ライフサイエンスコーパス: SREBP2

1 sterol regulatory element binding protein 2 (SREBP2).

2 ment-binding transcription factor 2 (SREBF2, SREBP2).

3 sterol regulatory element binding protein 2 (SREBP2).

4 gulatory element-binding protein (SREBP1 and SREBP2).

5 by accumulation and stabilization of mature SREBP2.

6 terol levels can be modulated by CO2 through SREBP2.

7 p requires an arginine residue in exon 18 of SREBP2.

8 icenses S1P to cleave its cognate substrate, SREBP2.

9 thways in HUVECs transfected with adenovirus-SREBP2.

10 creased activity of the transcription factor SREBP2.

11 ding the key cholesterol synthesis regulator SREBP2.

12 s and its facilitation of the recruitment of SREBP2.

13 MAPK and caspase-3 mediate the activation of SREBP2.

14 vastatin, and 3) shRNA-mediated knockdown of SREBP2.

15 gether with their protein levels, except for SREBP2.

16 asis through control of TFII-I expression by SREBP2.

17 sterol regulatory element binding protein 2 (SREBP2), a master regulator of cholesterol synthesis.

18 Importantly, our study identified SREBP2, a major regulator of sterol and fatty acid synth

19 ulates key hepatic lipogenic genes including Srebp2, a master regulator of lipid metabolism.

20 increased in all vegetable oil diets as was SREBP2, a master transcriptional regulator of these path

21 e areas of mouse aortas, suggesting that the SREBP2-activated NLRP3 inflammasome causes functionally

22 Our data thus identify SREBP2-activated transcription as a mechanism for promot

23 ation in which glutamine uptake is enhanced, SREBP2 activation and cellular cholesterol were increase

24 s upregulate Ch25h to maintain repression of SREBP2 activation and cholesterol synthesis.

25 Srebp2 activation and Notch up-regulation are associated

26 erlying mechanism suggests that CO2 triggers SREBP2 activation through changes in endoplasmic reticul

27 Furthermore, SREBP2 activation was dependent on NF-kappaB DNA binding

28 e inhibitors increased SCAP phosphorylation, SREBP2 activation, and subsequent expression of choleste

29 es NLRP3 inflammasome in endothelium through SREBP2 activation.

30 We show that inhibition of SREBP2 activity reduced TFII-I induction in response to

31 limits lipogenesis by inhibiting SREBP1 and SREBP2 activity.

32 to secondary feedback inhibition of hepatic SREBP2 activity.

33 Induction of SREBP2 also coinduces intronic microRNA-33a (miR-33a) in

34 nus of SREBP2 (SREBP2(N)), an active form of SREBP2, also inhibited the ABCA1 promoter activity.

35 sterol regulatory element-binding protein-2 (SREBP2), an ER-localized transcription factor that direc

36 acking p75 exhibited decreased activation of SREBP2 and a reduction in 7-dehydrocholesterol (7-DHC) r

37 hanistically, DAXX interacts with SREBP1 and SREBP2 and activates SREBP-mediated transcription.

38 ularly in the membrane fraction that harbors SREBP2 and caspase-2.

39 ermore, we identified SND1 as a link between SREBP2 and CCL19, an inflammatory chemokine that is redu

40 We show that the upregulation of SREBP2 and cholesterol by reduced aPKC levels is essenti

41 versus WT mice, with no further increase in SREBP2 and down-regulation of HMG-CoA reductase protein.

42 etention of SCAP enhanced transactivation of SREBP2 and expression of 3-hydroxy-3-methyl-glutaryl coe

43 sults showed that sterol depletion activated SREBP2 and increased its target, low density lipoprotein

44 Oscillatory flow activates SREBP2 and induces NLRP3 inflammasome in endothelial cel

45 dings reveal a novel pathway linking Parkin, SREBP2 and LPL in neuronal lipid homeostasis that may be

46 otein 2 (BMP2) is the downstream effector of Srebp2 and Lrp2, and Bmp2 is suppressed by SREBP2 transc

47 ances cholesterol biosynthesis by recruiting Srebp2 and Pol II in the promoter regions of cholesterol

48 er cells activate the mevalonate pathway via SREBP2 and promote the synthesis of ubiquinone that play

49 mma inhibition disrupts its association with SREBP2 and reduces chromatin acetylation at cholesterol-

50 tor gamma (RORgamma), which acts upstream of SREBP2 and serves as master regulator of the cholesterol

51 ter region of the master metabolic regulator Srebp2 and show that it directly interacts with coactiva

52 Ca(2+) depletion promotes the activation of SREBP2 and subsequent transcription of PCSK9.

53 serum starvation enhanced the association of SREBP2 and the ABCA1 promoter in ECs.

