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1 ely, PTG did not affect PP1 activity against hormone-sensitive lipase.
2 -stimulated cholesterol esterase and not the hormone-sensitive lipase.
3 are blocked by pharmacological inhibition of hormone-sensitive lipase.
4 nses were correlated with phosphorylation of hormone-sensitive lipase.
5 substrate for the consecutive hydrolysis by hormone-sensitive lipase.
6 ctivation of adipose triglyceride lipase and hormone-sensitive lipase.
7 lipolysis through an increased expression of hormone-sensitive lipase.
8 ts RE hydrolysis catalyzed by GS2 lipase and hormone-sensitive lipase.
9 t the hormonally regulated redistribution of hormone-sensitive lipase.
11 nd fatty acid oxidation, while inhibition of hormone-sensitive lipase activity results in a reduction
12 sis, measured by free fatty acid release and hormone-sensitive lipase activity, and lipogenesis, meas
15 ission, and phosphorylation of perilipin and hormone sensitive lipase - all hallmarks of lipolysis.
16 rotein levels of the key lipolytic effectors hormone-sensitive lipase and adipose triglyceride lipase
17 n increased expression of the genes encoding hormone-sensitive lipase and adipose triglyceride lipase
18 blocks leptin-stimulated phosphorylation of hormone-sensitive lipase and consequent lipolysis, as do
19 s in adipocytes to induce phosphorylation of hormone-sensitive lipase and consequently activate lipol
20 s showed that SR1555 inhibited activation of hormone-sensitive lipase and increased fatty acid oxidat
22 pogenesis, which are controlled primarily by hormone-sensitive lipase and lipoprotein lipase (LPL), r
23 lpha-mediated reduction in protein levels of hormone-sensitive lipase and perilipin A, two proteins i
24 dence has accrued of the interaction between hormone-sensitive lipase and perilipin, the protein that
26 vimentin), or almost completely eliminated (hormone-sensitive lipase and proteins >93 kDa) in the is
28 ripheral droplets are the sites of attack by hormone-sensitive lipase, and 3) perilipin and hormone-s
29 RgammaKO CR mice showed lower levels of both hormone-sensitive lipase, and its phosphorylated form.
30 olysis through reversible phosphorylation of hormone-sensitive lipase, and simultaneously inhibit LPL
31 ter-4, hexokinase-2, muscle-pyruvate kinase, hormone-sensitive lipase, and uncoupling proteins-2 and
32 l TG-transfer protein (MTP), hepatic lipase, hormone-sensitive lipase, apolipoprotein (apo) B, apo CI
33 rmone-sensitive lipase, and 3) perilipin and hormone-sensitive lipase are continuously colocalized fo
34 in-protein interaction between AFABP/aP2 and hormone sensitive lipase but does not activate PPARgamma
35 nzymes, adipose triglyceride (TG) lipase and hormone-sensitive lipase, by self-sustained adipocyte cl
36 est that the cardiomyocyte clock inactivates hormone-sensitive lipase during the active/awake phase b
37 esses amino acid domains homologous with the hormone-sensitive lipase family and the conserved active
39 reased the basal mRNA level of hexokinase-2, hormone sensitive lipase, glutathione peroxidase-1, and
41 vious in vitro studies have established that hormone sensitive lipase (HSL) and adipocyte fatty acid-
42 ipolysis secondary to enhanced expression of hormone sensitive lipase (HSL) and beta3-adrenergic (Adr
43 ein lipase (LPL), fatty acid synthase (FAS), hormone sensitive lipase (HSL) and perilipin 1 (PLIN1),
44 mRNA concentrations were also determined for hormone sensitive lipase (HSL), perilipin (lipid droplet
46 re assessed by protein expression studies of hormone-sensitive lipase (HSL) (84 kDa) and lipoprotein
47 that adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) act sequentially in catal
48 We tested the hypothesis that the actions of hormone-sensitive lipase (HSL) affect the microenvironme
51 AFABP/aP2) forms a physical complex with the hormone-sensitive lipase (HSL) and AFABP/aP2-null mice e
52 nt protein kinase (PKA) which phosphorylates hormone-sensitive lipase (HSL) and increases adipocyte l
54 is requires the phosphorylation of cytosolic hormone-sensitive lipase (HSL) and perilipin 1 (Plin1) i
55 nificant decreases of cAMP levels and of the hormone-sensitive lipase (HSL) and perilipin phosphoryla
56 mice also show defective phosphorylation of hormone-sensitive lipase (HSL) at S565, with higher phos
58 vation of adipocytes is the translocation of hormone-sensitive lipase (HSL) from the cytosol to the s
59 n in a manner that depended on activation of hormone-sensitive lipase (HSL) in cultured adipocytes an
60 ion of perilipin-2 and decreased activity of hormone-sensitive lipase (HSL) in HCV-infected hepatocyt
69 easured insulin-stimulated glucose uptake in hormone-sensitive lipase (HSL) knockout (KO) mice after
71 that adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) plays in the induction of
74 meshift deletion in exon 9 of LIPE, encoding hormone-sensitive lipase (HSL), a key enzyme for lipolys
75 ), and LSDP5, control lipolysis catalyzed by hormone-sensitive lipase (HSL), a major lipase in adipoc
76 e hydrolyzed by a cAMP-dependent enzyme like hormone-sensitive lipase (HSL), in separate studies, we
77 ssion of adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL), lipolysis, lipogenesis,
78 in, genes encoding lipoprotein lipase (LPL), hormone-sensitive lipase (HSL), peroxisome proliferator-
79 he phosphorylation of another PKA substrate, hormone-sensitive lipase (HSL), remains Akt dependent.
80 results in the phosphorylation of Peri A and hormone-sensitive lipase (HSL), the predominant lipase i
81 represents the critical second messenger and hormone-sensitive lipase (HSL), the rate-determining enz
82 , diacylglycerol acyltransferase (DGAT), and hormone-sensitive lipase (HSL), three key enzymes of lip
89 pressions of adipose triglyceride lipase and hormone sensitive lipase in adipose tissue further corro
90 polysis, cAMP levels, and phosphorylation of hormone sensitive lipase in response to isoproterenol or
93 f perilipin, a major lipid coat protein, and hormone-sensitive lipase in three preparations that exhi
94 ymes identified in both preparations include hormone-sensitive lipase, lanosterol synthase, NAD(P)-de
95 rase for short fatty acyl chains, similar to hormone-sensitive-lipase-like proteins that share less t
96 d decreased expression of lipolytic enzymes (hormone-sensitive lipase, lipoprotein lipase, and fatty
97 f adipocyte-abundant genes, including GLUT4, hormone sensitive lipase, long-chain fatty acyl-CoA synt
98 nd does not inhibit other lipases, including hormone-sensitive lipase, monoacylglycerol lipase, lipop
99 se macrophages, which showed the presence of hormone-sensitive lipase mRNA but not the bile salt-stim
102 ormal norepinephrine-stimulated p38 MAPK and hormone-sensitive lipase phosphorylation and Pgc1a and U
103 enol-stimulated increases in cAMP levels and hormone-sensitive lipase phosphorylation in human adipoc
104 The demonstration that adipocytes lacking hormone-sensitive lipase still display lipolysis has led
105 horylation of perilipin and translocation of hormone-sensitive lipase to the surfaces of lipid drople
108 results in the reversible phosphorylation of hormone-sensitive lipase, which is the primary mediator
109 In contrast, oligonucleotide primers for hormone-sensitive lipase yielded positive reactions only
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