ライフサイエンスコーパス: hormone-sensitive lipase

1 tion of both adipose triglyceride lipase and hormone sensitive lipase.

2 t the hormonally regulated redistribution of hormone-sensitive lipase.

3 ely, PTG did not affect PP1 activity against hormone-sensitive lipase.

4 -stimulated cholesterol esterase and not the hormone-sensitive lipase.

5 ytic enzymes adipose triglyceride lipase and hormone-sensitive lipase.

6 are blocked by pharmacological inhibition of hormone-sensitive lipase.

7 nses were correlated with phosphorylation of hormone-sensitive lipase.

8 substrate for the consecutive hydrolysis by hormone-sensitive lipase.

9 ctivation of adipose triglyceride lipase and hormone-sensitive lipase.

10 lipolysis through an increased expression of hormone-sensitive lipase.

11 ts RE hydrolysis catalyzed by GS2 lipase and hormone-sensitive lipase.

12 Adiponectin suppressed hormone-sensitive lipase activation without altering adi

13 nd fatty acid oxidation, while inhibition of hormone-sensitive lipase activity results in a reduction

14 sis, measured by free fatty acid release and hormone-sensitive lipase activity, and lipogenesis, meas

15 adipocytes in a manner that also depends on hormone-sensitive lipase activity.

16 Moreover, GE induced the expressions of hormone-sensitive lipase, adipose triglyceride lipase en

17 ission, and phosphorylation of perilipin and hormone sensitive lipase - all hallmarks of lipolysis.

18 Adipose triglyceride lipase, but not hormone sensitive lipase, also has transacylation activi

19 factors that regulate lipid metabolism (e.g. hormone sensitive lipase and fatty acid translocase; P <

20 rotein levels of the key lipolytic effectors hormone-sensitive lipase and adipose triglyceride lipase

21 n increased expression of the genes encoding hormone-sensitive lipase and adipose triglyceride lipase

22 blocks leptin-stimulated phosphorylation of hormone-sensitive lipase and consequent lipolysis, as do

23 s in adipocytes to induce phosphorylation of hormone-sensitive lipase and consequently activate lipol

24 s showed that SR1555 inhibited activation of hormone-sensitive lipase and increased fatty acid oxidat

25 as indicated by elevated phosphorylation of hormone-sensitive lipase and increased lipolysis.

26 pogenesis, which are controlled primarily by hormone-sensitive lipase and lipoprotein lipase (LPL), r

27 lpha-mediated reduction in protein levels of hormone-sensitive lipase and perilipin A, two proteins i

28 dence has accrued of the interaction between hormone-sensitive lipase and perilipin, the protein that

29 hich stimulates lipolysis by phosphorylating hormone-sensitive lipase and perilipin.

30 vimentin), or almost completely eliminated (hormone-sensitive lipase and proteins >93 kDa) in the is

31 The homology of AADA with hormone-sensitive lipase and the tissue distribution of

32 id droplets, LD-associated perilipins 2/3/5, hormone-sensitive lipase, and 1-acylglycerol-3-phosphate

33 ripheral droplets are the sites of attack by hormone-sensitive lipase, and 3) perilipin and hormone-s

34 RgammaKO CR mice showed lower levels of both hormone-sensitive lipase, and its phosphorylated form.

35 olysis through reversible phosphorylation of hormone-sensitive lipase, and simultaneously inhibit LPL

36 ter-4, hexokinase-2, muscle-pyruvate kinase, hormone-sensitive lipase, and uncoupling proteins-2 and

37 l TG-transfer protein (MTP), hepatic lipase, hormone-sensitive lipase, apolipoprotein (apo) B, apo CI

38 rmone-sensitive lipase, and 3) perilipin and hormone-sensitive lipase are continuously colocalized fo

39 in-protein interaction between AFABP/aP2 and hormone sensitive lipase but does not activate PPARgamma

40 nzymes, adipose triglyceride (TG) lipase and hormone-sensitive lipase, by self-sustained adipocyte cl

41 ental datasets, including P001-Y, Na(X), and hormone-sensitive lipase dimer, all affected by preferre

42 est that the cardiomyocyte clock inactivates hormone-sensitive lipase during the active/awake phase b

43 esses amino acid domains homologous with the hormone-sensitive lipase family and the conserved active

44 ed expression of beta-adrenergic receptor or hormone-sensitive lipase genes.