54 at oscillatory flow caused the activation of SREBP2 and therefore attenuated ABCA1 promoter activity

55 the activation of SREBP proteins (SREBP1 or SREBP2) and the transcription of downstream lipogenesis-

56 sterol regulatory element-binding protein 2 (SREBP2) and, consequently, reduced activation of SREBP2-

57 latory element binding protein (SREBP) 1 and SREBP2 are ubiquitously expressed transcription factors

58 enzymes, resulting in optimal recruitment of SREBP2 at these sites.

59 tory element-binding transcription factor 2 (SREBP2) at key regulatory regions controlling the expres

60 Thus, a 25-HC-SREBP2 axis shapes the humoral response at the intestina

61 ly regulated at the transcriptional level by SREBP2, but also through uptake of extracellular cholest

62 te modest reduction of HNF1alpha and nuclear SREBP2 by BBR led to a strong suppression of PCSK9 trans

63 rol levels through interference with nuclear SREBP2 clearance.

64 with pro-inflammatory cytokines upregulated SREBP2 cleavage and cholesterol biosynthetic gene expres

65 e (p38 MAPK) and activation of caspase-3 and SREBP2 cleavage following NGF and pro-NGF stimulations.

66 to heightened sterol sensing and downstream SREBP2 cleavage.

67 art, to the recruitment of HDAC1 to the ATF6-SREBP2 complex.

68 P2) and, consequently, reduced activation of SREBP2-controlled genes in the cholesterol biosynthesis

69 ls induced rapid PC differentiation, whereas SREBP2 deficiency reduced PC output in vitro and in vivo

70 SREBP2 degradation in hypoxia overrides the normal stero

71 the expression of cholesterogenic genes in a SREBP2-dependent manner and modulates cellular cholester

72 Our studies outline an AIBP-regulated Srebp2-dependent paradigm for HSPC emergence in developm

73 ning cholesterol synthesis through regulated SREBP2-dependent protein degradation.

74 However, the role of SREBP2-dependent transcription in HIV-1 biology has not

75 ) depletion, including thapsigargin, induced SREBP2-dependent up-regulation of PCSK9 expression.

76 ly, we show that inhibition of either LPL or SREBP2 exacerbates rotenone-induced cell death.

77 Mechanistically, UA- or MSU-induced SREBP2 expression and its transcriptional activity.

78 Perhexiline maleate decreases SREBP2 expression levels and reverses the KRAS mutant-in

79 -treated cells, the mRNA levels of SREBP1-c, SREBP2, fatty-acid synthase, acetyl-CoA carboxylase, ATP

80 duces intronic microRNA-33a (miR-33a) in the SREBP2 gene in Cyp7a1-tg mice.

81 Supporting this, SREBP2 genetic ablation abolished Parkin effect on LPL e

82 sterol regulatory element-binding protein 2 (SREBP2) has an unanticipated function in the retinal pig

83 Basal protein levels of SREBP2, HMG-CoA reductase, and steroidogenic acute regul

84 tionally active N-terminal fragment of human SREBP2 (hSREBP2).

85 In vivo, mice with knockout of SREBP2 in astrocytes have impaired brain development and

86 sterol, which is a newly defined function of SREBP2 in ECs in addition to its role in cholesterol upt

87 VEGF activated SREBP1 and SREBP2 in ECs, as demonstrated by the increased SREBPs,

88 r intima from transgenic mice overexpressing SREBP2 in endothelium or mice with hyperuricemia exhibit

89 Ectopic expression of SREBP2 in germinal center B cells induced rapid PC diffe

90 we demonstrated that knockdown of endogenous SREBP2 in HepG2 cells lowered ACSL1 mRNA and protein lev

91 esponses, confirming the requirement of SCAP-SREBP2 in steroidogenesis.

92 We investigated the regulation of ABCA1 by SREBP2 in vascular endothelial cells (ECs).

93 iption regulator of cholesterol homeostasis, SREBP2, in the EC responses to inflammatory stress.

94 Srebp2 inhibition impairs hypercholesterolemia-induced H

95 ced than the effects of fatostatin, a direct SREBP2 inhibitor.

96 After SREBP2 is cleaved in Golgi, its CTD remains bound to Sca

97 Since SREBP2 is difficult to target, we performed pharmacologi

98 o the CTD of Scap, this signal is masked and SREBP2 is stabilized.

99 sterol-responsive element-binding protein 2 (SREBP2) is the key protein regulating cholesterol synthe

100 neurite outgrowth, and this is reduced with SREBP2 knockdown astrocytes.

