ライフサイエンスコーパス: ATGL

1 ATGL and HSL are robustly expressed by adipocytes that w

2 ATGL biosynthetic transacylase activity is present in hu

3 ATGL could constitute a new therapeutic strategy to targ

4 ATGL deficient INS1 cells and human pseudoislets showed

5 ATGL gene mutations cause a severe phenotype especially

6 ATGL inhibition induced metabolic plasticity, causing a

7 ATGL promotes prostate cancer metabolic plasticity and p

8 ATGL was further involved in transesterification and rem

9 ATGL-deficient INS1 cells and human pseudoislets showed

10 ected small hairpin RNAs demonstrate that 1) ATGL activity is required for all PKA-stimulated FA and

11 nabled ABHD4 (ABHD4 N303R/S332G) to activate ATGL in Cos7 cells, brown adipocytes, and artificial lip

12 1 restrain the ability of CGI-58 to activate ATGL under basal conditions.

13 In addition, ATGL mediates the effects of beta-adrenergic signaling o

14 Additionally, ATGL knockdown in HepG2 cells attenuated LPS/OP21-induce

15 tively disrupted lipolysis without affecting ATGL lipid droplet translocation or ABHD5 interactions w

16 sive lipolysis, and impairment of GSIS after ATGL silencing.

17 sive lipolysis, and impairment of GSIS after ATGL silencing.

18 ctivity of the HCV core protein with altered ATGL binding to CGI-58 and the enhanced association of b

19 Although ATGL deficiency is compatible with normal skin developme

20 Although ATGL gain and loss of function did not alter hepatic TAG

21 prevention of lipid overload occurred in an ATGL-dependent manner.

22 he proliferation and invasion, suggesting an ATGL-independent role of ABHD5 in modulating PCa aggress

23 ells expressing both ectopic perilipin 5 and ATGL showed a 3-fold increase in lipolysis following act

24 muscle lipolysis depends on both CGI-58 and ATGL.

25 ts a direct functional role for both HSL and ATGL in hepatic lipid homeostasis and identifies these e

26 ed 3-5 days after infection in both HSL- and ATGL-overexpressing male mice, suggesting an increase in

27 Gs and diacylglycerols in both wild-type and ATGL-deficient hepatocytes.

28 palmitoyltransferase 1 alpha) in both WT and ATGL KO mice.

29 Wild-type (WT) and ATGL knockout (KO) mice were challenged with tunicamycin

30 olysis independently of adipocyte-autonomous ATGL, and thereby worsen organ failure.

31 Because ATGL preferentially generates sn-1,3 and sn-2,3, it sugg

32 xpectedly, increased the interaction between ATGL and its activator CGI-58 as well as the recruitment

33 late an epidermal triglyceride lipase beyond ATGL required for the adequate provision of fatty acids

34 ased by ATGL overexpression and decreased by ATGL knockdown.

35 etion, fatty acid oxidation was increased by ATGL overexpression and decreased by ATGL knockdown.

36 cetylase activity is positively regulated by ATGL to promote PGC-1alpha signaling.

37 n) murine models of type 1 diabetes, cardiac ATGL protein expression and TAG content were significant

38 shows that after diabetes, increased cardiac ATGL expression is an adaptive, albeit insufficient, res

39 xamined whether alterations in cardiomyocyte ATGL impact cardiac function during uncontrolled type 1

40 ounced hepatic steatosis, dietary-challenged ATGL LKO mice showed lower hepatic inflammation, reflect

41 ounced hepatic steatosis, dietary-challenged ATGL LKO mice showed lower hepatic inflammation, reflect

42 hepatic phenotype in MCD- or LPS-challenged ATGL-knockout (KO) mice.

43 atohepatitis, and heart disease, classifying ATGL as a promising drug target.

44 diet (HFD)-induced obesity despite complete ATGL deficiency in WAT and normal adipocyte differentiat

45 Consequently, ATGL knockdown reduced maximal oxidation of fatty acids,

46 Genetic perturbation in the COP1-ATGL axis disrupts lipid homeostasis, leading to liver s

47 and the expression of Egr1 while decreasing ATGL levels in epididymal fat.