45 reased the basal mRNA level of hexokinase-2, hormone sensitive lipase, glutathione peroxidase-1, and

46 Murine carboxylesterases and hormone sensitive lipase have been shown to have this ac

47 vious in vitro studies have established that hormone sensitive lipase (HSL) and adipocyte fatty acid-

48 ipolysis secondary to enhanced expression of hormone sensitive lipase (HSL) and beta3-adrenergic (Adr

49 ein lipase (LPL), fatty acid synthase (FAS), hormone sensitive lipase (HSL) and perilipin 1 (PLIN1),

50 Early enzymatic studies showed that hormone sensitive lipase (HSL) hydrolyzes luteal cholest

51 mRNA concentrations were also determined for hormone sensitive lipase (HSL), perilipin (lipid droplet

52 zymes adipose triglyceride lipase (ATGL) and hormone sensitive lipase (HSL).

53 mic reticulum (ER) stress triggers excessive hormone sensitive lipases (HSL) mediated lipolysis which

54 re assessed by protein expression studies of hormone-sensitive lipase (HSL) (84 kDa) and lipoprotein

55 that adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) act sequentially in catal

56 We tested the hypothesis that the actions of hormone-sensitive lipase (HSL) affect the microenvironme

57 The hormone-sensitive lipase (HSL) and adipocyte fatty acid-

58 In this study, we have demonstrated that hormone-sensitive lipase (HSL) and adipose triglyceride

59 AFABP/aP2) forms a physical complex with the hormone-sensitive lipase (HSL) and AFABP/aP2-null mice e

60 nt protein kinase (PKA) which phosphorylates hormone-sensitive lipase (HSL) and increases adipocyte l

61 in kinase (PKA)-stimulated lipolysis by both hormone-sensitive lipase (HSL) and non-HSL(s).

62 is requires the phosphorylation of cytosolic hormone-sensitive lipase (HSL) and perilipin 1 (Plin1) i

63 nificant decreases of cAMP levels and of the hormone-sensitive lipase (HSL) and perilipin phosphoryla

64 mice also show defective phosphorylation of hormone-sensitive lipase (HSL) at S565, with higher phos

65 Hormone-sensitive lipase (HSL) catalyzes the hydrolysis

66 vation of adipocytes is the translocation of hormone-sensitive lipase (HSL) from the cytosol to the s

67 n in a manner that depended on activation of hormone-sensitive lipase (HSL) in cultured adipocytes an

68 ion of perilipin-2 and decreased activity of hormone-sensitive lipase (HSL) in HCV-infected hepatocyt

69 ence of the importance of lipid droplets and hormone-sensitive lipase (HSL) in regulating the aggress

70 Hormone-sensitive lipase (HSL) is a cytosolic neutral li

71 Hormone-sensitive lipase (HSL) is a cytosolic neutral li

72 Hormone-sensitive lipase (HSL) is a cytosolic neutral li

73 Hormone-sensitive lipase (HSL) is a rate-limiting enzyme

74 Hormone-sensitive lipase (HSL) is a vital enzyme in lipi

75 Hormone-sensitive lipase (HSL) is an intracellular lipas

76 Hormone-sensitive lipase (HSL) is responsible for the ne

77 Hormone-sensitive lipase (HSL) is the predominant lipase

78 easured insulin-stimulated glucose uptake in hormone-sensitive lipase (HSL) knockout (KO) mice after

79 Hormone-sensitive lipase (HSL) mediates the hydrolysis o

80 that adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) plays in the induction of

81 In this study, we show that Hormone-sensitive lipase (Hsl) specifically controls SE

82 Mice lacking ATGL or hormone-sensitive lipase (HSL) were challenged with a me

83 This reaction is mediated by hormone-sensitive lipase (HSL), a cytosolic enzyme, and

84 meshift deletion in exon 9 of LIPE, encoding hormone-sensitive lipase (HSL), a key enzyme for lipolys

