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 is an evolutionarily conserved regulator of lipid

3 SREBP was required in BAT for the thermogenic response t

4 SREBP-1 and endoplasmic reticulum stress thus provide po

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

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

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

8 SREBPs are cleaved in the Golgi through the combined act

9 SREBPs are critical for the production and metabolism of

10 SREBPs are inhibited by a complex composed of INSIG prot

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), fatty acid synthase (FASN), hormone-sensitive

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

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

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

17 ation of the transcription factors (SREBP-1, SREBP-2, and E2F1) in liver.

18 turn, promotes nuclear activation of sbp-1/ SREBP, a key regulator of sterol and fatty acid synthesi

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

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

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

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

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

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

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

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

31 culum cholesterol, as indicated by activated SREBP.

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

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

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

35 rol from PM to ER ceased, thereby activating SREBP transcription factors and increasing cholesterol s

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

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

38 be recycled to bind and transport additional SREBPs.

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 Depletion of LIMP-2 alters SREBP-2-mediated cholesterol regulation, as well as LDL-

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

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

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

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

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

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

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

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

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

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

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

53 Mga2 and SREBP-1 regulate triacylglycerol and glycerophospholipid

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

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

56 int multiple SREBP proteolytic processes and SREBP-regulated lipid biosynthesis pathways, including t

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

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

66 ry element binding transcription factor 1-c (SREBP-1c) binding site; inhibition of SREBP-1 by using s

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

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

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

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

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

72 ed levels of BAT free cholesterol, decreased SREBP targets, and induced the expression of genes invol

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

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

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

76 ) and cholesterol blood levels, and elevated SREBP-dependent signaling.

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

78 hen cholesterol levels are low, Scap escorts SREBPs from the ER to the Golgi, where the actions of tw

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

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

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

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

83 thesis is controlled by transcription factor SREBP in many eukaryotes.

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

85 via modulation of the transcription factors (SREBP-1, SREBP-2, and E2F1) in liver.

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

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

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

89 2 as a rhomboid family protease required for SREBP proteolytic processing.

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

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

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

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

94 ntify a function and mechanism of action for SREBPs in augmenting TNF-induced macrophage activation a

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

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

97 However, SREBP functions beyond lipid metabolism are less underst

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

99 letion of the nuclear forms of SREBPs, as in SREBP cleavage-activating protein knockout mice, impaire

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

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

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

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

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

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

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

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

108 morigenesis and is associated with increased SREBP-2 maturation.

109 e strongly reduces CDK8 levels but increases SREBP activity.

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

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

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

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

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

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

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

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

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

119 , is a target gene of the two SREBP isoforms SREBP-1a/c.

120 Because of its potent iNOS suppression, low SREBP induction, and activation of RXR, MSU-42011 was se

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

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

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

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

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

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

127 Mechanistic studies pinpoint multiple SREBP proteolytic processes and SREBP-regulated lipid bi

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

129 Overexpression of nuclear SREBP-1a under the control of the phosphoenolpyruvate ca

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

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

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

133 Genetic ablation of SREBP activity in myeloid cells or topical pharmacologic

134 Genetic ablation of SREBP function shifted the balance of macrophage polariz

135 ex to the Golgi apparatus, the activation of SREBP proteins (SREBP1 or SREBP2) and the transcription

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

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

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

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

140 -2a expression, leading to the activation of SREBP-1c and its downstream lipogenic target enzymes.

141 p53 blocks activation of SREBP-2, the master transcriptional regulator of this pa

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

143 lgi and consequent proteolytic activation of SREBP.

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

145 The CTD of SREBP remains bound to Scap but must be eliminated so th

146 response to norepinephrine, and depletion of SREBP prevented maintenance of body temperature both dur

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

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

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

153 Inhibition of SREBP function blocked lipid biosynthesis in hypoxic can

154 lls or topical pharmacological inhibition of SREBP improved skin wound healing under homeostatic and

155 resulted in GSC loss, whereas inhibition of SREBP rescued GSC loss triggered by depletion of dMfn.