48 K-ASKO ablation show no changes in desnutrin/ATGL levels but have defective phosphorylation of desnut

49 es have been identified, including desnutrin/ATGL, greatly expanding our understanding of adipocyte l

50 lipase A(2) (PLA(2))zeta and mouse desnutrin/ATGL) has been described in adipose cells as a member of

51 phosphorylation and regulation of desnutrin/ATGL and HSL and thus adipose lipolysis.

52 have defective phosphorylation of desnutrin/ATGL at S406 to decrease its triacylglycerol (TAG) hydro

53 hat the evolutionarily conserved mTORC1-Egr1-ATGL regulatory pathway represents an important componen

54 utrophil-specific deletion of genes encoding ATGL or ATGL inhibitory factors altered neutrophil lipid

55 nd regulates its interaction with endogenous ATGL promotors.

56 with this mechanism, deletion of endothelial ATGL markedly increased lesion size in a model of athero

57 odel that core reduces lipolysis by engaging ATGL.

58 s redistribution of the key lipolytic enzyme ATGL to lipid droplets and increases lipolysis.

59 We used "healthy" AKO mice expressing ATGL exclusively in cardiomyocytes (AKO/cTg) to circumve

60 MCD-fed ATGL-KO mice, although partially protected from peripher

61 Mutations in the genes coding for ATGL or CGI-58 in humans cause neutral lipid storage dis

62 or CGI-58, indicating a predominant role for ATGL.

63 This peptide is highly selective for ATGL and does not inhibit other lipases, including hormo

64 In embryonic fibroblasts derived from ATGL KO mice, exogenous free fatty acids did not affect

65 been presumed that fatty acids derived from ATGL-catalyzed lipolysis act as PPAR-alpha ligands.

66 results demonstrate a crucial role for FSP27-ATGL interactions in regulating lipolysis, triglyceride

67 Knocking down hepatic ATGL completely abrogated the increase in serum insulin

68 Hence, we tested the contribution of hepatic ATGL on mediating glucose tolerance and insulin action.

69 Adenovirus-mediated knockdown of hepatic ATGL resulted in steatosis in mice and decreased hydroly

70 target genes in mice with suppressed hepatic ATGL expression.

71 Mice with suppressed hepatic ATGL had reduced hepatic glucose production in vivo, and

72 en together, these data suggest that hepatic ATGL knockdown enhances glucose tolerance by increasing

73 reptozotocin-diabetic mice with heterozygous ATGL deficiency and cardiomyocyte-specific ATGL overexpr

74 reptozotocin-diabetic mice with heterozygous ATGL deficiency displayed increased TAG accumulation, li

75 fully capable of inhibiting mouse and human ATGL.

76 the first small-molecule inhibitor of human ATGL.

77 In humans, ATGL deficiency causes neutral lipid storage disease wit

78 In addition to altering TAG hydrolysis, ATGL was shown to play a significant role in partitionin

79 TM increased hepatic TG accumulation in ATGL KO, but not in WT, mice.

80 ic lipolysis and increased PPARd activity in ATGL/PNPLA2 deficiency may counteract hepatic inflammati

81 ipolysis and increased PPARdelta activity in ATGL/PNPLA2 deficiency may counteract hepatic inflammati

82 The marked increase in ATGL protein levels in cardiac muscle of CGI-58KOM mice

83 down-regulated by TM in WT and even more in ATGL KO mice, which displayed strongly reduced serum VLD

84 ted likely through reduced palmitoylation in ATGL deficient INS1 cells.

85 ted likely through reduced palmitoylation in ATGL-deficient INS1 cells.

86 inositol-requiring enzyme 1a were reduced in ATGL LKO mice fed with MCD diet.

87 itol-requiring enzyme 1alpha were reduced in ATGL LKO mice fed with MCD diet.

88 hanges in PAT composition but also increased ATGL, suggesting a relative PAT deficiency.