85 ), and LSDP5, control lipolysis catalyzed by hormone-sensitive lipase (HSL), a major lipase in adipoc

86 ein 1 (SREBP-1), fatty acid synthase (FASN), hormone-sensitive lipase (HSL), and acyl dehydrogenases

87 e hydrolyzed by a cAMP-dependent enzyme like hormone-sensitive lipase (HSL), in separate studies, we

88 ases, adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in TAG estolide and FAHF

89 ssion of adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL), lipolysis, lipogenesis,

90 in, genes encoding lipoprotein lipase (LPL), hormone-sensitive lipase (HSL), peroxisome proliferator-

91 he phosphorylation of another PKA substrate, hormone-sensitive lipase (HSL), remains Akt dependent.

92 results in the phosphorylation of Peri A and hormone-sensitive lipase (HSL), the predominant lipase i

93 represents the critical second messenger and hormone-sensitive lipase (HSL), the rate-determining enz

94 , diacylglycerol acyltransferase (DGAT), and hormone-sensitive lipase (HSL), three key enzymes of lip

95 We investigated the effects of leptin on hormone-sensitive lipase (HSL), which acts as a neutral

96 and utilization of LD through regulation of hormone-sensitive lipase (HSL), which was downregulated

97 Lipotransin is a novel hormone-sensitive lipase (HSL)-interacting protein that

98 ylation of cholesterol-ester hydrolase (CEH)/hormone-sensitive lipase (HSL).

99 bolism in mice, nor the "downstream" lipase, hormone-sensitive lipase (HSL).

100 on of fatty acid-binding protein (FABP) with hormone-sensitive lipase (HSL).

101 pases adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL).

102 pressions of adipose triglyceride lipase and hormone sensitive lipase in adipose tissue further corro

103 polysis, cAMP levels, and phosphorylation of hormone sensitive lipase in response to isoproterenol or

104 ing phosphorylation and translocation of the hormone-sensitive lipase in 3T3-L1 adipocytes.

105 Genetic knockout of hormone-sensitive lipase in mice has implicated the pres

106 f perilipin, a major lipid coat protein, and hormone-sensitive lipase in three preparations that exhi

107 ymes identified in both preparations include hormone-sensitive lipase, lanosterol synthase, NAD(P)-de

108 rase for short fatty acyl chains, similar to hormone-sensitive-lipase-like proteins that share less t

109 d decreased expression of lipolytic enzymes (hormone-sensitive lipase, lipoprotein lipase, and fatty

110 f adipocyte-abundant genes, including GLUT4, hormone sensitive lipase, long-chain fatty acyl-CoA synt

111 nd does not inhibit other lipases, including hormone-sensitive lipase, monoacylglycerol lipase, lipop

112 se macrophages, which showed the presence of hormone-sensitive lipase mRNA but not the bile salt-stim

113 n adipose triglyceride lipase (ATGL) and not hormone-sensitive lipase or monoacylglycerol lipase.

114 associated with altered expression levels of hormone-sensitive lipase or perilipin.

115 ha, and adiponectin) and lipid accumulation (hormone-sensitive lipase, perilipin A, and LDs).

116 ormal norepinephrine-stimulated p38 MAPK and hormone-sensitive lipase phosphorylation and Pgc1a and U

117 enol-stimulated increases in cAMP levels and hormone-sensitive lipase phosphorylation in human adipoc

118 The demonstration that adipocytes lacking hormone-sensitive lipase still display lipolysis has led

119 related genes, including LIPE, which encodes hormone sensitive lipase, the rate-limiting enzyme in li

120 horylation of perilipin and translocation of hormone-sensitive lipase to the surfaces of lipid drople

121 Furthermore, increased expression of hormone-sensitive lipase was measured with CD36 expressi

122 ceride lipase (ATGL) nor phosphorylations of hormone-sensitive lipase were altered.

123 acids, glycerol, and the phosphorylation of hormone-sensitive lipase were attenuated in iWAT of Gcgr

124 results in the reversible phosphorylation of hormone-sensitive lipase, which is the primary mediator

125 In contrast, oligonucleotide primers for hormone-sensitive lipase yielded positive reactions only