ライフサイエンスコーパス: SREBP

1 SREBP activity is tightly regulated to maintain lipid ho

2 SREBP regulates SCAP in human cells and yeast, indicatin

3 SREBP-1 and endoplasmic reticulum stress thus provide po

4 SREBP-1 is critical for OGT-mediated regulation of cell

5 SREBP-1 is highly expressed in mature WAT and plays a cr

6 SREBP-1c activates the transcription of all genes necess

7 SREBP-2 cleavage and nuclear translocation were not affe

8 SREBP-2 cleavage and translocation steps are well establ

9 SREBPs are cleaved in the Golgi through the combined act

10 SREBPs are critical for the production and metabolism of

11 increased sterol element binding protein 1 (SREBP-1) activity.

12 sterol regulatory element binding protein 1 (SREBP-1) and its transcriptional targets both in cancer

13 sterol regulatory element-binding protein 1 (SREBP-1)-dependent manner.

14 sterol regulatory element-binding protein 1 (SREBP-1, ADD1) processing.

15 Sterol regulatory element-binding protein-1 (SREBP-1) is a key transcription factor that regulates ge

16 t/sterol response element-binding protein-1 (SREBP-1) signaling pathway in SEB-1 sebocytes, and reduc

17 terol regulatory element binding protein 1c (SREBP-1c) and its downstream target, fatty acid synthase

18 terol regulatory element-binding protein 1c (SREBP-1c) is a central regulator of lipogenesis whose ac

19 terol-regulatory element binding protein 1c (SREBP-1c) seen in NAFLD patients in vivo.

20 terol regulatory element-binding protein 1c (SREBP-1c), leading to increased hepatic triglyceride syn

21 terol regulatory element-binding protein-1c (SREBP-1), accumulation of cellular triglycerides, and se

22 terol regulatory element binding protein-1c (SREBP-1c) gene expression.

23 terol regulatory element binding protein-1c (SREBP-1c), resulting in indirect MAFB upregulation.

24 terol regulatory element-binding protein-1c (SREBP-1c).

25 on in kidney in part by decreasing SREBP-1c, SREBP-2, ChREBP, FATP1, HMGCoAR, and LDL receptor, and i

26 sterol regulatory element-binding protein 2 (SREBP-2) and SREBP-1, respectively, are transcribed in c

27 sterol regulatory element binding protein 2 (SREBP-2) cholesterol genetic regulatory pathway in a hep

28 urated phosphatidylcholine to ER accelerated SREBP-1c processing through a mechanism that required an

29 lerosis and that angiotensin II can activate SREBP-1 in tubular cells.

30 tins, which respectively inhibit or activate SREBP, further supports SREBP-mediated regulation of IDH

31 exploits the NLRP3 inflammasome to activate SREBPs and host lipid metabolism, leading to liver disea

32 Activated SREBP-2 translocates to the nucleus, where it binds to a

33 g and colleagues find that glucose activates SREBP by stabilizing SCAP, a central regulator of the SR

34 e thus investigated whether mTORC1 activates SREBP-2 by reducing cholesterol delivery to the ER.

35 uce TGF-beta upregulation despite activating SREBP-1.

36 glucose promotes lipogenesis via activating SREBP transcription factors.

37 clines in cellular cholesterol by activating SREBPs, increasing cholesterol uptake and synthesis.

38 k5(toku/toku) mice, transcriptionally active SREBPs accumulated in the skin, but not in the liver; th

39 chain composition of ER phospholipids affect SREBP-1c maturation in physiology and disease.

40 ress was identified as a key mediator of Akt-SREBP-1 activation, and inhibition of endoplasmic reticu

41 However, notably missing is an SREBP-1 analog that regulates triacylglycerol and glycer

42 l that PLIN2 deletion suppressed SREBP-1 and SREBP-2 target genes involved in de novo lipogenesis and

43 latory element-binding protein (SREBP)-1 and SREBP-2 transcription factors.

44 ows for coordinate regulation of SREBP-1 and SREBP-2.