89 dentification-58 (CGI-58) strongly increased ATGL-mediated TG catabolism in cell culture experiments.

90 xidative metabolism in response to increased ATGL-mediated lipolysis.

91 To determine whether increased ATGL expression during diabetes is detrimental or benefi

92 sts with FoxO1-encoding lentivirus increases ATGL expression and renders it sensitive to regulation b

93 down of Egr1 in 4E-BP1/2-null MEFs increases ATGL expression and decreases fat storage.

94 oth PKA activation and isoproterenol-induced ATGL translocation to the LD periphery.

95 Thus, by inhibiting ATGL, HIG2 acts downstream of HIF-1 to sequester FAs in

96 on AMPK activation was blocked by inhibiting ATGL, the rate-limiting enzyme for triacylglycerol hydro

97 eptide corresponding to this region inhibits ATGL in a noncompetitive manner in the nanomolar range.

98 lates, but forced expression of SRA inhibits ATGL expression and free fatty acids (FFA) beta-oxidatio

99 SRA inhibits ATGL promoter activity, primarily by inhibiting the othe

100 Hepatocyte-specific ATGL knockout (ATGL LKO) mice were challenged with methionine-choline-d

101 Mice lacking ATGL or hormone-sensitive lipase (HSL) were challenged w

102 ts in adipose tissue, compatible with latent ATGL stimulation.

103 we show that 4E-BP1/2-null MEFs express less ATGL and accumulate more fat than control cells, while k

104 We provide an alternate mechanism that links ATGL to PPAR-alpha signaling.

105 ysis as indicated by elevation of the lipase ATGL, the lipolysis marker glycerol and release of fatty

106 ivation of the conserved triglyceride lipase ATGL-1, triggers a feedback transcriptional loop that in

107 t loss via the adipocyte triglyceride lipase ATGL-1.

108 at deletion of the enzyme adipose TG lipase (ATGL) in the endothelium led to neutral lipid accumulati

109 repressing the adipose triglyceride lipase (ATGL) activity in neutrophils in prostaglandin E2-depend

110 he discovery of adipose triglyceride lipase (ATGL) and comparative gene identification-58 (CGI-58) as

111 polytic enzymes adipose triglyceride lipase (ATGL) and hormone sensitive lipase (HSL).

112 udies show that adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) act sequentiall

113 d the role that adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) plays in the in

114 abolic lipases, adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in TAG estolid

115 tosolic lipases adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL).

116 Adipose triglyceride lipase (ATGL) and its coactivator comparative gene identificatio

117 dependent upon adipose triglyceride lipase (ATGL) and not hormone-sensitive lipase or monoacylglycer

118 have identified adipose triglyceride lipase (ATGL) as a major lipase in adipose tissue, although its

119 with increased adipose triglyceride lipase (ATGL) at the LD surface.

120 Adipose triglyceride lipase (ATGL) critically determines the release of fatty acids f

121 e LD-associated Adipose Triglyceride Lipase (ATGL) disrupts both actin bundle formation and cortical

122 rol hydrolysis, adipose triglyceride lipase (ATGL) has been proposed to influence the storage/product

123 Silencing adipose triglyceride lipase (ATGL) in human pseudoislets (shATGL) increased triglycer

124 Silencing adipose triglyceride lipase (ATGL) in human pseudoislets with shRNA targeting ATGL (s

125 have shown that adipose triglyceride lipase (ATGL) increases the activity of the nuclear receptor PPA

126 Adipose triglyceride lipase (ATGL) initiates intracellular triglyceride (TG) cataboli

127 Adipose triglyceride lipase (ATGL) is rate-limiting for the initial step of triacylgl

128 Adipose triglyceride lipase (ATGL) is the predominant triacylglycerol (TAG) hydrolase

129 lysis in global adipose triglyceride lipase (ATGL) knockout mice reduced free PAHSA levels and uncove

130 otein levels of adipose triglyceride lipase (ATGL) nor phosphorylations of hormone-sensitive lipase w

131 Adipose triglyceride lipase (ATGL) plays a key role in intracellular lipolysis, the m

132 ipolysis enzyme adipose triglyceride lipase (ATGL) resulted in large cytoplasmic LDs, whereas lysosom

133 In liver, adipose triglyceride lipase (ATGL) serves as a major triacylglycerol (TAG) lipase and

134 unaffected, and adipose triglyceride lipase (ATGL) was suppressed.

