ライフサイエンスコーパス: PGES

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1 PGES type 2 (mPGES-2) is a membrane-associated enzyme, w

2 PGES was seen in 15/30 (50%) case and 35/92 (38%) contro

3 can express a suboptimal profile of PGHS and PGES isoforms, resulting in diminished levels of PGE(2)

4 same protein expression pattern for PGIS and PGES in 108 different non-small cell lung cancer biopsie

5 ive was to determine the association between PGES, as a possible identifiable EEG marker of profound

6 ctive inhibitor CAY10526, but not mPGES-2, c-PGES or PU.1, attenuated LPS-induced burst of PGE(2) pro

7 data show that mPGES-1, but not mPGES-2 or c-PGES isomerase, mediates LPS-induced late-phase burst of

8 matopoietic-PGDS (H-PGDS), cytosolic-PGES (c-PGES), or mPGES-2 in BMDM was not affected by LPS treatm

9 cked by RU486 and, second, repression of COX/PGES is antagonized by RU486.

10 ases (microsomal PGES1, PGES2 and cystosolic PGES) was down-regulated by the TZDs.

11 osomal PGES1 (mPGES1), mPGES2, and cytosolic PGES (cPGES) were present in FLO EA cells.

12 significant effect of diagnosis on cytosolic PGES (cPGES) protein levels in the frontal cortex, with

13 OX-1, hematopoietic-PGDS (H-PGDS), cytosolic-PGES (c-PGES), or mPGES-2 in BMDM was not affected by LP

14 More importantly, PGES(-/-) mice harbor significantly higher Mtb lung burd

15 -2 has been reported to be a GSH-independent PGES, the crystal structure and sequence analysis indica

16 Microsomal PGES (mPGES) is inducible and works more efficiently wit

17 Microsomal PGES-1(-/-) (mPGES-1(-/-)) mice were crossed into low-de

18 ereas the increased expression of microsomal PGES (mPGES)-1 and a myeloid cell transcription factor P

19 s, for each 1-second increase in duration of PGES, the odds of SUDEP increased by a factor of 1.7%(p

20 ncreased in direct proportion to duration of PGES.

21 ctional as indicated by a 3-fold increase of PGES activity in synoviocytes following treatment with I

22 Prolonged PGES (>50 seconds) appears to identify refractory epilep

23 Several putative PGES have been identified and cloned, including the memb

24 ite effects in lung AC (PGIS down-regulated; PGES up-regulated).

25 d electroencephalographic (EEG) suppression (PGES) and apnea are implicated in SUDEP.

26 hione-dependent prostaglandin E(2) synthase (PGES) genes has yielded important insights into the term

27 ) and inducible prostaglandin E(2) synthase (PGES) were joint classifiers that showed opposite effect

28 clooxygenase (COX)/prostaglandin E synthase (PGES) activity and COX-2 expression, RU486 (<1 microm) w

29 The prostaglandin E synthase (PGES) responsible for acid-induced PGE2 production in BE

30 that infection of prostaglandin E synthase (PGES)(-/-) macrophages in vitro with H37Rv resulted in s

31 Prostaglandin E2 synthase (PGES) catalyzes the isomerization of PGH2 to PGE2.

32 med from PGH(2) by a series of PGE synthase (PGES) enzymes.

33 nents of this cascade, two PGE(2) synthases (PGES), have very recently been identified as glutathione

34 by the prostanoid isomerases, PGE synthases (PGES) and PGD synthases (PGDS), respectively.

35 oid endoperoxides by specific PGE synthases (PGES).

36 COX) and one of the terminal PGE2 synthases (PGES) in postmortem tissue provided by The Stanley Medic

37 A Mann-Whitney U test showed that PGES was significantly longer in the generalized motor s

38 ed significantly elevated odds of SUDEP with PGES durations of >50 seconds (p < 0.05).

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