45 er is independently regulated by SREBP-2 and SREBP-1c, respectively.

46 tory element-binding protein 2 (SREBP-2) and SREBP-1, respectively, are transcribed in concert with t

47 expression of other target genes, ABCG1 and SREBP-1c.

48 sterol ligand required for LXR activity and SREBP-1c expression.

49 This results in disruption of AKT, AMPK, and SREBP signaling, leading to altered insulin, glucose, an

50 embrane proteolysis (RIP) of OASIS, ATF6 and SREBP transcription factors, consistent with decreased p

51 se in HF fraction while increasing GIRK4 and SREBP-1 expression.

52 to increase when mTORC1 activity is low, and SREBP-2 is activated.

53 Mga2 and SREBP-1 regulate triacylglycerol and glycerophospholipid

54 ic crosstalk was due to decreased mTORC1 and SREBP activity in PTG knockout mice or knockdown cells,

55 t cancer tissues, the levels of p54(nrb) and SREBP-1a proteins were positively correlated with each o

56 Moreover, both p54(nrb) and SREBP-1a were required for breast cancer cell growth in

57 ional interaction between endogenous SHP and SREBP-2 and inhibits SREBP-2 target genes, and these eff

58 cerophospholipid synthesis, whereas Sre1 and SREBP-2 regulate sterol synthesis.

59 In vivo, endoplasmic reticulum stress and SREBP-1-dependent effects were induced in glomeruli of a

60 In cultured myocytes, insulin treatment and SREBP-1 overexpression decreased, whereas SREBP-1 interf

61 tress-activated lipogenesis through the ATF6/SREBP-1c pathway in vitro.

62 t Rbd2 activity controls the balance between SREBP activation and degradation.

63 olves the sterol regulatory element-binding (SREBP) transcription factors SREBP1 and 2, whose activat

64 t HCV infection increases expression of both SREBP-1c and FASN.

65 Release of membrane-bound SREBP requires SREBP cleavage-activating protein (SCAP)

66 ide synthesis that are normally regulated by SREBP-1c.

67 ) in the liver is independently regulated by SREBP-2 and SREBP-1c, respectively.

68 es a description of genetic transcription by SREBP-2 which is subsequently translated to mRNA leading

69 creased mRNA and protein levels of canonical SREBP targets in primary human breast cancer samples.

70 LATS2 down-regulation caused SREBP activation and accumulation of excessive cholester

71 am transcriptional responses by coactivating SREBP-1, which subsequently enhanced lipogenic enzyme ex

72 olesterol from increasing and, consequently, SREBP-2 is activated without mTORC1 activation.

73 knockout (Lats2-CKO) displayed constitutive SREBP activation and overexpressed SREBP target genes an

74 rium of the Akita mouse results in decreased SREBP-1, attenuation of parasympathetic modulation of he

75 a dominant-active GSK3beta mutant decreased SREBP-1 and GIRK4 expression.

76 n HCV-infected cells significantly decreased SREBP-1c and FASN expression.

77 LSD1 knockdown decreases SREBP-1a at the transcription level.

78 accumulation in kidney in part by decreasing SREBP-1c, SREBP-2, ChREBP, FATP1, HMGCoAR, and LDL recep

79 ipogenesis and is required for LXR-dependent SREBP-1c activation.

80 pression of shTRAP80 inhibited LXR-dependent SREBP-1c expression and RNA polymerase II recruitment to

81 ol binding protein-like 3 (OSBPL3), enhanced SREBP-1 processing, and promoted de novo lipogenesis.

82 ith overexpression of miR-24, which enhanced SREBP processing.

83 cleavage-activating protein (SCAP) to escort SREBP from the endoplasmic reticulum (ER) to the Golgi f

84 hat ectopic expression of OSBPL3 facilitates SREBP-1 processing in WT mice, while silencing hepatic O

85 n through activation of the lipogenic factor SREBP-1.