135 us inhibitor of adipose triglyceride lipase (ATGL), a key enzyme in intracellular lipolysis.

136 lipolysis by adipocyte triglyceride lipase (ATGL), a key lipase in adipocytes and non-adipose cells.

137 an inhibitor of adipose triglyceride lipase (ATGL), a key mediator of intracellular triacylglycerol (

138 vels of SRA and adipose triglyceride lipase (ATGL), a major hepatic triacylglycerol (TAG) hydrolase,

139 degradation of adipose triglyceride lipase (ATGL), a rate limiting enzyme of TAG hydrolysis.

140 t expression of adipose triglyceride lipase (ATGL), an enzyme that controls lipid droplet homeostasis

141 nase (POX), and adipose triglyceride lipase (ATGL), as well as markedly reduced lipid droplet size.

142 by attenuating adipose triglyceride lipase (ATGL), but repression of oncogene-induced transformation

143 polytic enzyme, adipose triglyceride lipase (ATGL), has two FoxO1-binding sites, and co-transfection

144 e expression of adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL), lipolysis, lipoge

145 l TAG hydrolase adipose triglyceride lipase (ATGL), in the regulation of cardiac lipolysis.

146 TAG hydrolase, adipose triglyceride lipase (ATGL), regulates baseline cardiac metabolism and functio

147 tive lipase and adipose triglyceride lipase (ATGL), suggesting a link between adipocyte oxygen sensin

148 ism mediated by adipose triglyceride lipase (ATGL), the key enzyme for intracellular lipolysis.

149 the activity of adipose triglyceride lipase (ATGL), the key lipolytic enzyme in the first step of TG

150 ) hydrolysis by adipose triglyceride lipase (ATGL), the major lipase in the liver.

151 ic inhibitor of adipose triglyceride lipase (ATGL), the rate-limiting enzyme for intracellular lipoly

152 express neither adipose triglyceride lipase (ATGL), the rate-limiting enzyme for triglyceride catabol

153 the activity of adipose triglyceride lipase (ATGL), the rate-limiting enzyme in triacylglycerol hydro

154 tes turnover of Adipose Triglyceride Lipase (ATGL), the rate-limiting lipolytic enzyme.

155 ipase (HSL) and adipose triglyceride lipase (ATGL), two enzymes critical for lipolysis in adipose tis

156 tic activity of adipose triglyceride lipase (ATGL), which catalyzes the hydrolysis of TGs to diacylgl

157 ed regulator of adipose triglyceride lipase (ATGL)-mediated lipolysis that plays important roles in m

158 n increase in adipocyte triglyceride lipase (ATGL)-mediated triglyceride breakdown and prolongation o

159 olonged drop in adipose triglyceride lipase (ATGL).

160 tic activity of adipose triglyceride lipase (ATGL).

161 he absence of adipocyte triglyceride lipase (ATGL).

162 ion, inhibiting adipose triglyceride lipase (ATGL)/patatin-like phospholipase domain containing 2 (PN

163 nteracting with adipose triglyceride lipase (ATGL, also called desnutrin or PNPLA2).

164 e we identified adipose triglyceride lipase (ATGL, also known as patatin-like phospholipase domain co

165 affect adipose or liver triglyceride lipase (ATGL, known also as Pnpla2) mRNA in Pnpla3(+/+) and Pnpl

166 lic regulators, adipose triglyceride lipase (ATGL/bmm) and transcriptional cofactor PGC-1.