101 the DAXX-SREBP interaction for lipogenesis, SREBP2 knockdown attenuates tumor growth in cells with D

102 The SREBP2 knockdown by siRNA partially abolished UA- or MSU

103 n treatment but increased in cells following SREBP2 knockdown.

104 lyceride levels by raising the expression of SREBP2, low-density lipoprotein receptor, HMGCo-A reduct

105 R, CD36), synthesis (HMGCR), and regulation (SREBP2, LXRA) was significantly lower in both ART-Treate

106 ed cells identified the transcription factor SREBP2, master regulator of cholesterol homeostasis.

107 Betulin inhibition of SREBP2 may restrain gout-induced endothelial dysfunction

108 monstrated the key role of this SRE motif in SREBP2-mediated activation of C-ACSL1 gene transcription

109 In conclusion, we propose that Qki-Srebp2-mediated cholesterol biosynthesis is essential fo

110 Thus, SREBP2-mediated cholesterol synthesis in astrocytes play

111 rain due to decreased insulin stimulation of SREBP2-mediated cholesterol synthesis in neuronal and gl

112 ntracellular cholesterol levels and augments SREBP2-mediated gene expression and LDL-cholesterol upta

113 c sterol content and increased expression of SREBP2-mediated genes.

114 This study suggests that a CYP7A1/SREBP2/miR-33a axis plays a critical role in regulation

115 rongly correlated with reductions in hepatic Srebp2 mRNA level and mature Srebp2 protein abundance.

116 In addition, srebp1 and srebp2 mRNA respond to replacement of dietary FO with VO

117 Functionally adenovirus-mediated SREBP2(N) expression increased cholesterol accumulation

118 ctional consequence, the lipogenic effect of SREBP2(N) in liver cells was suppressed by ATF6(N).

119 Furthermore sterol depletion and SREBP2(N) overexpression induced the binding of SREBP2(N

120 BP2(N) overexpression induced the binding of SREBP2(N) to both consensus and ABCA1-specific E-box.

121 Overexpression of the N terminus of SREBP2 (SREBP2(N)), an active form of SREBP2, also inhibited the

122 onserved E-box motif was responsible for the SREBP2(N)-mediated inhibition since mutation of the E-bo

123 tation assays revealed that ATF6(N) bound to SREBP2(N).

124 moter and abolished the inhibitory effect of SREBP2(N).

125 ATF6(N) formed a complex with the SRE-bound SREBP2(N).

126 Consistently, SREBP2, NADPH oxidase 2, and NLRP3 levels were elevated

127 phosphorylation of AMPKalpha Thr172, reduced SREBP2 nuclear translocation, and Srebf2 mRNA expression

128 stimulation extended the genomic profile of SREBP2 occupancy to include binding to and activation of

129 detailed molecular dissection of the CTD of SREBP2, one of three SREBP isoforms expressed in mammals

130 NA (siRNA)-mediated gene silencing of either SREBP2 or TFII-I significantly reduced HIV-1 production

131 Collectively, we propose that SREBP2 participates in CO2 signaling and that cellular c

132 We conclude that glial SREBP2 participates in Huntington's disease brain pathog

133 asmic reticulum (ER), where it regulates the SREBP2 pathway and undergoes esterification.

134 sses cholesterol synthesis via the AMPKalpha-SREBP2 pathway.

135 flammatory response, such as RXRA, EGFR, and SREBP2 precursor.

136 on NF-kappaB DNA binding and canonical SCAP-SREBP2 processing.

137 marked up-regulation of ACAT2 and suppressed SREBP2 processing.

138 sterol regulatory element-binding protein 2 (SREBP2) processing, and U18666A is an inhibitor of the v

139 teraction with SCAP and PAQR3 and subsequent SREBP2-processing.

140 Hypoxia-mediated degradation of SREBP2 protects cells from statin-induced cell death by

141 ions in hepatic Srebp2 mRNA level and mature Srebp2 protein abundance.

142 ically, this outcome was driven by increased SREBP2 protein expression accompanied by amplified targe

143 ion of SCAP in SCAP-deficient cells restored SREBP2 protein expression and partially restored steroid

144 During postnatal development, SREBP2 protein expression in the RPE decreases whereas t

145 l1 mRNA, and decreased Hmgr mRNA and nuclear SREBP2 protein.

146 steroid response element-binding protein 2 (SREBP2)-regulated cholesterol metabolic network and abse

147 sterol regulatory element-binding protein 2 (SREBP2)-regulated transcription.

