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1 ostaglandin E2 (PGE2) from prostaglandin H2 (PGH2).
2 arachidonic acid (AA) into prostaglandin H2 (PGH2).
3 ses (COXs), convert arachidonic acid (AA) to PGH2.
4 HS peroxidase (POX) activity reduces PGG2 to PGH2.
5 en and a peroxidase that reduces the PGG2 to PGH2.
6 talyze the conversion of arachidonic acid to PGH2.
7         TBXAS1 metabolizes prostaglandin H2 (PGH2), a cyclooxygenase (COX) product of arachidonic aci
8 gation response stimulated by thromboxane or PGH2 analogs.
9 btained for the bicycloendoperoxides U44069, PGH2, and U46619 (Ki = 29-39 nM).
10 te kinetic study revealed that TXAS consumed PGH2 at a rate of 3,800 min(-1) and that the k(cat)/K(m)
11  mutations in TBXAS result in an increase in PGH2 availability for other PG synthases.
12 c parameters of TXAS-catalyzed reaction are: PGH2 bound TXAS at a rate of 1.2-2.0 x 10(7) M(-1) s(-1)
13 tadecatrienoic acid and malondialdehyde from PGH2, but not formation of PGE2.
14 ently converted to the unstable intermediate PGH2 by cyclooxygenase-2 (COX-2), and PGH2 undergoes an
15 ly all of the LG predicted to be formed from PGH2 can be accounted for as adducts of the PGH-synthase
16 to prostaglandin (PG) G2 (catalytic step 1), PGH2 (catalytic step 2), and PGI2 (catalytic step 3).
17                      Given that the cellular PGH2 concentration is quite low, we concluded that under
18 f 3,800 min(-1) and that the k(cat)/K(m) for PGH2 consumption was 3 x 10(6) M(-1) s(-1).
19 ES-2h has significant catalytic activity for PGH2 degradation.
20        Incubations of cells carried out with PGH2 demonstrated that PGE2 synthase activity was increa
21 sozymes and terminal enzymes by developing a PGH2-divided model.
22 w a cell processes the unstable endoperoxide PGH2 during the inactivation of a major metabolic outlet
23                        Further metabolism of PGH2-EA and PGH2-G by prostaglandin synthases produces a
24 ol (2-AG), to prostaglandin-H2-ethanolamide (PGH2-EA) and -glycerol ester (PGH2-G), respectively.
25           An important structural feature of PGH2 formed by COX is the trans-configuration of side ch
26 donic acid to the prostaglandin endoperoxide PGH2, from which all other prostaglandins are formed.
27            Further metabolism of PGH2-EA and PGH2-G by prostaglandin synthases produces a variety of
28 -ethanolamide (PGH2-EA) and -glycerol ester (PGH2-G), respectively.
29  with heme ligands in binding study and with PGH2 in enzymatic study.
30 nal absorbance changes upon mixing TXAS with PGH2, indicating minimal accumulation of any heme-derive
31  PGE synthases catalyze the isomerization of PGH2 into PGE2.
32 he conversion of prostaglandin endoperoxide (PGH2) into thromboxane A2 (TxA2) which plays a crucial r
33     The first COX product, prostaglandin H2 (PGH2) is also a command substrate for other prostanoid e
34                                              PGH2-like endoperoxides are intermediates in this pathwa
35 rize the contribution of mPGES-1 to cellular PGH2 metabolism in murine macrophages by studying the sy
36 in E synthases involved in prostaglandin H2 (PGH2) metabolism.
37 ce between the heme and the protein, where a PGH2 might be able to bind.
38 nase-2 (COX-2), converts arachidonic acid to PGH2 PGHS-2 is a conformational heterodimer composed of
39                          During reactions of PGH2 synthase I with arachidonic acid (AA) and ethyl hyd
40 und I and compound II observed with EtOOH in PGH2 synthase II suggest that peroxidative cleavage is n
41                              Aspirin-treated PGH2 synthase II was found to produce 15-HETE, and the a
42                However, when aspirin-treated PGH2 synthase II was reacted with AA, a unique spectral
43                         When aspirin-treated PGH2 synthase II was reacted with EtOOH, a normal peroxi
44                        During reactions with PGH2 synthase II with AA, compound I and compound II wer
45                 However, during reactions of PGH2 synthase II with EtOOH, compound I and compound II
46 d peroxidase activities of prostaglandin H2 (PGH2) synthase I and II were monitored by stopped-flow s
47 ngs question mechanisms of catalysis in both PGH2 synthases.
48 ting the prostaglandin pathway downstream of PGH2 synthesis and avoiding suppression of antithromboti
49 ey step in the conversion of arachidonate to PGH2, the immediate substrate for a series of cell speci
50 nthase (PGES) catalyzes the isomerization of PGH2 to PGE2.
51 hat specifically catalyzes the conversion of PGH2 to PGE2.
52 tic function of PGIS in the isomerization of PGH2 to prostacyclin.
53 ) s(-1); the rate of catalytic conversion of PGH2 to TXA2 or MDA was at least 15,000 s(-1) and the lo
54  molecular oxygen, it uses prostaglandin H2 (PGH2) to catalyze either an isomerization reaction to fo
55                                    U46619, a PGH2/TxA2 mimetic, induced specific phosphorylation of b
56 ediate PGH2 by cyclooxygenase-2 (COX-2), and PGH2 undergoes an isomerization reaction to generate PGE