86 vation of the lipogenic transcription factor SREBP and by controlling the expression of the low-densi

87 tial coactivator of the transcription factor SREBP and thus of lipid biosynthesis, resulted in signif

88 t overexpression of the transcription factor SREBP-1 induces glomerular sclerosis and that angiotensi

89 Cdc48-Ufd1 and Cdc48-Rbd2, are required for SREBP activation and low-oxygen adaptation in S. pombe.

90 vating protein (SCAP), which is required for SREBP activation.

91 ablished Cdc48 cofactor Ufd1 is required for SREBP cleavage but does not interact with the Cdc48-Rbd2

92 2 as a rhomboid family protease required for SREBP proteolytic processing.

93 Although not required for SREBP-1 activation by angiotensin II, EGF receptor signa

94 PP2A activity was required for SREBP-2 DNA binding.

95 t of Rbd2 bypassed the Cdc48 requirement for SREBP cleavage, demonstrating that Cdc48 likely plays a

96 zation of SHP sites with published sites for SREBP-2, a master transcriptional activator of cholester

97 holesterol is a well-established trigger for SREBP-2 activation.

98 adenoviral vector, we have silenced hepatic SREBP-1 in normal and obese mice.

99 of Insig-2, Insig-2a, which in turn hinders SREBP-1c activation and inhibits hepatic de novo lipogen

100 While the homeostatic SREBP regulation is well studied, stimuli-dependent regu

101 erature, the model is used to understand how SREBP-2 transcription and regulation affects cellular ch

102 erformed a biochemical screen and identified SREBP-1a, a master activator for genes involved in lipid

103 hosphorylation state, causing an increase in SREBP-2 binding to an LDLR SRE site.

104 er show that the statin mediated increase in SREBP-2 directly activates expression of patatin-like ph

105 accumulation concomitant with an increase in SREBP-2 driven autophagy in mice fed a high-fat diet (HF

106 Reductions in SREBP cleavage lead to SCAP degradation in lysosomes, pr

107 onstrating that Cdc48 likely plays a role in SREBP recognition.

108 ter site-1 protease cleavage of the inactive SREBP transmembrane precursor protein, RIP of the anchor

109 element-binding proteins (SREBPs) including SREBP-2, a master regulator of cholesterol synthesis.

110 o reduces the ability of insulin to increase SREBP-1c mRNA.

111 Known Nrf2 activators increased SREBP-1C promoter reporter activity in HepG2 cells.

112 sed LATS2 mRNA in association with increased SREBP target gene expression was observed in a subset of

113 e strongly reduces CDK8 levels but increases SREBP activity.

114 or SREBP-1 prevented angiotensin II-induced SREBP-1 binding to the TGF-beta promoter, TGF-beta upreg

115 hermore, UDCA treatment repressed T7-induced SREBP-1c, FAS, and ACC protein levels, whereas knockdown

116 or regulator of lipid metabolism by inducing SREBP-1c, fatty acid synthase (FAS), and acetyl-CoA carb

117 fatty acids, which others have shown inhibit SREBP activation and de novo lipogenesis.

118 Thus Fatostatin's ability to inhibit SREBP activity and cell division could prove beneficial

119 ion of Insig-2a in hepatocytes and inhibited SREBP-1c activation.

120 ir C-terminal regulatory domains, inhibiting SREBP processing and activation.

121 ween endogenous SHP and SREBP-2 and inhibits SREBP-2 target genes, and these effects were blunted in

122 These findings thus establish ROR/INSIG2/SREBP as a molecular pathway by which circadian clock co

123 through a mechanism that required an intact SREBP cleavage-activating protein (SCAP) pathway.

124 Interestingly, SREBP cleavage required Rbd2 binding of Cdc48, consisten

125 Knocking SREBP-1 down in db/db mice resulted in a significant red

126 eostasis in S. pombe, analogous to mammalian SREBP-1.

127 In mammals, SREBP-2 controls cholesterol biosynthesis, whereas SREBP

128 ynthetic pathway is required for the maximal SREBP-1c expression and high rates of FA synthesis.