167 Since adipose triglyceride lipase (ATGL/PNPLA2) is the key enzyme for intracellular hydroly

168 the absence of adipose triglyceride lipase (ATGL/PNPLA2)-the main enzyme for intracellular lipolysis

169 in (also called adipose triglyceride lipase [ATGL]) in adipocytes (aP2-desnutrin) and also performed

170 ranscription of adipose triglyceride lipase, ATGL.

171 he de novo lipogenic program and the lipases ATGL and HSL.

172 fasting in mice, and the expression of liver ATGL was induced by SRAKO under normal and high fat diet

173 After short hairpin RNA-mediated ATGL knockdown, HepG2 cells were treated with lipopolysa

174 contrast, myosin heavy chain promoter (MHC)-ATGL mice were resistant to diabetes-induced increases i

175 Moreover, hearts from diabetic MHC-ATGL mice exhibited decreased reliance on palmitate oxid

176 Moreover, ATGL-KO mice challenged by LPS showed enhanced hepatic i

177 into perilipin 5 by 2-fold, whereas neither ATGL nor CGI-58 was labeled under the incubation conditi

178 nduced exclusively in TM-treated WT, but not ATGL KO, mice.

179 Our studies establish perilipin 5 as a novel ATGL partner and provide evidence that the protein compo

180 hese effects were reversed by co-ablation of ATGL.

181 prevent excessive obesity in the absence of ATGL.

182 ulates lipolysis primarily via activation of ATGL expression.

183 ion to LDs and CGI-58-mediated activation of ATGL.

184 s and mobilizes CGI-58 for the activation of ATGL.

185 drolase domain containing-5, an activator of ATGL, and negatively with mRNA levels of lipid droplet p

186 e LD surface regulates lipolytic activity of ATGL.

187 ABHD5 is an essential coactivator of ATGL, the rate-limiting triglyceride (TG) lipase in many

188 The compatibility of ATGL deficiency with normal epidermal function indicated

189 Thus, we tested the contribution of ATGL to hepatic lipid metabolism and signaling.

190 ucing LD growth and enhancing degradation of ATGL.

191 Mice with a genetic deletion of ATGL (AKO) also accumulate TG in many tissues.

192 r, reducing lipolysis by either depletion of ATGL or expression of exogenous full-length FSP27 or ami

193 PNPLA3 was not caused by the displacement of ATGL from LDs.

194 onism was unable to normalize the effects of ATGL knockdown on PPAR-alpha target gene expression, and

195 als; however, the tissue-specific effects of ATGL outside of adipose tissue have not been well charac

196 T3-L1 adipocytes decreases the expression of ATGL and attenuates basal and isoproterenol-stimulated l

197 ic expression of Rheb inhibits expression of ATGL and HSL at the level of transcription, suppresses l

198 in human adipocytes increases expression of ATGL at the level of transcription, whereas overexpressi

199 the ATGL promoter in vitro and expression of ATGL in cultured adipocytes.

200 Co-expression of ATGL reverses the changes in LD phenotype induced by LDA

201 While expression of ATGL, HSL and CGI-58 remains mostly unaffected, TNF-alph

202 adipocytes by controlling the expression of ATGL.

203 provide evidence that targeted expression of ATGL/bmm in the offspring of HFD-fed parents protects th

204 in livers or mouse embryonic fibroblasts of ATGL(-/-) mice no longer decreases TG degradation as obs

205 ating evidence suggests that inactivation of ATGL has beneficial effects on lipotoxicity-driven disor

206 ed transformation by G0S2 was independent of ATGL inhibition.

207 Combined inhibition of ATGL and LAL resulted in large LDs, suggesting that lipo

208 nt of metabolic disorders, the inhibition of ATGL by G0S2-derived peptides may represent a novel ther

209 Pharmacological inhibition of ATGL enzyme activity similarly reduced triglyceride-hydr

210 Pharmacological inhibition of ATGL may prove useful to prevent HFD-induced obesity and

211 steatosis by CGI-58-dependent inhibition of ATGL on LDs.