148 nges in the mRNA levels of the LDLR or other SREBP2-regulated genes, in line with this phenotype bein

149 the ER, evidenced by increased expression of SREBP2-regulated genes.

150 eprivation activated ATF6 but suppressed the SREBP2-regulated transcription.

151 ranslocation and the expression of a nuclear SREBP2 rescued mevalonate pathway activity during glutam

152 amino acids encoded in exon 19 that mediates SREBP2's proteasomal degradation in the absence of Scap.

153 SREBP1 and SREBP2 share approximately 47% sequence identity and map

154 REBP) and cleavage-activating protein (SCAP)-SREBP2 signaling in patients with CKD, hyperphosphatemic

155 d SCAP levels with aberrantly activated SCAP-SREBP2 signaling.

156 Overexpression of the N terminus of SREBP2 (SREBP2(N)), an active form of SREBP2, also inhib

157 ia, as the main ubiquitin ligase controlling SREBP2 stability.

158 Furthermore, SREBP2 (sterol regulatory element-binding protein 2) pro

159 macologic inhibition or genetic silencing of SREBP2 suppresses ZIKV infection of DCs.

160 ific overexpression of the activated form of SREBP2 synergized with hyperlipidemia to increase athero

161 anscription in activated T cells, as a novel SREBP2 target gene.

162 sion of sterol regulatory-binding protein 2 (SREBP2) target genes, and activation of liver X receptor

163 of ATF6(N) had similar inhibitory effects on SREBP2-targeted genes.

164 ulatory element-binding proteins (SREBP1 and SREBP2) that are required for oncogene-induced lipid syn

165 sterol regulatory element-binding protein-2 (SREBP2) that regulates genes involved in lipid metabolis

166 Sterol Regulatory Element Binding Protein 2 (SREBP2), the key transcription factor driving sterol pro

167 king of SCAP that licenses the activation of SREBP2, the major transcriptional regulator of cholester

168 nd inhibits the processing and activation of SREBP2, the master regulator of cholesterol biosynthesis

169 phages and revealed late-phase activation of SREBP2, the master regulator of cholesterol biosynthesis

170 ted cholesterol efflux activates endothelial Srebp2, the master transcription factor for cholesterol

171 tary and cellular cholesterol levels through SREBP2, the master transcriptional regulator of choleste

172 n of the sterol-sensing transcription factor SREBP2, thereby regulating B cell cholesterol biosynthes

173 sterol regulatory element binding protein 2 (SREBP2) through activation of the extracellular signal-r

174 sterol regulatory element-binding protein 2 (SREBP2) through microRNA-124 downregulation.

175 nesis in vivo and that AAV-based delivery of SREBP2 to astrocytes counteracts key features of the dis

176 tsRNA-Glu-CTC interacts with SREBP2 to regulate its own transcription through an E-bo

177 a novel mechanism by which ATF6 antagonizes SREBP2 to regulate the homeostasis of lipid and glucose.

178 ificantly attenuated the activity of nuclear SREBP2 to transactivate PCSK9 promoter.

179 y physically linking or 'tethering' STING to SREBP2 trafficking.

180 The underlying mechanisms involve SREBP2 transactivating NADPH oxidase 2 and NLRP3.

181 UA or MSU causes endothelial dysfunction via SREBP2 transactivation of YAP.

182 eostasis pathway, which is controlled by the SREBP2 transcription factor, is repressed in gonadal adi

183 tronic microRNA within the gene encoding the SREBP2 transcription factor.

184 sterol regulatory element-binding protein 2 (SREBP2) transcriptional program, which includes genes in

185 f Srebp2 and Lrp2, and Bmp2 is suppressed by SREBP2 transcriptionally but activated by Lrp2.

186 SREBP2 transcriptionally represses low density lipoprote

187 in using sequencing (ATAC-seq) indicate that Srebp2 transregulates Notch pathway genes required for h

188 ls polarization through control of SIRT6 and SREBP2 ubiquitination.

189 cholesterol-biosynthesis program, dominating SREBP2 via its binding to cholesterol-biosynthesis genes

190 ered an unprecedented link between ACSL1 and SREBP2 via the specific regulation of the C-ACSL1 transc

191 The attenuated transcriptional activity of SREBP2 was due, in part, to the recruitment of HDAC1 to

192 oform of the ubiquitous transcription factor SREBP2, which in somatic cells is required for homeostat

193 a novel isoform of the transcription factor SREBP2, which is highly enriched in rat and mouse sperma

194 These effects are most likely mediated by SREBP2, which responds to reductions in dietary choleste

195 Usp25(-/-) or Usp25(C178S) cells, activating Srebp2, with increased cholesterol flux and attenuated T