ライフサイエンスコーパス: lipid body

1 core surface of a cellular organelle named 'lipid body'.

2 the form of intracellular inclusions termed 'lipid bodies'.

3 ed the formation and function of cytoplasmic lipid bodies.

4 at the oleosin was largely restricted to the lipid bodies.

5 ne, GIM1, that is able to restore import and lipid bodies.

6 G) E2 and LTB4 correlated with the number of lipid bodies.

7 cally diagnosed as organizing pneumonia with lipid bodies.

8 nd contribute to CE formation for storage in lipid bodies.

9 LO and LTC(4) S at perinuclear locations and lipid bodies.

10 d (FA) synthesis during the expansion of the lipid bodies.

11 into the PV or esterifies it for storage in lipid bodies.

12 is in turn required for breakdown of TAG in lipid bodies.

13 ic reticulum (ER) and subsequent transfer to lipid bodies.

14 5beta PI3K subunits were present at isolated lipid bodies.

15 l eicosanoid production through formation of lipid bodies.

16 ls of cPLA2 and contain numerous cytoplasmic lipid bodies.

17 osolic phospholipase A2 (cPLA2) localizes at lipid bodies.

18 ases, including ERK1, ERK2, p85, and p38, in lipid bodies.

19 ncordant with fluorescent fatty-acid-labeled lipid bodies.

20 ivated protein (MAP) kinases, co-localize at lipid bodies.

21 n was present mostly on the periphery of the lipid bodies.

22 addition, mutant etfb(-) displayed elevated lipid body accumulation and reduced ATP synthesis.

23 hat deletion of this TF results in increased lipid body accumulation, and that ATF3 directly regulate

24 e details in cell shape, cytoplasm, nucleus, lipid bodies and cytoskeletal structures in 3D with unpr

25 as a model system, we provide evidence that lipid bodies and peroxisomes have a close physiological

26 eroxisomes oxidize lipids, the metabolism of lipid bodies and peroxisomes is thought to be largely un

27 CAT2 parasites have reduced CE levels, fewer lipid bodies, and accumulate free cholesterol, which cau

28 tion of thylakoid membranes, accumulation of lipid bodies, and alterations of cell-surface morphology

29 led that evident changes in starch granules, lipid bodies, and cell walls thickness of the SAM in C.

30 formation, intracellular LTC(4) formation at lipid bodies, and priming for enhanced calcium ionophore

31 Peroxisomes adhere stably to lipid bodies, and they can even extend processes into li

32 s in membrane lipids, which are deposited in lipid bodies; and (5) when sinks for photosynthetic ener

33 esis and sequestration of TAG into cytosolic lipid bodies appear to be a protective mechanism by whic

34 Lipid bodies are eukaryotic structures for temporary sto

35 Lipid bodies are inducible lipid domains abundantly pres

36 Because lipid bodies are potential reservoirs of esterified arac

37 Thus, lipid bodies are structurally distinct, inducible, nonnu

38 ding proteins, cellular cholesterol sensors, lipid-body-associated proteins and secreted autocrine fa

39 nts and composition of the transformed yeast lipid bodies but replaced some of the native proteins as

40 110beta catalytic subunits were localized to lipid bodies by immunocytochemistry and/or immunoblottin

41 Overall reorientation of the lipid body, consisting of the phosphorus, glycerol, and

42 ies, and they can even extend processes into lipid body cores.

43 Lipid bodies, cytoplasmic inclusions that develop in cel

44 rotein kinases both elicits the formation of lipid body domains and promotes LTC(4) formation at thes

45 of eosinophils and moves to the granules and lipid bodies during fMLP-mediated activation.

