1.1.1.141: 15-hydroxyprostaglandin dehydrogenase (NAD+)

This is an abbreviated version, for detailed information about 15-hydroxyprostaglandin dehydrogenase (NAD+), go to the full flat file.

Reaction

(5Z,13E,15S)-11alpha,15-dihydroxy-9-oxoprost-5,13-dienoate
+
NAD+
=
(5Z,13E)-11alpha-hydroxy-9,15-dioxoprost-5,13-dienoate
+
NADH
+
H+

Synonyms

11alpha,15-dihydroxy-9-oxoprost-13-enoate:NAD+ 15-oxidoreductase, 15-hydroxy prostaglandin dehydrogenase, 15-hydroxyprostaglandin dehydrogenase, 15-hydroxyprostaglandin-dehydrogenase, 15-hydroxyprostanoic dehydrogenase, 15-OH-PGDH, 15-PGDH, 15-prostaglandin dehydrogenase, dehydrogenase, 15-hydroxyprostaglandin, HPGD, NAD+ dependent 15-hydroxyprostaglandin dehydrogenase, NAD+ dependent PGDH, NAD+-15-hydroxy prostanoate oxidoreductase, NAD+-dependent 15-hydroxyprostaglandin dehydrogenase, NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (type I), NAD+-dependent 15-PGDH, NAD+-linked 15-hydroxyprostaglandin dehydrogenase, NAD-dependent 15-hydroxyprostaglandin dehydrogenase, NAD-specific 15-hydroxyprostaglandin dehydrogenase, PGDH, prostaglandin dehydrogenase

ECTree

     1 Oxidoreductases
         1.1 Acting on the CH-OH group of donors
             1.1.1 With NAD+ or NADP+ as acceptor
                1.1.1.141 15-hydroxyprostaglandin dehydrogenase (NAD+)

Engineering

Engineering on EC 1.1.1.141 - 15-hydroxyprostaglandin dehydrogenase (NAD+)

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ENGINEERING
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
A13G/A14S/Q15K/D36S/W37R
-
no activity
A140P
-
naturally occuring mutation in patients with pulmonary hypertropic osteoarthropathy. Homozygous individuals develop pulmonary hypertrophic osteoarthropathy secondary to chronically elevated prostaglandin E2 levels. Heterozygous relatives also show milder biochemical and clinical manifestations. After expression in Escherichia coli, the mutations renders the protein largely insoluble at 37C, but mostly souble at 20C. Mutant exhibits less than 1.5% of wild-type activity; the mutant shows no detectable activity, the A140P substitution renders the enzyme largely insoluble at 37C, at 27C, the mutant protein is partially soluble, and at 20C it is mostly soluble
A14S/Q15K/D36S/W37R
-
no activity
C152A
-
similar activity as wild-type
C152F
-
no activity
C182A
-
no activity
C182F
-
no activity
C42A
-
similar activity as wild-type
C45F
-
similar activity as wild-type
C63A
-
similar activity as wild-type
C63F
-
10% of wild-type activity
D64E
-
no activity
D64K
-
low activity
D64N
-
similar activity as wild type
D86E
-
similar activity as wild type
D86N
-
similar activity as wild type
I17A
-
270% of wild-type activity
I17E
-
no activity
I17K
-
no activity
I17L
-
364% of wild-type activity
I17V
-
300% of wild-type activity
K155L
-
inactive enzyme
K155Q
-
inactive enzyme
L155L
-
no activity
L155Q
-
no activity
N91A
-
136% of wild-type activity
N91D
-
86% of wild-type activity
N91K
-
no activity
N91L
-
no activity
Q15K
-
approx. 200% of wild-type activity
Q15K/D36A/W37R
-
no activity with NAD+ as cofactor, low activity with NADP+ as cofactor
Q15K/D36S/W37R
-
no activity with NAD+ as cofactor, low activity with NADP+ as cofactor
Q15K/W37K
-
approx. 350% of wild-type activity
Q15K/W37R
-
approx. 350% of wild-type activity, strong activity with NADP+ as cofactor
Q15R
-
approx. 100% of wild-type activity
Q15R/W37K
-
approx. 200% of wild-type activity
Q15R/W37R
-
approx. 200% of wild-type activity, strong activity with NADP+ as cofactor
S138A
-
no activity
S193P
-
the missense mutation in exon 6 of the human HPGD gene encoding NAD+ dependent 15-hydroxyprostaglandin dehydrogenase is involved in the pathogenesis of isolated congenital nail clubbing
T11A
-
no activity
T11C
-
no activity
T11S
-
110% of wild-type activity
T188A
-
no activity
T188S
-
substantial activity, lower than wild-type
T188Y
-
no activity
V186A
-
143% of wild-type activity
V186D
-
no activity
V186I
-
468% of wild-type activity
V186K
-
71% of wild-type activity
W37K
-
approx. 100% of wild-type activity
W37R
-
approx. 100% of wild-type activity
Y151L/K155E
-
inactive
additional information