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1  core surface of a cellular organelle named 'lipid body'.
2 the form of intracellular inclusions termed 'lipid bodies'.
3 ncordant with fluorescent fatty-acid-labeled lipid bodies.
4 ivated protein (MAP) kinases, co-localize at lipid bodies.
5 n was present mostly on the periphery of the lipid bodies.
6 ed the formation and function of cytoplasmic lipid bodies.
7  into the PV or esterifies it for storage in lipid bodies.
8 at the oleosin was largely restricted to the lipid bodies.
9 ne, GIM1, that is able to restore import and lipid bodies.
10 G) E2 and LTB4 correlated with the number of lipid bodies.
11 cally diagnosed as organizing pneumonia with lipid bodies.
12 asma membrane, and cytosolic accumulation of lipid bodies.
13 nd contribute to CE formation for storage in lipid bodies.
14 LO and LTC(4) S at perinuclear locations and lipid bodies.
15  is in turn required for breakdown of TAG in lipid bodies.
16 ic reticulum (ER) and subsequent transfer to lipid bodies.
17 5beta PI3K subunits were present at isolated lipid bodies.
18 l eicosanoid production through formation of lipid bodies.
19 d (FA) synthesis during the expansion of the lipid bodies.
20 ls of cPLA2 and contain numerous cytoplasmic lipid bodies.
21 osolic phospholipase A2 (cPLA2) localizes at lipid bodies.
22 ases, including ERK1, ERK2, p85, and p38, in lipid bodies.
23  addition, mutant etfb(-) displayed elevated lipid body accumulation and reduced ATP synthesis.
24 hat deletion of this TF results in increased lipid body accumulation, and that ATF3 directly regulate
25 e details in cell shape, cytoplasm, nucleus, lipid bodies and cytoskeletal structures in 3D with unpr
26 as they rounded up, accumulated vacuoles and lipid bodies and displayed subtle but consistent differe
27  as a model system, we provide evidence that lipid bodies and peroxisomes have a close physiological
28 eroxisomes oxidize lipids, the metabolism of lipid bodies and peroxisomes is thought to be largely un
29 CAT2 parasites have reduced CE levels, fewer lipid bodies, and accumulate free cholesterol, which cau
30 tion of thylakoid membranes, accumulation of lipid bodies, and alterations of cell-surface morphology
31 led that evident changes in starch granules, lipid bodies, and cell walls thickness of the SAM in C.
32 formation, intracellular LTC(4) formation at lipid bodies, and priming for enhanced calcium ionophore
33                 Peroxisomes adhere stably to lipid bodies, and they can even extend processes into li
34 s in membrane lipids, which are deposited in lipid bodies; and (5) when sinks for photosynthetic ener
35 esis and sequestration of TAG into cytosolic lipid bodies appear to be a protective mechanism by whic
36                                              Lipid bodies are eukaryotic structures for temporary sto
37                                              Lipid bodies are inducible lipid domains abundantly pres
38                                      Because lipid bodies are potential reservoirs of esterified arac
39                                        Thus, lipid bodies are structurally distinct, inducible, nonnu
40  Lipid droplets, also known as oil bodies or lipid bodies, are plant organelles that compartmentalize
41 ding proteins, cellular cholesterol sensors, lipid-body-associated proteins and secreted autocrine fa
42 nts and composition of the transformed yeast lipid bodies but replaced some of the native proteins as
43 110beta catalytic subunits were localized to lipid bodies by immunocytochemistry and/or immunoblottin
44                 Overall reorientation of the lipid body, consisting of the phosphorus, glycerol, and
45 ses to NO in vitro, demonstrated by changing lipid body content, tgs1 transcription, and bacterial to
46 ies, and they can even extend processes into lipid body cores.
47                                              Lipid bodies, cytoplasmic inclusions that develop in cel
48                                     Although lipid body determination is a potential biomarker for su
49 rotein kinases both elicits the formation of lipid body domains and promotes LTC(4) formation at thes
50 of eosinophils and moves to the granules and lipid bodies during fMLP-mediated activation.