46 op into spores, while cells that do not form lipid bodies end up becoming peripheral rods, which are

47 or stimulation of human PMN with PAF to form lipid bodies enhanced eicosanoid production in response

48 ed three multivariate factors interpreted as lipids, body fat/insulin/glucose/CRP, and blood pressure

49 Lipid bodies form autonomous intracellular structures in

50 LL-37 stimulates lipid body formation and activates cys-LT-synthesizing e

51 Chemokine-induced lipid body formation and enhanced LTC(4) release were bo

52 in this study that IgG or IL-5 also induces lipid body formation and subsequent leukotriene C4 produ

53 Aspirin and NSAIDs inhibited both induced lipid body formation and the enhanced capacity for formi

54 heximide inhibited not only the induction of lipid body formation by PAF, but also the PAF-induced "p

55 We demonstrate that macrophage lipid body formation can be induced by modified lipoprot

56 late, was as potent as aspirin in inhibiting lipid body formation elicited by cis-fatty acids.

57 re, 5-HETE was equally effective in inducing lipid body formation in both wild-type and 5-LO genetica

58 Lipid body formation in eosinophils was a rapidly (<1 h)

59 X inhibition, inhibit cis-fatty acid-induced lipid body formation in leukocytes and in concert inhibi

60 arachidonic and oleic acids) rapidly induced lipid body formation in leukocytes, and this lipid body

61 Moreover, it appears that lipid body formation in M. xanthus is an important initi

62 mes may localize, we evaluated mechanisms of lipid body formation in neutrophils (PMN).

63 Our studies indicate that lipid body formation is an inducible early response in l

64 y, NSAIDs inhibited arachidonic acid-induced lipid body formation likewise in macrophages from wild-t

65 Corroborating the dependency of PAF-induced lipid body formation on 5-LO, PMN and macrophages from w

66 e inhibitory effect of aspirin and NSAIDs on lipid body formation was independent of cyclooxygenase (

67 Second, cis-fatty acid-induced lipid body formation was not impaired in macrophages fro

68 The 5-LO product inducing lipid body formation was not LTB4 but was 5(S)-hydroxyei

69 Both PAF- and 5(S)-HETE-induced lipid body formation were inhibited by protein kinase C

70 dose dependently (0.01-100 nM) elicited new lipid body formation, intracellular LTC(4) formation at

71 hr concordantly with cis-fatty acid-induced lipid body formation.

72 ive proteins were associated with a floating lipid body fraction obtained from a tapetal/locular flui

73 Lipid body fractions free of cytosol and other organelle

74 fatty acids promote novel structures within lipid bodies ("gnarls"), which may be organized arrays o

75 Formed at the onset of starvation, these lipid bodies gradually disappear until they are complete

76 erculosis, and accumulation of intracellular lipid bodies has been proposed to identify a persister p

77 Retinosomes, particles reminiscent of lipid bodies, have been identified in retinal pigment ep

78 localized to native as well as newly induced lipid bodies in intact and enucleated eosinophils.

79 overed an unexpected function of Viperin and lipid bodies in interferon induction by Toll-like recept

80 iated signaling is active within cytoplasmic lipid bodies in leukocytes.

81 TLR stimulation promotes the accumulation of lipid bodies in macrophages and consequently foam cell f

82 ignalling pathways modulate the formation of lipid bodies in macrophages and thereby cellular accumul

83 , the compartmentalization of lipids to form lipid bodies in PMN is dependent on specific cellular re

84 iene (LT) B4, induced the rapid formation of lipid bodies in PMN.

85 PpoA localizes in lipid bodies in these tissues.

86 t plant oleosin is correctly targeted to the lipid bodies in transformed yeast and that yeast may be

87 t oleosin could be correctly targeted to the lipid bodies in transformed yeast.

88 spholipids or SDS, did not bind to the yeast lipid bodies in vitro.

89 he ER and hence subsequent deposition on the lipid bodies in vivo.

90 The lipid bodies in yeast have not been previously subjected

91 o a distinct intracellular site, cytoplasmic lipid bodies, in leukocytes.