156 r 1-c (SREBP-1c) binding site; inhibition of SREBP-1 by using specific inhibitors as well as small in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 endoplasmic reticulum and the activation of SREBPs(1,2).

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

178 kinase activity of PCK1 in the activation of SREBPs, lipogenesis and the development of HCC.

179 ght a previously unknown role for the CTD of SREBPs in regulating SREBP activity.

180 ranes, the carboxyl-terminal domain (CTD) of SREBPs binds to the CTD of Scap.

181 teases release the amino-terminal domains of SREBPs that travel to the nucleus to up-regulate express

182 r-specific depletion of the nuclear forms of SREBPs, as in SREBP cleavage-activating protein knockout

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

199 r Sterol regulatory element binding protein (SREBP) also resulted in GSC loss, whereas inhibition of

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

201 Sterol regulatory element binding protein (SREBP) cleavage-activating protein (SCAP) is a cholester

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

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

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

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

206 f sterol regulatory element binding protein (SREBP) is both necessary and sufficient to cause synapti

207 d sterol regulatory element binding protein (SREBP) is shown to interact with AM580, which accounts f

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

209 , sterol regulatory element-binding protein (SREBP) signaling, bone morphogenetic protein (BMP) signa

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

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

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

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

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

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

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

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

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

219 f sterol regulatory element-binding protein (SREBP).

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

221 (sterol regulatory element-binding protein [SREBP], acetyl-CoA carboxylase [ACC], peroxisome prolife

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

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

224 sterol regulatory element-binding proteins (SREBPs) are a family of transcription factors best known

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

226 sterol regulatory element-binding proteins (SREBPs) has a central role in this process.

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

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

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

230 sterol regulatory element-binding proteins (SREBPs), BbSre1, was shown to be involved in BbOhmm-medi

231 sterol regulatory element-binding proteins (SREBPs), membrane-bound transcription factors whose prot

232 sterol regulatory element-binding proteins (SREBPs).

233 sterol regulatory element-binding proteins (SREBPs).

234 ted by a complex composed of INSIG proteins, SREBP cleavage-activating protein (SCAP) and sterols in

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

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

237 to endoplasmic reticulum pools that regulate SREBP transcription factors.

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

239 own role for the CTD of SREBPs in regulating SREBP activity.

240 ith the known effects of Hamp up-regulation, SREBP-1a-overexpressing mice displayed signs of dysregul

241 nce to human viral infections and represents SREBP as a potential target for the development of broad

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

243 human opportunistic fungal pathogens require SREBP activation for virulence.

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

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

246 is critical for the dissociation of the SCAP-SREBP complex from the endoplasmic reticulum and the act

247 AP, leading to the translocation of the SCAP-SREBP complex to the Golgi apparatus, the activation of

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

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

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

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

258 Our studies demonstrate that SREBP regulates synaptic vesicle levels by interacting w

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 Moreover, ChIP experiments revealed that SREBP-1a binds to the Hamp gene promoter.

264 Here, we show that SREBP orthologs are not involved in the regulation of st

265 research, the present findings suggest that SREBP signaling plays an essential role in epidermal dif

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

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

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

273 Knockdown of PSEN1 or inhibition of the SREBP pathway restores Ca(2+) homeostasis, corrects diff

274 ol in the PM, as well as the activity of the SREBP pathway.

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

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

277 re, mature, active, and nuclear forms of the SREBP-1a/c proteins induce endogenous Hamp gene expressi

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

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

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

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

282 mp Together, these results indicate that the SREBP-1a/c transcription regulators activate hepcidin ex

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

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

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

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

287 -33, an intronic microRNA encoded within the SREBP loci, the expression of which is decreased with ra

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

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

290 issection of the CTD of SREBP2, one of three SREBP isoforms expressed in mammals.

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

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

293 nd inflammation, is a target gene of the two SREBP isoforms SREBP-1a/c.

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

295 2 controls cholesterol biosynthesis, whereas SREBP-1 controls triacylglycerol and glycerophospholipid

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

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

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

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

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