51 op into spores, while cells that do not form lipid bodies end up becoming peripheral rods, which are
52 or stimulation of human PMN with PAF to form lipid bodies enhanced eicosanoid production in response
53 ore and after the intervention, intrahepatic lipids, body fat distribution, fasting and postprandial
54 ed three multivariate factors interpreted as lipids, body fat/insulin/glucose/CRP, and blood pressure
55                                              Lipid bodies form autonomous intracellular structures in
56                             LL-37 stimulates lipid body formation and activates cys-LT-synthesizing e
57                            Chemokine-induced lipid body formation and enhanced LTC(4) release were bo
58  in this study that IgG or IL-5 also induces lipid body formation and subsequent leukotriene C4 produ
59    Aspirin and NSAIDs inhibited both induced lipid body formation and the enhanced capacity for formi
60 heximide inhibited not only the induction of lipid body formation by PAF, but also the PAF-induced "p
61               We demonstrate that macrophage lipid body formation can be induced by modified lipoprot
62 late, was as potent as aspirin in inhibiting lipid body formation elicited by cis-fatty acids.
63 re, 5-HETE was equally effective in inducing lipid body formation in both wild-type and 5-LO genetica
64                                              Lipid body formation in eosinophils was a rapidly (<1 h)
65 X inhibition, inhibit cis-fatty acid-induced lipid body formation in leukocytes and in concert inhibi
66 arachidonic and oleic acids) rapidly induced lipid body formation in leukocytes, and this lipid body
67                    Moreover, it appears that lipid body formation in M. xanthus is an important initi
68 mes may localize, we evaluated mechanisms of lipid body formation in neutrophils (PMN).
69                    Our studies indicate that lipid body formation is an inducible early response in l
70 y, NSAIDs inhibited arachidonic acid-induced lipid body formation likewise in macrophages from wild-t
71  Corroborating the dependency of PAF-induced lipid body formation on 5-LO, PMN and macrophages from w
72 e inhibitory effect of aspirin and NSAIDs on lipid body formation was independent of cyclooxygenase (
73               Second, cis-fatty acid-induced lipid body formation was not impaired in macrophages fro
74                    The 5-LO product inducing lipid body formation was not LTB4 but was 5(S)-hydroxyei
75              Both PAF- and 5(S)-HETE-induced lipid body formation were inhibited by protein kinase C
76  dose dependently (0.01-100 nM) elicited new lipid body formation, intracellular LTC(4) formation at
77  hr concordantly with cis-fatty acid-induced lipid body formation.
78 ive proteins were associated with a floating lipid body fraction obtained from a tapetal/locular flui
79                                              Lipid body fractions free of cytosol and other organelle
80  fatty acids promote novel structures within lipid bodies ("gnarls"), which may be organized arrays o
81     Formed at the onset of starvation, these lipid bodies gradually disappear until they are complete
82 erculosis, and accumulation of intracellular lipid bodies has been proposed to identify a persister p
83 ls in sputum containing triacylglycerol-rich lipid bodies have been shown to be associated with treat
84        Retinosomes, particles reminiscent of lipid bodies, have been identified in retinal pigment ep
85 localized to native as well as newly induced lipid bodies in intact and enucleated eosinophils.
86 overed an unexpected function of Viperin and lipid bodies in interferon induction by Toll-like recept
87 iated signaling is active within cytoplasmic lipid bodies in leukocytes.
88 TLR stimulation promotes the accumulation of lipid bodies in macrophages and consequently foam cell f
89 ignalling pathways modulate the formation of lipid bodies in macrophages and thereby cellular accumul
90 , the compartmentalization of lipids to form lipid bodies in PMN is dependent on specific cellular re
91 iene (LT) B4, induced the rapid formation of lipid bodies in PMN.
92 that produces an excess of 30% dry weight as lipid bodies in the form of triacylglycerol.
93                            PpoA localizes in lipid bodies in these tissues.
94 t plant oleosin is correctly targeted to the lipid bodies in transformed yeast and that yeast may be
95 t oleosin could be correctly targeted to the lipid bodies in transformed yeast.
96 spholipids or SDS, did not bind to the yeast lipid bodies in vitro.
97 he ER and hence subsequent deposition on the lipid bodies in vivo.
98                                          The lipid bodies in yeast have not been previously subjected
99 o a distinct intracellular site, cytoplasmic lipid bodies, in leukocytes.
100 umulation of the cellular activation marker, lipid bodies, in mouse macrophages and the release of im
101              These observations suggest that lipid bodies, including retinosomes, carry out specific
102 associated with phosphorylated Lyn kinase in lipid bodies induced to form in human polymorphonuclear
103                                              Lipid body induction by PAF required 5-lipoxygenase (LO)
104 lipid body formation in leukocytes, and this lipid body induction was inhibited by aspirin and nonste
105 bpopulations of cells occur: cells that form lipid bodies invariably develop into spores, while cells
106 tant for rotation about the long axis of the lipid body, is difficult to determine precisely because
107        DCs in tumor-bearing hosts accumulate lipid bodies (LB) containing electrophilic oxidatively t
108                                              Lipid bodies (LB; lipid droplets) are cytoplasmic organe
109 restored the capability of TAG synthesis and lipid body (LB) formation in H1246.
