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1                                              PPAR delta likely mediates this antiapoptotic effect bec
2                                              PPAR-delta activation also reduced HTT-induced neurotoxi
3                                              PPAR-delta also has a relatively high expression in the
4                                              PPAR-delta overexpression in colonic epithelial cells pr
5                                              PPAR-delta promotes colonic tumorigenesis.
6                                              PPAR-delta+ NG2 cell numbers were significantly higher t
7                                              PPAR-delta+ oligodendrocyte numbers declined at 1 dpi an
8 e (P = 0.026), and 2.25 +/- 0.25 in 15-LOX-1-PPAR-delta-Gut mice (P = 0.0006).
9 ession in colonic epithelial cells (15-LOX-1-PPAR-delta-Gut mice) suppressed these effects: the numbe
10 MP-7, CCND1 (Cyclin D1), CX43 (Connexin 43), PPAR-delta, and ITF2 genes in OEAs with deregulated beta
11 ings indicate cyclin D1, MMP-7, connexin 43, PPAR-delta, and ITF-2, likely play important roles in th
12 ewal potential of these organoid bodies in a PPAR-delta-dependent manner.
13          Notably, HFD- and agonist-activated PPAR-delta signalling endow organoid-initiating capacity
14 oding other PPAR family members (PPAR alpha, PPAR delta, or NUC-1) were unchanged or decreased.
15 roliferator-activated receptor (PPAR)-alpha, PPAR-delta, PPAR-gamma, cd36/Fat, and Ucp2, which coinci
16 ator-activated receptors (PPARs; PPAR-alpha, PPAR-delta, and PPAR-gamma) comprise a family of nuclear
17 ceptor isoforms, PPAR gamma, PPAR alpha, and PPAR delta, encoded by different genes.
18 echanistic relationship between 15-LOX-1 and PPAR-delta was previously unknown.
19 phosphorylation, IL-6 promoter activity, and PPAR-delta mRNA and protein expression.
20 ivated receptors (PPAR-alpha, PPAR-gamma and PPAR-delta) exemplify this connection, regulating divers
21 ts that activate PPAR-alpha, PPAR-gamma, and PPAR-delta alone or in combination have the potential to
22 ceptors (PPARs), PPAR-alpha, PPAR-gamma, and PPAR-delta.
23 A-7 cells express this receptor, and another PPAR delta agonist, docosahexaenoic acid, mimics the eff
24 by sulindac sulfone but can be bound by both PPAR delta and PPAR gamma.
25  oligodendrocytes in uninjured spinal cords; PPAR-delta was also detected in NG2 cells (potential oli
26 on in skeletal muscle resulting in decreased PPAR-delta activation.
27 (i) 13-S-HODE binds to PPAR-delta, decreases PPAR-delta activation, and down-regulates PPAR-delta exp
28   We show that mice deficient in PPAR-delta (PPAR-delta(-/-)) develop a severe inflammatory response
29 isome proliferator-activated receptor delta (PPAR-delta) interacts with HTT and that mutant HTT repre
30 isome proliferator-activated receptor delta (PPAR-delta) signature in intestinal stem cells and proge
31 isome proliferator-activated receptor delta (PPAR-delta)-fatty-acid oxidation (FAO) pathway for the m
32 isome proliferator-activated receptor-delta (PPAR-delta) is induced when macrophages engulf apoptotic
33 isome proliferator-activated receptor-delta (PPAR-delta) may have important roles in FAO.
34 isome proliferator-activated receptor-delta (PPAR-delta), which is implicated in bile acid homoeostas
35 isome proliferator-activated receptor-delta (PPAR-delta).
36 isome proliferator-activated receptor-delta (PPAR-delta; also known as PPAR-beta) is expressed at hig
37 iating capacity to progenitors, and enforced PPAR-delta signalling permits these progenitors to form
38 played by PPAR nuclear receptors, especially PPAR-delta (Lee et al.), in the modulation of inflammato
39    A large proportion of NG2 cells expressed PPAR-delta after SCI, especially along lesion borders.
40 such that >20% of oligodendrocytes expressed PPAR-delta after SCI compared with approximately 10% in
41 ignificantly greater in mice nullizygous for PPAR-delta.