92 These observations suggest that lipid bodies, including retinosomes, carry out specific

93 associated with phosphorylated Lyn kinase in lipid bodies induced to form in human polymorphonuclear

94 Lipid body induction by PAF required 5-lipoxygenase (LO)

95 lipid body formation in leukocytes, and this lipid body induction was inhibited by aspirin and nonste

96 bpopulations of cells occur: cells that form lipid bodies invariably develop into spores, while cells

97 tant for rotation about the long axis of the lipid body, is difficult to determine precisely because

98 DCs in tumor-bearing hosts accumulate lipid bodies (LB) containing electrophilic oxidatively t

99 Lipid bodies (LB; lipid droplets) are cytoplasmic organe

100 Newly lipid body (LB)-associated proteins included MRP-14, pot

101 Lipid bodies (LBs) in the coral gastrodermal tissues are

102 Lipid bodies (LBs), multifunctional organelles present i

103 Lipid bodies, lipid rich cytoplasmic inclusions, are cha

104 moking, fasting status, month of blood draw, lipids, body mass index, and other cardiovascular diseas

105 BP, serum lipids, body mass index, and smoking were assessed in al

106 After adjustment for age, education, lipids, body mass index, smoking, diabetes, hypertension

107 in resistance; fasting glucose, insulin, and lipids; body mass index (BMI); and blood pressure.

108 lly activating protein kinases suggests that lipid bodies may be structurally distinct intracellular

109 and LTB4 production in PMN, the induction of lipid bodies may have a role in the formation of eicosan

110 These data indicate that lipid bodies not only fuel cellular differentiation but

111 ed eosinophils, the PAF-induced increases in lipid body numbers correlated with enhanced production o

112 Chemokine-elicited lipid body numbers correlated with increased calcium ion

113 Since increases in lipid body numbers correlated with priming for enhanced

114 Arachidonic and oleic acid-induced lipid body numbers correlated with the enhanced levels o

115 Our results show that BaP accumulates in the lipid bodies of Chlorella sp. and that there is Forster

116 ompartmentalization within arachidonate-rich lipid bodies of cPLA2 and its potentially activating pro

117 sinophils and the synthesis at intracellular lipid bodies of LTC(4), the dominant 5-lipoxygenase-deri

118 ally accumulate within the large cytoplasmic lipid bodies of tapetal cells.

119 d with DGAT activity, were isolated from the lipid bodies of the oleaginous fungus Mortierella ramann

120 from 5-LO genetically deficient mice, formed lipid bodies on exposure to PAF both in vitro and in viv

121 roplets in plants (also known as oil bodies, lipid bodies, or oleosomes) are well characterized in se

122 ing the induced formation of new cytoplasmic lipid body organelles.

123 sugar, and storage triacylglycerol (TAG) and lipid bodies persist in green cotyledons.

124 um cultures and calculated the percentage of lipid body-positive acid-fast bacilli (%LB + AFB) on spu

125 om wild-type cells initiates development and lipid body production in a csgA mutant to bypass the mut

126 ive physical contact between peroxisomes and lipid bodies promotes the coupling of lipolysis within l

127 ration processes, including seed-storage and lipid-body proteins.

128 Here, we present evidence that intracellular lipid bodies provide the necessary metabolic fuel for th

129 ments and proteomic analysis of the purified lipid bodies suggest that these processes are limited to

130 Unexpectedly, the gim1-1 mutant lacks lipid bodies, suggesting a heretofore unknown role of th

131 co-localization of cPLA2 and MAP kinases at lipid bodies was confirmed by subcellular fractionation

132 ted the effects of resistant starch on blood lipids, body weight, and defining resistant starch-induc

133 Serum lipids, body weight, and glucose metabolism were the sam

134 stigated the impact of glucomannan on plasma lipids, body weight, fasting blood glucose (FBG), and bl

135 did not significantly change serum glucose, lipids, body weight, or fat mass.

136 With time, the lipid bodies were metabolized in an ATP-dependent fashio

137 ent localization of newly formed eicosanoid, lipid bodies were the predominant sites of LTC(4) synthe

138 lised in the interior of tapetal cytoplasmic lipid bodies where they were associated with a regular h

139 e lysosome and promoting the accumulation of lipid bodies, which serve as a bacterial source of nutri

140 es promotes the coupling of lipolysis within lipid bodies with peroxisomal fatty acid oxidation.

141 asurements indicate that the chlorosome is a lipid body with a rod-like shape, and that the self-asse