110                                        Newly lipid body (LB)-associated proteins included MRP-14, pot
111                                              Lipid bodies (LBs) in the coral gastrodermal tissues are
112                                              Lipid bodies (LBs), multifunctional organelles present i
113                                              Lipid bodies, lipid rich cytoplasmic inclusions, are cha
114 moking, fasting status, month of blood draw, lipids, body mass index, and other cardiovascular diseas
115                                    BP, serum lipids, body mass index, and smoking were assessed in al
116                                  Based on 12 lipids, body mass index, aspartate aminotransferase, and
117         After adjustment for age, education, lipids, body mass index, smoking, diabetes, hypertension
118 in resistance; fasting glucose, insulin, and lipids; body mass index (BMI); and blood pressure.
119 lly activating protein kinases suggests that lipid bodies may be structurally distinct intracellular
120 and LTB4 production in PMN, the induction of lipid bodies may have a role in the formation of eicosan
121                     These data indicate that lipid bodies not only fuel cellular differentiation but
122                                              Lipid bodies, not observable in uninfected mature leaves
123 ed eosinophils, the PAF-induced increases in lipid body numbers correlated with enhanced production o
124                           Chemokine-elicited lipid body numbers correlated with increased calcium ion
125                           Since increases in lipid body numbers correlated with priming for enhanced
126           Arachidonic and oleic acid-induced lipid body numbers correlated with the enhanced levels o
127 Our results show that BaP accumulates in the lipid bodies of Chlorella sp. and that there is Forster
128 ompartmentalization within arachidonate-rich lipid bodies of cPLA2 and its potentially activating pro
129 sinophils and the synthesis at intracellular lipid bodies of LTC(4), the dominant 5-lipoxygenase-deri
130 ally accumulate within the large cytoplasmic lipid bodies of tapetal cells.
131 d with DGAT activity, were isolated from the lipid bodies of the oleaginous fungus Mortierella ramann
132 from 5-LO genetically deficient mice, formed lipid bodies on exposure to PAF both in vitro and in viv
133 roplets in plants (also known as oil bodies, lipid bodies, or oleosomes) are well characterized in se
134 ing the induced formation of new cytoplasmic lipid body organelles.
135 sugar, and storage triacylglycerol (TAG) and lipid bodies persist in green cotyledons.
136 uencing variability in sputum frequencies of lipid body-positive (%LB(+)) M tuberculosis in patients
137 um cultures and calculated the percentage of lipid body-positive acid-fast bacilli (%LB + AFB) on spu
138 om wild-type cells initiates development and lipid body production in a csgA mutant to bypass the mut
139 ive physical contact between peroxisomes and lipid bodies promotes the coupling of lipolysis within l
140 ration processes, including seed-storage and lipid-body proteins.
141 Here, we present evidence that intracellular lipid bodies provide the necessary metabolic fuel for th
142 ments and proteomic analysis of the purified lipid bodies suggest that these processes are limited to
143        Unexpectedly, the gim1-1 mutant lacks lipid bodies, suggesting a heretofore unknown role of th
144  co-localization of cPLA2 and MAP kinases at lipid bodies was confirmed by subcellular fractionation
145 ted the effects of resistant starch on blood lipids, body weight, and defining resistant starch-induc
146                                        Serum lipids, body weight, and glucose metabolism were the sam
147 ases in hyperglycemia and decreases in serum lipids, body weight, and SAT, with preserved VAT and mus
148 stigated the impact of glucomannan on plasma lipids, body weight, fasting blood glucose (FBG), and bl
149       A low systolic blood pressure, altered lipids, body weight, higher VPT, and gender may determin
150  did not significantly change serum glucose, lipids, body weight, or fat mass.
151                               With time, the lipid bodies were metabolized in an ATP-dependent fashio
152 ent localization of newly formed eicosanoid, lipid bodies were the predominant sites of LTC(4) synthe
153 lised in the interior of tapetal cytoplasmic lipid bodies where they were associated with a regular h
154 e lysosome and promoting the accumulation of lipid bodies, which serve as a bacterial source of nutri
155 es promotes the coupling of lipolysis within lipid bodies with peroxisomal fatty acid oxidation.
156 asurements indicate that the chlorosome is a lipid body with a rod-like shape, and that the self-asse

 
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