42 L >> LDL > HDL), PPAR isoform (PPAR alpha >> PPAR delta > PPAR gamma), and among fatty acid-releasing
43  resultant induction of apoptosis; and (iii) PPAR-delta is an important signaling receptor for 13-S-H
44                        Our results implicate PPAR-delta in the regulation of intestinal adenoma growt
45 8 in wild-type littermates, 6.67 +/- 0.83 in PPAR-delta-Gut mice (P = 0.026), and 2.25 +/- 0.25 in 15
46               We show that mice deficient in PPAR-delta (PPAR-delta(-/-)) develop a severe inflammato
47               The most prominent increase in PPAR-delta+ oligodendrocytes was along lesion borders wh
48  cellular differentiation, the early rise in PPAR-delta+ NG2 cells followed by an increase in new PPA
49                                    Increased PPAR-delta transactivation ameliorated mitochondrial dys
50  These findings highlight how diet-modulated PPAR-delta activation alters not only the function of in
51 in liver and heart, in mouse skeletal muscle PPAR delta is severalfold more abundant than either PPAR
52                     Thus, chronic myocardial PPAR-delta deficiency leads to lipotoxic cardiomyopathy.
53              Expression of dominant-negative PPAR-delta in the central nervous system of mice was suf
54              Expression of dominant-negative PPAR-delta specifically in the striatum of medium spiny
55 ta+ NG2 cells followed by an increase in new PPAR-delta+ oligodendrocytes suggests that this transcri
56 evious reports suggesting that activation of PPAR-delta potentiates colon polyp formation, here we sh
57 em cells), and pharmacological activation of PPAR-delta recapitulates the effects of a HFD on these c
58 se models of HD, pharmacologic activation of PPAR-delta using the agonist KD3010 improved motor funct
59 of mice with a synthetic ligand activator of PPAR-delta, GW0742, ameliorates experimental autoimmune
60 sion of these T helper subsets in the CNS of PPAR-delta(-/-) mice occurred as a result of a constella
61                          Genetic deletion of PPAR-delta decreases expression of opsonins such as comp
62 ediated cardiomyocyte-restricted deletion of PPAR-delta in mice downregulates constitutive expression
63              We also show that the effect of PPAR-delta in inhibiting the production of IFN-gamma and
64  to examine the spatiotemporal expression of PPAR-delta in naive and injured spinal cords from adult
65                   We have found that loss of PPAR-delta or inhibition of mitochondrial FAO induces lo
66  a critical step in NSAID down-regulation of PPAR-delta and the resultant induction of apoptosis; and
67 indings indicate that the down-regulation of PPAR-delta by 15-LOX-1 through 13-S-HODE is an apoptotic
68                      We examined the role of PPAR-delta in colon carcinogenesis using PPAR-delta-defi
69    Identification of 15-LOX-1 suppression of PPAR-delta to inhibit IL-6/STAT3 signaling-driven CAC tu
70 crease the affinity for the same peptides on PPAR delta and in one case on PPAR alpha.
71 liferator-activated receptor (PPAR)-alpha or PPAR-delta activation stimulates keratinocyte differenti
72                                      Overall PPAR-delta+ cell numbers declined at 1 day post injury (
73                     Mechanistically, the PML-PPAR-delta-FAO pathway controls the asymmetric division
74 the tail group modifications imparted potent PPAR delta agonist activity, improvement of PPAR alpha a
75 es PPAR-delta activation, and down-regulates PPAR-delta expression in colorectal cancer cells; (ii) t
76 rs to terminate inflammation, down-regulates PPAR-delta.
77                      As previously reported, PPAR-delta was expressed by neurons and oligodendrocytes
78 racts with HTT and that mutant HTT represses PPAR-delta-mediated transactivation.
79              After spinal cord injury (SCI), PPAR-delta mRNA and protein were present early and incre
80 an and rodent myocytes, the highly selective PPAR delta agonist GW742 increased fatty acid oxidation
81                              NSAIDs suppress PPAR-delta activity in colon cancer cells.
82 ed from individuals with HD, indicating that PPAR-delta activation may be beneficial in HD and relate
83 tes colon polyp formation, here we show that PPAR-delta attenuates colon carcinogenesis.
84                 Together, our data show that PPAR-delta is a crucial determinant of constitutive myoc
85                              We suggest that PPAR-delta is a potential therapeutic target in treating
86    Collectively, these findings suggest that PPAR-delta serves as an important molecular brake for th
87       We report the crystal structure of the PPAR delta ligand-binding domain (LBD) bound to either t
88             Exposure of Apc(min) mice to the PPAR-delta ligand GW501516 resulted in a significant inc
89 ect was on polyp size; mice treated with the PPAR-delta activator had a fivefold increase in the numb
90 (2) promotes survival of colonocytes through PPAR delta activation.
91                                        Thus, PPAR-delta has a pivotal role in orchestrating the timel
92 rent study shows that (i) 13-S-HODE binds to PPAR-delta, decreases PPAR-delta activation, and down-re
93  of PPAR-delta in colon carcinogenesis using PPAR-delta-deficient (Ppard(-/-)) mice.
94 d oligodendrocytes (bromodeoxyuridine+) were PPAR-delta+.
95 ic commitment of HSC daughter cells, whereas PPAR-delta activation increased asymmetric cell division
96               But it remains unclear whether PPAR-delta is required for maintaining basal myocardial
97               Incubation of macrophages with PPAR-delta agonists was shown to inhibit foam cell forma
98 s of HSC maintenance, whereas treatment with PPAR-delta agonists improved HSC maintenance.

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