129 inding to Rbd2 is required for Rbd2-mediated SREBP cleavage.

130 ansitions (EcR activity) and fat metabolism (SREBP activity) during the larval-pupal transition.

131 These data suggest that the mTORC1/SREBP pathway is a major mechanism through which common

132 Although LSD1 affects nuclear SREBP-1 abundance indirectly through SIRT1, it is also r

133 clear SREBP-1a caused an increase of nuclear SREBP-1a protein stability.

134 creased membrane saturation, reduced nuclear SREBP-1c abundance, and blunted the lipogenic response t

135 Interestingly, p54(nrb) binding to nuclear SREBP-1a caused an increase of nuclear SREBP-1a protein

136 th in vitro, and p54(nrb) binding to nuclear SREBP-1a was also critical for breast tumor development

137 xic and hypoxic cells and that activation of SREBP was required to maintain the expression of fatty a

138 Angiotensin II-induced activation of SREBP-1 required signaling through the angiotensin II ty

139 protein (SCAP) and consequent activation of SREBP-1, an ER-bound transcription factor with central r

140 I induced the upregulation and activation of SREBP-1.

141 -2a expression, leading to the activation of SREBP-1c and its downstream lipogenic target enzymes.

142 n of cholesterol in the ER and activation of SREBP-2.

143 lgi and consequent proteolytic activation of SREBP.

144 er induce the already elevated activities of SREBP-2 or HMGR in Insig-deficient enterocytes.

145 Increased binding of SREBP-1 to this DNA region was confirmed in the heart of

146 We analyzed the effect of SREBP activity inhibitors including Fatostatin, PF-42924

147 d increases in adiponectin and expression of SREBP-1, IR, and PPARgamma mRNA.

148 vestigation suggested that the expression of SREBP-1c and FASN is controlled by the transcription fac

149 uired for its binding to the nuclear form of SREBP-1a.

150 ied by low ER cholesterol and an increase of SREBP-2 activation.

151 Insulin induction of SREBP-1c requires LXRalpha, a nuclear receptor.

152 are required for the feedback inhibition of SREBP and HMG-CoA reductase (HMGR).

153 an antitumor agent due to its inhibition of SREBP and its effect on lipid metabolism, we show that F

154 Inhibition of SREBP function blocked lipid biosynthesis in hypoxic can

155 cently discovered as a specific inhibitor of SREBP cleavage-activating protein (SCAP), which is requi

156 recycling of SCAP-SREBP until initiation of SREBP cleavage.

157 vestigated the labile anchor intermediate of SREBP-1 using NMR spectroscopy.

158 ta inhibitor Kenpaullone increased levels of SREBP-1 and expression of GIRK4 and IKACh, whereas a dom

159 The levels of SREBP-1 are significantly elevated in obese patients and

160 ment to the LXR responsive element (LXRE) of SREBP-1c, but not to the LXRE of ABCA1.

161 and of lipid synthesis, as overexpression of SREBP-1 rescues lipogenic defects associated with OGT su

162 s SHP as a global transcriptional partner of SREBP-2 in regulation of sterol biosynthetic gene networ

163 nsport to Golgi and subsequent processing of SREBP-2.

164 controls circadian chromatin recruitment of SREBP-1, resulting in the cyclic regulation of genes imp

165 Thus, TAK1 regulation of SREBP critically contributes to the maintenance of liver

166 d paralleling a selective down-regulation of SREBP target gene expression, whereas mRNAs involved in

167 echanism allows for coordinate regulation of SREBP-1 and SREBP-2.

168 tion, lipid metabolism and the regulation of SREBP-1 in cancer and suggests a crucial role for O-GlcN

169 our data suggest that p54(nrb) regulation of SREBP-1a supports the increased cellular demand of lipid

170 esis subsequently leads to the regulation of SREBP-2 via a negative feedback formulation.

171 nclude that p54(nrb) is a novel regulator of SREBP-1a in the nucleus, and our data suggest that p54(n

172 icantly reversed UDCA-mediated repression of SREBP-1c, FAS, and ACC protein levels.

