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1                                              L-PGDS (50 microg/ml) was able to significantly inhibit
2                                              L-PGDS expression also increased 50% upon the differenti
3                                              L-PGDS expression was detected in whole lung and alveola
4                                              L-PGDS overexpressing transgenic mice improved clearance
5                                              L-PGDS promotes cell surface expression of DP1, but not
6 es caveolin-1 expression by > 2.5-fold in an L-PGDS-dependent manner.
7 n of microsomal PGE synthase-1 (mPGES-1) and L-PGDS.
8  mucosa showed significantly higher COX2 and L-PGDS mRNA expression, and significantly higher PGD2 le
9 face is dependent on the interaction between L-PGDS and the C-terminal MEEVD residues of Hsp90.
10              Surprisingly, PGD2 synthesis by L-PGDS is promoted by coexpression of DP1, suggesting a
11 ulated ERK phosphorylation was unaffected by L-PGDS pretreatment in both cell lines.
12           Enzymatic products of stromal cell L-PGDS included high levels of PGD2 and 15-deoxy-delta(1
13 s abolished by AT-56, a specific competitive L-PGDS inhibitor.
14                                 In contrast, L-PGDS knockout mice were impaired in their ability to r
15 nsating for a lack of PPARgamma2, we crossed L-PGDS KO mice to PPARgamma2 KO mice to generate Double
16 concentrations (20 mm) resulted in decreased L-PGDS expression in control cells but actually stimulat
17 R (DP1) promotes the activity of the enzyme (L-PGDS) that produces its agonist (PGD2) and in which th
18 this study, we report on the 50% increase in L-PGDS protein expression observed in vascular smooth mu
19 ridization revealed significant increases in L-PGDS expression in the arcuate and ventromedial nucleu
20 d focal adhesion kinase expression levels in L-PGDS KO vascular smooth muscle cells and controls.
21 erial endotoxin (LPS) or Pseudomonas induced L-PGDS expression.
22 der cold-acclimated conditions, mice lacking L-PGDS had elevated reliance on carbohydrate to provide
23  increases glucose utilization, mice lacking L-PGDS had improved glucose tolerance after high-fat fee
24                                    Moreover, L-PGDS knockout mice exhibited increased expression of g
25  production, suggesting that H-PGDS, but not L-PGDS, mediates LPS-induced PGD(2) production in BMDM.
26                        Catalytic activity of L-PGDS produces PGD2, an endogenous somnogen.
27       Furthermore, we examined the effect of L-PGDS incubation on insulin-stimulated Akt, glycogen sy
28 tion, we demonstrate differential effects of L-PGDS treatment on cell proliferation and apoptosis in
29 Rs, in HEK293 and HeLa cells, independent of L-PGDS enzyme activity.
30  Together, our results identify induction of L-PGDS expression by inflammatory stimuli or bacterial i
31                 To determine if induction of L-PGDS was compensating for a lack of PPARgamma2, we cro
32     Consistent with the concept that lack of L-PGDS increases glucose utilization, mice lacking L-PGD
33 erial infection, the regulatory mechanism of L-PGDS induction, and the protective role of L-PGDS expr
34 triguing possibility that E(2) modulation of L-PGDS plays a role in the regulation of sleep-wake stat
35 ng DKO mice we demonstrated a requirement of L-PGDS for maintenance of subcutaneous WAT (scWAT) funct
36 L-PGDS induction, and the protective role of L-PGDS expression in host immune response.
37  However, the regulation and significance of L-PGDS expression in macrophages are unknown.
38                    Epigenetic suppression of L-PGDS expression in macrophages blunted a majority of P
39          As predicted from E2 suppression of L-PGDS transcript levels, the responses of the locked nu
40 dy suggests a potential therapeutic usage of L-PGDS or PGD(2) against Pseudomonas pneumonia.
41                                     Overall, L-PGDS and PPARgamma2 coordinate to regulate carbohydrat
42 ts inhibitor HQL-79, but not lipocalin PGDS (L-PGDS) siRNA and its inhibitor AT-56, significantly att
43                               Thus, reducing L-PGDS in the VLPO of oil-treated females mimicked the e
44                              In this regard, L-PGDS increases the formation of a DP1-ERK1/2 complex a
45 ion in control cells but actually stimulated L-PGDS expression in SHR.
46                                Surprisingly, L-PGDS gene expression is reduced 2-fold after E(2) trea
47  lipocalin-type prostaglandin D(2) synthase (L-PGDS), a protein found at elevated levels in type 2 di
48 ng is lipocalin prostaglandin D(2) synthase (L-PGDS), which catalyzes the conversion of prostaglandin
49 hat lipocalin-type prostaglandin D synthase (L-PGDS) and prostaglandin D2 (PGD2) metabolites produced
50 ns, Lipocalin-type prostaglandin D synthase (L-PGDS) expression by neurons and glial cells was analyz
51 evels of Lipocalin prostaglandin D synthase (L-PGDS) expression in BAT and subcutaneous white adipose
52 role for lipocalin prostaglandin D synthase (L-PGDS) in the control of metabolic fuel utilization by
53  in lipocalin-type prostaglandin D synthase (L-PGDS) transcript levels, after E2 treatment, in the ve
54 ers lipocalin-like prostaglandin D synthase (L-PGDS), alpha(1) -acid glycoprotein (AAG), transferrin
55    Lipocalin-type prostaglandin D2 synthase (L-PGDS) has recently been linked to a variety of pathoph
56 neuronal cells, lipocalin-type PGD synthase (L-PGDS) is detected in the macrophages infiltrated to at
57 calin-type prostaglandin D2 (PGD2) synthase (L-PGDS) interacts intracellularly with the GPCR DP1 in a
58                             We conclude that L-PGDS plays an important role regulating insulin sensit
59                          We demonstrate that L-PGDS expression in BAT is positively correlated with B
60 , we demonstrate, immunocytochemically, that L-PGDS is also expressed in a population of VLPO neurons
61                              We propose that L-PGDS is involved in the balance of VSMC proliferation
62 romatin immunoprecipitation assays show that L-PGDS induction was regulated positively by AP-1, but n
63                        Our results show that L-PGDS KO mice become glucose-in-tolerant and insulin-re
64                   Immunostaining showed that L-PGDS was expressed in the neurons of human myenteric a
65   Taken together, these results suggest that L-PGDS plays an important role in the regulation of gluc
66  Adipocytes were significantly larger in the L-PGDS KO mice compared with controls on the same diets.
67                        In addition, only the L-PGDS KO mice developed nephropathy and an aortic thick
68 te and elevated serum FFA levels compared to L-PGDS KO alone.
69 ieties (an improved technology), targeted to L-PGDS mRNA, (ii) scrambled sequence control oligos, or
70                             Finally, whereas L-PGDS has been reported to be expressed primarily in ol
71 und that when WKY cells were pretreated with L-PGDS, insulin could actually induce apoptosis and fail

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