ライフサイエンスコーパス: SREBP2

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

2 sterol regulatory element binding protein 2 (SREBP2).

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

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

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

6 gether with their protein levels, except for SREBP2.

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

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

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

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

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

12 es NLRP3 inflammasome in endothelium through SREBP2 activation.

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

14 to secondary feedback inhibition of hepatic SREBP2 activity.

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

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

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

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

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

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

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

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

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

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

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

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

27 rol levels through interference with nuclear SREBP2 clearance.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 n treatment but increased in cells following SREBP2 knockdown.

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

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

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

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

48 Thus, SREBP2-mediated cholesterol synthesis in astrocytes play

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

84 ls polarization through control of SIRT6 and SREBP2 ubiquitination.

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

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

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

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

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