173 recycles to the ER for additional rounds of SREBP binding and transport.

174 PLIN2 deletion contribute to suppression of SREBP activation, we isolated endoplasmic reticulum memb

175 nase 1 (IDH1) as a transcriptional target of SREBP across a spectrum of cancer cell lines and human c

176 Transcription of SREBP-1c also requires transcription factor C/EBPbeta, b

177 80 selectively promotes the transcription of SREBP-1c but not ABCA1.

178 , activated mTORC1 triggers translocation of SREBP-2, an endoplasmic reticulum (ER) resident protein,

179 Golgi, followed by proteolytic activation of SREBPs by S1P and S2P in the Golgi.

180 In general, activation of SREBPs occurs during cholesterol depletion.

181 gly, during HCV infection, the activation of SREBPs occurs under normal cholesterol levels, but the u

182 tory domains of ER to suppress activation of SREBPs, halting cholesterol uptake and synthesis; and (3

183 lesterol synthesis by blocking activation of SREBPs.

184 t TAK1 binds to and inhibits mature forms of SREBPs.

185 Pharmacological inhibition of SREBPs alleviated the steatosis and reduced the expressi

186 ysis revealed that the Dsc E3 ligase acts on SREBP prior to cleavage by Rbd2.

187 tem cell function, was strongly dependent on SREBP function.

188 erestingly, the impact of LATS2 depletion on SREBP-mediated transcription was clearly distinct from t

189 sympathetic dysfunction through an effect on SREBP-1, supporting GSK3beta as a new therapeutic target

190 processing of its close homolog ATF6beta or SREBP (a cholesterol-regulated transcription factor), bo

191 nhibition of endoplasmic reticulum stress or SREBP-1 prevented angiotensin II-induced SREBP-1 binding

192 stitutive SREBP activation and overexpressed SREBP target genes and developed spontaneous fatty liver

193 OCS3 overexpression, further inducing PCSK9, SREBP-1, fatty acid synthase, and apoB mRNA.

194 This leads to accumulation of precursor SREBP-1 and ATF6, and development of insufficient reserv

195 ted cells confirms accumulation of precursor SREBP-1 and ATF6.

196 ifically block Dsc1-Ubc4 interaction prevent SREBP cleavage, indicating that SREBP activation require

197 As expected, miR-24 knockdown prevented SREBP processing, and subsequent expression of lipogenic

198 o liver X receptor (LXR) activation promoted SREBP-1c processing by driving the incorporation of poly

199 that protein phosphatase 2A (PP2A) promotes SREBP-2 LDLR promoter binding in response to cholesterol

200 n sterol regulatory element-binding protein (SREBP) activity and the expression of lipid metabolism g

201 d sterol regulatory element-binding protein (SREBP) activity in enterocytes to support increased lipi

202 d Sterol Regulatory Element Binding Protein (SREBP) activity in neurons leading to LD accumulation in

203 f sterol regulatory element-binding protein (SREBP) cleavage-activating protein (SCAP) and consequent

204 f sterol regulatory element-binding protein (SREBP) cleavage-activating protein (SCAP), an essential

205 [sterol-regulatory element-binding protein (SREBP) cleavage-activating protein] acts as a cholestero

206 e sterol regulatory element-binding protein (SREBP) family of transcription factors are critical regu

207 Sterol regulatory element binding protein (SREBP) is a major transcriptional regulator of the enzym

208 ol regulatory element (SRE)-binding protein (SREBP) pathway, and RSV treatment increased the C-ACSL1

209 ing sterol response element-binding protein (SREBP) processing to reduce Il1b transcription and to br

210 r sterol regulatory element-binding protein (SREBP) transcription factor activation that shows archit

211 Sterol regulatory element-binding protein (SREBP) transcription factors are central regulators of c

212 e sterol regulatory element-binding protein (SREBP) transcription factors have become attractive targ

213 e sterol regulatory element-binding protein (SREBP) transcription factors regulate lipid homeostasis.

