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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
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
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
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
23 A-7 cells express this receptor, and another PPAR delta agonist, docosahexaenoic acid, mimics the eff
25 oligodendrocytes in uninjured spinal cords; PPAR-delta was also detected in NG2 cells (potential oli
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
34 isome proliferator-activated receptor-delta (PPAR-delta), which is implicated in bile acid homoeostas
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
40 such that >20% of oligodendrocytes expressed PPAR-delta after SCI compared with approximately 10% in
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
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
48 cellular differentiation, the early rise in PPAR-delta+ NG2 cells followed by an increase in new PPA
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
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
62 ediated cardiomyocyte-restricted deletion of PPAR-delta in mice downregulates constitutive expression
64 to examine the spatiotemporal expression of PPAR-delta in naive and injured spinal cords from adult
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
69 Identification of 15-LOX-1 suppression of PPAR-delta to inhibit IL-6/STAT3 signaling-driven CAC tu
71 liferator-activated receptor (PPAR)-alpha or PPAR-delta activation stimulates keratinocyte differenti
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
80 an and rodent myocytes, the highly selective PPAR delta agonist GW742 increased fatty acid oxidation
82 ed from individuals with HD, indicating that PPAR-delta activation may be beneficial in HD and relate
86 Collectively, these findings suggest that PPAR-delta serves as an important molecular brake for th
89 ect was on polyp size; mice treated with the PPAR-delta activator had a fivefold increase in the numb
92 rent study shows that (i) 13-S-HODE binds to PPAR-delta, decreases PPAR-delta activation, and down-re
95 ic commitment of HSC daughter cells, whereas PPAR-delta activation increased asymmetric cell division
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