G-G476S, strong E329G-A419S, E329G-A348T and moderate E329G-S383C,E329G-F486L interaction
E37K
non-synonymous single nucleotide polymorphism
E484K
mutation forms high-affinity complexes (~40% more than wild-type)
E484K/N501Y
variant possesses both enhanced affinity and antibody resistance
F72V
variant exhibits lower binding to SARS-CoV-2 S protein
G211R
G326E
variant exhibits lower binding to SARS-CoV-2 S protein
G352V
variant exhibits lower binding to SARS-CoV-2 S protein
G726R
non-synonymous single nucleotide polymorphism
H345A
-
no activity with (7-methoxycoumarin-4-yl)acetyl-APK-2,4-dinitrophenyl
H345L
-
no activity with (7-methoxycoumarin-4-yl)acetyl-APK-2,4-dinitrophenyl
H34R
variant exhibits lower binding to SARS-CoV-2 S protein
H378R
H505A
-
1.5% of wild-type activity with (7-methoxycoumarin-4-yl)acetyl-APK-2,4-dinitrophenyl as substrate
H505L
-
no activity with (7-methoxycoumarin-4-yl)acetyl-APK-2,4-dinitrophenyl
I21V
the variant in the binding region increases disease susceptibility towards SARS-CoV-2
I468V
deleterious missense variant
K31R
variant exhibits lower binding to SARS-CoV-2 S protein
K341R
deleterious missense variant
K417T/E484K/N501Y
variant possesses both enhanced affinity and antibody resistance
K481Q
angiotensin I cleavage activity is 21% of wild-type activity, angiotensin II cleavage activity is 71.8% of wild-type activity
K68E
variant exhibits lower binding to SARS-CoV-2 S protein
L584A
the point mutation in the ACE2 ectodomain markedly attenuates shedding. The resultant ACE2-L584A mutant trafficks to the cell membrane and facilitates SARS-CoV entry into target cells
L595V
non-synonymous single nucleotide polymorphism
L731F
deleterious missense variant
L79I
mutation increases binding of SARS-CoV-2 spike protein
M62V
variant exhibits lower binding to SARS-CoV-2 S protein
N33I
variant exhibits lower binding to SARS-CoV-2 S protein
N501Y
mutation forms high-affinity complexes (~40% more than wild-type)
N51S
variant exhibits lower binding to SARS-CoV-2 S protein
N580A
the mutation in the ectodomain has no effect on sACE2 release
N64K
the variant in the binding region increases disease susceptibility towards SARS-CoV-2
N720D
P263S
non-synonymous single nucleotide polymorphism
P284S
non-synonymous single nucleotide polymorphism
P583A
the mutation in the ectodomain has no effect on sACE2 release
Q102P
the variant in the binding region increases disease susceptibility towards SARS-CoV-2
Q35K
variant exhibits lower binding to SARS-CoV-2 S protein
Q37K
variant exhibits lower binding to SARS-CoV-2 S protein
Q388L
variant exhibits lower binding to SARS-CoV-2 S protein
Q42L
mutation increases binding of SARS-CoV-2 spike protein
R169Q
R169QK481QR514Q
angiotensin I cleavage activity is 53.2% of wild-type activity, angiotensin II cleavage activity is 203.4% of wild-type activity
R219C
deleterious missense variant
R219H
deleterious missense variant
R273K
-
no activity with (7-methoxycoumarin-4-yl)acetyl-APK-2,4-dinitrophenyl
R273Q
-
no activity with (7-methoxycoumarin-4-yl)acetyl-APK-2,4-dinitrophenyl
R514Q
R582A
the mutation in the ectodomain has no effect on sACE2 release
R697G
deleterious missense variant
R768W
non-synonymous single nucleotide polymorphism
S477N
mutation forms high-affinity complexes (~40% more than wild-type)
S477N/E484K
variant possesses both enhanced affinity and antibody resistance
S547C
deleterious missense variant
S563L
non-synonymous single nucleotide polymorphism
S692P
deleterious missense variant
T27A
the variant in the binding region increases disease susceptibility towards SARS-CoV-2
T92I
the variant in the binding region increases disease susceptibility towards SARS-CoV-2
V581A
the mutation in the ectodomain has no effect on sACE2 release
V604A
the mutation in the ectodomain has no effect on sACE2 release
W271A
angiotensin I cleavage activity is 5.3% of wild-type activity, angiotensin II cleavage activity is 0.9% of wild-type activity. Lacks any significant chloride sensitivity with the substrate angiotensin I
W459C
non-synonymous single nucleotide polymorphism
Y252N
non-synonymous single nucleotide polymorphism
Y50F
variant exhibits lower binding to SARS-CoV-2 S protein
Y83H
variant exhibits lower binding to SARS-CoV-2 S protein
Q42L
mutation increases binding of SARS-CoV-2 spike protein
additional information