214 s sterol regulatory element-binding protein (SREBP) transcription factors, and human opportunistic fu

215 e sterol regulatory element binding protein (SREBP), a key regulator of cholesterol metabolism protei

216 f sterol regulatory element binding protein (SREBP), the master regulator of intracellular lipid home

217 n sterol regulatory element-binding protein (SREBP)-1 and SREBP-2 transcription factors.

218 e sterol regulatory element-binding protein (SREBP)-1-mediated lipogenic program.

219 e sterol regulatory element-binding protein (SREBP)-encoding genes and control cholesterol/lipid home

220 g sterol regulatory element-binding protein (SREBP-1), insulin receptor (IR), and PPARgamma in liver

221 the sterol response element-binding protein (SREBP-1).

222 ted sterol response element-binding protein (SREBP-2).

223 ort of the SREBP cleavage-activating protein.SREBP complex from the endoplasmic reticulum to the Golg

224 sterol regulatory element-binding proteins (SREBPs) and transports them from the endoplasmic reticul

225 Sterol-regulatory element-binding proteins (SREBPs) are key transcription factors regulating cholest

226 Sterol regulatory element-binding proteins (SREBPs) in the fission yeast Schizosaccharomyces pombe r

227 sterol regulatory element-binding proteins (SREBPs) including SREBP-2, a master regulator of cholest

228 sterol regulatory element-binding proteins (SREBPs) play a pivotal role in stimulating lipid biosynt

229 sterol regulatory element-binding proteins (SREBPs) through their C-terminal regulatory domains, inh

230 sterol-regulatory element binding proteins (SREBPs), in the HCV-mediated stimulation of LDLR transcr

231 sterol regulatory element-binding proteins (SREBPs), transcription factors that activate lipid synth

232 sterol regulatory element-binding proteins (SREBPs).

233 sterol regulatory element-binding proteins (SREBPs).

234 In the absence of functional Rbd2, SREBP precursor is degraded by the proteasome, indicatin

235 in hepatocytes of mice also markedly reduced SREBP-1c and the expression of all genes involved in FA

236 to endoplasmic reticulum pools that regulate SREBP transcription factors.

237 els of CDK8, EcR and USP, yet down-regulates SREBP activity.

238 OGT regulates SREBP-1 protein expression via AMP-activated protein kin

239 The phosphatase(s) regulating SREBP-2 represents a novel pharmacological target for tr

240 sterol-25-hydroxylase (Ch25h) and repressing SREBP transcription factors.

241 human opportunistic fungal pathogens require SREBP activation for virulence.

242 Release of membrane-bound SREBP requires SREBP cleavage-activating protein (SCAP) to escort SREBP

243 As a result, SREBPs are no longer processed, cholesterol synthesis an

244 sms regulating ER-to-Golgi transport of SCAP-SREBP are understood in molecular detail, but little is

245 ctively prevents premature recycling of SCAP-SREBP until initiation of SREBP cleavage.

246 conformational changes that prevent the Scap-SREBP complex from leaving the ER.

247 demonstrate a novel role for LH/cAMP in SCAP/SREBP activation and subsequent regulation of steroidoge

248 tion with Insig-1, allowing movement of SCAP/SREBP to the Golgi and consequent proteolytic activation

249 processes, including activation of the SCAP/SREBP pathway.

250 Several SREBP-2 phosphorylation sites have been mapped and funct

251 The soluble SREBP N-terminal transcription factor domain is then rel

252 mice with hepatocyte- or adipocyte-specific SREBP-1c overexpression as models of PRIM and SEC.

253 As a result, p54(nrb) stimulates SREBP-1-meidated transcription of lipogenic genes and li

254 inhibit or activate SREBP, further supports SREBP-mediated regulation of IDH1 and, in cells with onc

255 tudies reveal that PLIN2 deletion suppressed SREBP-1 and SREBP-2 target genes involved in de novo lip

256 ven when mTORC1 activity is high, suppresses SREBP-2 activation.