212 Chemical inhibition of ATGL or genetic deletion of Atgl inhibits FAHFA biosynth

213 HIG2), a HIF-1 target, as a new inhibitor of ATGL.

214 e, but with opposite effects; interaction of ATGL with CGI-58 increased lipolysis, whereas interactio

215 increased lipolysis, whereas interaction of ATGL with perilipin 5 decreased lipolysis.

216 l culture model, we examined interactions of ATGL and its co-lipase CGI-58 with perilipin 1 (perilipi

217 rmed in Hepa1.6 cells after the knockdown of ATGL before FA and TM treatment.

218 Knockdown of ATGL reduced cAMP-mediated induction of genes involved i

219 Interestingly, knockdown of ATGL, the best-known molecular target of ABHD5, impeded

220 in brown adipocytes with stable knockdown of ATGL.

221 Lack of ATGL may protect from hepatic ER stress through alterati

222 both chow and high-fat diets, modulation of ATGL-mediated IMTG hydrolysis did not significantly infl

223 as RFWD2) binds to the consensus VP motif of ATGL and targets it for proteasomal degradation by K-48

224 Conversely, overexpression of ATGL amplifies the cAMP response, yielding increased glu

225 ted deletion or transgenic overexpression of ATGL exclusively in skeletal muscle.

226 As expected, overexpression of ATGL in cultured hepatoma (HuH-7) cells depleted the cel

227 Overexpression of ATGL in these cells antagonized the lipogenic effect of

228 f myocardial TAG, and that overexpression of ATGL is sufficient to ameliorate diabetes-induced cardio

229 Interestingly, overexpression of ATGL restored the lipolytic rates in cells with silenced

230 ted PKA, which led to the phosphorylation of ATGL and HSL and their recruitment to the LD surface.

231 d triglyceride breakdown and prolongation of ATGL half-life in adipose tissue.

232 his screen, we expressed a fusion protein of ATGL covering residues M1-D288 flanked with N-terminal a

233 However, regulation of ATGL expression and its functional implications in hepat

234 a new model of transcriptional regulation of ATGL.

235 However, the physiological relevance of ATGL-mediated triacylglycerol hydrolysis in skeletal mus

236 ting hepatic steatosis through repression of ATGL expression.

237 c adaptation, through specific repression of ATGL/Brummer lipase gene expression in adipose (fat body

238 ly unknown and highly conserved repressor of ATGL-1 called HLH-11/AP4.

239 findings unravel a novel protective role of ATGL against hepatic inflammation which could have impor

240 g through PPARalpha, we explored the role of ATGL in hepatic inflammation in mouse models of NASH and

241 cid 2:1 (OP21) to explore the direct role of ATGL in inflammation in vitro.

242 The selectivity of ATGL broadens to the sn-1 position upon stimulation of t

243 Silencing of ATGL expression in adipocytes almost completely abolishe

244 sis by reducing nascent protein synthesis of ATGL, thereby suppressing adipocyte thermogenesis.

245 of hepatic lipid metabolism requires optimum ATGL expression for its metabolic outcome.

246 Adenoviral overexpression of HSL and/or ATGL reduced liver triglycerides by 40-60% in both ob/ob

247 -specific deletion of genes encoding ATGL or ATGL inhibitory factors altered neutrophil lipid profile

248 In summary, hepatic overexpression of HSL or ATGL can promote fatty acid oxidation, stimulate direct

249 lls with adenoviral overexpression of HSL or ATGL showed that reduced cellular triglycerides could be

250 imulated lipolysis mediated by overexpressed ATGL or CGI-58.

251 ivated FOXO1 to promote expression of Pnpla2/ATGL.

252 alpha) and d-akap1, the lipase genes Pnplaz (ATGL) and Lipe (HSL), and lipid droplet protein genes fs

253 We conclude that G0S2 acts as a potent ATGL inhibitor in the heart modulating cardiac substrate

254 Both proteins independently recruited ATGL to the LD surface, but with opposite effects; inter

255 ring LD formation and suppressed by reducing ATGL.