257 Furthermore, targeting SREBP-inflammasome pathways can be a therapeutic strateg

258 Srebf-2 from hepatocytes and confirmed that SREBP-2 regulates all genes involved in cholesterol bios

259 We found that SREBP induces the expression of oncogenic IDH1 and influ

260 We found that SREBP transcriptional activity was induced by serum depl

261 tion prevent SREBP cleavage, indicating that SREBP activation requires Dsc E3 ligase activity.

262 ally, gene expression analysis revealed that SREBP defines a gene signature that is associated with p

263 However, we show that SREBP actively prevents premature recycling of SCAP-SREB

264 Current models suggest that SREBP plays a passive role prior to cleavage.

265 Here we demonstrate that SREBPs are regulated by a previously uncharacterized mec

266 The SREBP-induced NOD-like receptor family pyrin domain-cont

267 However, little is known about the SREBP-mediated control of processes that indirectly supp

268 or depends on fat metabolism mediated by the SREBP-SCD pathway, an acetyl-CoA carboxylase (ACC) and c

269 Mutations of the genes in the SREBP-SCD pathway reduce satiety quiescence.

270 s subsequently leads to the transport of the SREBP cleavage-activating protein.SREBP complex from the

271 xygen stimulates proteolytic cleavage of the SREBP homolog Sre1, generating the active transcription

272 n II-infused mice, and administration of the SREBP inhibitor fatostatin prevented angiotensin II-indu

273 d biosynthesis known to be downstream of the SREBP pathway in mammals.

274 stabilizing SCAP, a central regulator of the SREBP pathway.

275 ignaling was necessary for activation of the SREBP-1 cotranscription factor Sp1, which provided a req

276 erol levels to the reciprocal actions of the SREBP-2 and LXR pathways.

277 RORalpha/gamma causes overactivation of the SREBP-dependent lipogenic response to feeding, exacerbat

278 fission yeast Schizosaccharomyces pombe, the SREBP-2 homolog Sre1 regulates sterol homeostasis in res

279 Proteolysis releases the SREBP transcription factor domains, which enter the nucl

280 y interacts with LC3 and we suggest that the SREBP-2/PNPLA8 axis represents a novel regulatory mechan

281 Thus, the SREBP pathway may represent a novel target for treating

282 additional negative feedback control to the SREBP pathway.

283 the LXRalpha-C/EBPbeta complex binds to the SREBP-1c promoter in a region that contains two binding

284 e LXRalpha-C/EBPbeta complex is bound to the SREBP-1c promoter in the absence or presence of insulin,

285 -33, an intronic microRNA encoded within the SREBP loci, the expression of which is decreased with ra

286 The SREBPs are also required for the growth factor-independe

287 s maintained through concerted action of the SREBPs and LXRs.

288 oncogenic signaling and fuel availability to SREBP-dependent lipogenesis.

289 hypothesis that these actions contribute to SREBP-regulated de novo lipogenesis involved in non-alco

290 nscriptional and posttranslational level via SREBPs and PCSK9 to promote lipid uptake and facilitate

291 um (ER) resident protein, to the Golgi where SREBP-2 is cleaved to translocate to the nucleus and act

292 2 controls cholesterol biosynthesis, whereas SREBP-1 controls triacylglycerol and glycerophospholipid

293 nd SREBP-1 overexpression decreased, whereas SREBP-1 interference increased, peroxisome proliferator-

294 Here we have addressed whether SREBP-1 is needed for regulating glucose homeostasis.

295 We thus studied whether SREBP-1 is activated by angiotensin II and mediates angi

296 entiation of human preadipocytes, along with SREBP-1.

297 rol depletion, PP2A directly interacted with SREBP-2 and altered its phosphorylation state, causing a

298 mportant for its functional interaction with SREBP-2 and reduction of liver/serum cholesterol levels.

299 Proteolytic release of fission yeast SREBPs from the membrane in response to low oxygen requi

300 In fission yeast, SREBP functions in an oxygen-sensing pathway to promote