256 he first demonstration that Peri A regulates ATGL-dependent lipolysis and identify serine 517 as the

257 n UCP1 mRNA (p = 0.03) and lipolysis-related ATGL mRNA (p = 0.04).

258 ockout mice, unlike obese adipocyte-specific ATGL knockouts, had lower visceral adipose tissue lipoly

259 s ATGL deficiency and cardiomyocyte-specific ATGL overexpression.

260 Hepatocyte-specific ATGL knockout (ATGL LKO) mice were challenged with methi

261 ent activity, informing strategies to target ATGL and lipid metabolism for cancer treatment.

262 ) in human pseudoislets with shRNA targeting ATGL (shATGL) increased triglycerides (TGs) and the numb

263 Glucose tolerance tests demonstrated that ATGL knockdown normalized glucose tolerance in HF-diet-f

264 and PG treatment of follicles indicate that ATGL acts upstream of Pxt to regulate actin remodeling.

265 d the number and size of LDs indicating that ATGL is the principal lipase in human beta cells.

266 the number and size of LDs, indicating that ATGL is the principal lipase in human beta-cells.

267 Here we show that ATGL exhibits a strong preference for the hydrolysis of

268 The results show that ATGL interacts with CGI-58 and perilipin 5; the latter i

269 Taken together, these data show that ATGL is a major hepatic TAG lipase that plays an integra

270 This suggests that ATGL and diacylglycerol-O-acyltransferase 2 act coordina

271 rget gene expression, and this suggests that ATGL influences PPAR-alpha activity independently of lig

272 s the expression of luciferase driven by the ATGL promotor.

273 However, the ATGL variant showed neither hydrolytic activity nor tran

274 a treatment caused a rapid abrogation of the ATGL inhibitory protein G0S2.

275 the effect of Tor1 on the expression of the ATGL ortholog in yeast.

276 rients and directly inhibits activity of the ATGL promoter in vitro and expression of ATGL in culture

277 FSP27 suppresses the activity of the ATGL promoter in vitro, and the proximal Egr1 binding si

278 s its association with and inhibition of the ATGL promoter.

279 reduction in expression of either HSL or the ATGL coactivator CGI-58.

280 hat core does not directly interact with the ATGL complex but, unexpectedly, increased the interactio

281 Therefore, ATGL is responsible for LD mobilization in human beta ce

282 Therefore, ATGL is responsible for LD mobilization in human beta-ce

283 Consistent with this, ATGL was enriched in larger-sized LDs, whereas lipophagi

284 eficiency, while augmented lipolysis through ATGL overexpression recovers adipocyte thermogenesis in

285 c acid (PA/OA) ratio in WT mice, compared to ATGL KO mice, at baseline.

286 r findings show that UBXD8 binds directly to ATGL and promotes dissociation of its endogenous coactiv

287 n than hearts with a lipolytic defect due to ATGL deficiency.

288 nfirm a PAHSA metabolite reservoir linked to ATGL-mediated lipolysis.

289 inflammation in both MCD-fed and LPS-treated ATGL-KO mice.

290 In vitro, the truncated ATGL variant demonstrated acyl-CoA-independent transacyl

291 PNLIP-knockout mice, unlike ATGL knockouts, were protected from adipocyte-induced pa

292 erol O-acyltransferase 1) and degrade LD via ATGL (adipocyte triglyceride lipase) after FA loading.

293 des in ovaries, and these are increased when ATGL is lost.

294 ssion of PNPLA3(wild type [WT] or 148M) with ATGL inhibited that depletion.

295 r perilipin 1 nor 2 interacted directly with ATGL.

296 s by direct protein-protein interaction with ATGL.

297 27, amino acids 120-220, that interacts with ATGL to inhibit its lipolytic function and promote trigl

298 d the hypothesis that PNPLA3 interferes with ATGL activity by interacting with its cofactor, comparat

299 S2 decreased hepatic TG content in mice with ATGL ablation.

300 Studies with ATGL-and HSL-directed small hairpin RNAs demonstrate tha