ライフサイエンスコーパス: SREBP1

1 SREBP1 and SREBP2 share approximately 47% sequence ident

2 SREBP1 cleavage is normally inhibited by increased stero

3 sterol regulatory element binding protein 1 (SREBP1) mediates the induction of steatosis by upregulat

4 , sterol response element binding protein 1 (SREBP1) was identified as a novel lamin A interactor.

5 e sterol response element-binding protein 1 (SREBP1) was implicated in the nutrient control of lipoge

6 Sterol regulatory element-binding protein 1 (SREBP1), when presented in its mature form (mSREBP1), en

7 sterol regulatory element-binding protein 1 (SREBP1)-directed transcription of its direct targets inc

8 sterol regulatory element-binding protein 1 (SREBP1)-mediated pathway through which miR-148a regulate

9 d sterol response element binding protein 1 (SREBP1).

10 e sterol response element binding protein 1 (SREBP1).

11 r sterol response element-binding protein-1 (SREBP1) and Spot 14 as biohydrogenation intermediate res

12 sterol regulatory element binding protein-1 (SREBP1) appear to be crucial for the response of the UCP

13 sterol regulatory element-binding protein 1(SREBP1/SREBF1), in a PI3K-mTORC1-dependent fashion.

14 genes (Insig1/2(Delta/Delta) mice) activated SREBP1, causing marked accumulation of lipids that consi

15 VEGF activated SREBP1 and SREBP2 in ECs, as demonstrated by the increas

16 l tissues was inversely correlated to active SREBP1.

17 rs including PPARgamma, the C/EBPs, and ADD1/SREBP1.

18 lement consensus and specifically binds ADD1/SREBP1.

19 The stimulation of PPARgamma by ADD1/SREBP1 does not require coexpression in the same cells;

20 th leptin and FAS are transactivated by ADD1/SREBP1.

21 supernatants from cultures that express ADD1/SREBP1 augment the transcriptional activity of PPARgamma

22 onstrate directly that cells expressing ADD1/SREBP1 produce and secrete lipid molecule(s) that bind d

23 that most if not all of this action of ADD1/SREBP1 is through an E-box motif at -64 to -59, containe

24 We show here that the expression of ADD1/SREBP1 specifically increases the activity of PPARgamma

25 A mutation in the basic domain of ADD1/SREBP1 that allows E-box binding but destroys sterol reg

26 This elevation of ADD1/SREBP1, leptin, and FAS that is induced by feeding in vi

27 These data establish that ADD1/SREBP1 can control the production of endogenous ligand(s

28 These results indicate that ADD1/SREBP1 is a key transcription factor linking changes in

29 red with the interaction between lamin A and SREBP1.

30 selective ER stress markers GRP78, CHOP, and SREBP1 was increased equivalently in both types of mice.

31 s pathway, such as PPARgamma, C/EBPalpha and SREBP1.

32 known partners, including actin, emerin, and SREBP1, but how these interactions are regulated is unkn

33 broblasts by significantly reducing LDLr and SREBP1 gene expression.

34 ; however, the connection between mTORC2 and SREBP1 has not been clearly established and hence is the

35 aster regulator of cholesterol biosynthesis, SREBP1.

36 Consistent with our in vitro data, SREBP1 was detected in newly developed microvasculatures

37 ranscription factors (PPARgamma, C/EBPalpha, SREBP1) of the adipogenesis pathway.

38 The gene encoding SREBP1 (SREBF1) has been cloned and characterized.

39 solated human adipocytes to insulin enhanced SREBP1 gene expression and promoted its proteolytic clea

40 ding of the adipoctye differentiation factor SREBP1 to lamin A.

41 lement-binding (SREBP) transcription factors SREBP1 and 2, whose activation and mRNA expression are s

42 ectly through SIRT1, it is also required for SREBP1 binding to the FAS promoter.

43 f evidence suggest that LSD1 is required for SREBP1-dependent activation of the FAS promoter in mamma

44 poorly or not activating the lipogenic genes SREBP1 and SCD1 or FASN, respectively.

45 andial rise in triglyceride synthesis genes (SREBP1-c, FAS, SCD-1).

46 pression and proteolytic maturation of human SREBP1 are positively modulated by insulin.

47 l clones provided an opportunity to identify SREBP1-regulated genes that may influence the assembly a

48 Oxysterols inactivated SREBP1 in wild type macrophages but not in LDLR(-/-) cel

49 transcription factors and enzymes, including SREBP1 and PNPLA3, as demonstrated by microarray analysi

50 yperinsulinemia also significantly increased SREBP1 gene expression in human skeletal muscle.

51 tive mechanism in WAT, which involves Insig1/SREBP1 and preserves the degree of lipid unsaturation un

52 ulatory feedback set point control of Insig1/SREBP1 represent an adaptive response that preserves WAT

53 p between (i) the cellular content of mature SREBP1 and 7alpha-hydroxylase protein, (ii) the relative

54 The increased cellular content of mature SREBP1 and increased secretion of apoB100 were concomita

55 l clones expressed varying amounts of mature SREBP1 protein.

56 terol, suggesting that the content of mature SREBP1, known to be decreased by 25-hydroxycholesterol,

57 inked through the cellular content of mature SREBP1.

58 Moreover, SREBP1 expression significantly increased the ability of

59 PUFA suppressed both the hepatic mRNA(SREBP1) through a PPARalpha-independent mechanism as wel

60 accumulated, glycogen stimulates the mTORC1/SREBP1 pathway to shift energy storage to lipogenesis.

61 In skeletal muscle, SREBP1 expression was significantly reduced in type 2 di

62 tely blocked the insulin-induced cleavage of SREBP1 protein.

63 The cleavage of SREBP1 requires it to be in complex with SREBP cleavage

64 thesis, under the transcriptional control of SREBP1, is regulated by the rapamycin-sensitive mTOR sig

65 he N-terminal transcription factor domain of SREBP1, between residues 227 and 487.

66 Importantly, ectopic expression of SREBP1, the master regulator of lipogenic genes, in MCF1

67 Within the diabetic group, the extent of SREBP1 suppression was inversely related to metabolic co

68 nd insulin-treated cells, the mRNA levels of SREBP1-c, SREBP2, fatty-acid synthase, acetyl-CoA carbox

69 ve response that promotes the maintenance of SREBP1 maturation and facilitates lipogenesis and availa

70 A role for mTORC1 in the regulation of SREBP1 activity has been suggested; however, the connect

71 d sterol regulatory element-binding protein (SREBP1 and SREBP2).

72 sterol regulatory element-binding proteins (SREBP1 and SREBP2) that are required for oncogene-induce

73 we show that LSD1 plays a role in regulating SREBP1-mediated gene expression.

74 In this report, we have assessed the role SREBP1 plays in the PUFA control of three hepatic genes,

75 in primary hepatocytes, CA-FoxO1 suppressed SREBP1-c expression and inhibited basal and insulin-indu

76 complex 1 (mTORC1) and its downstream target SREBP1.

77 sterol homeostasis (where it has been termed SREBP1).

78 We find that SREBP1 and 2 promote proliferation downstream of mTORC1,

79 using short hairpin RNA (shRNA) showed that SREBP1 cleavage and the induction of lipogenic genes and

80 alpha(i2) promoter activity, suggesting that SREBP1 may play a role in the regulation of Galpha(i2) e

81 on correlates with increased cleavage of the SREBP1 precursors to form the mature active transcriptio

82 They also show that the SREBP1-mediated induction of hepatic steatosis in ob/ob

83 The binding of lamin A to SREBP1 was noticeably reduced by FPLD mutations.

84 In turn, SREBP1 regulates the expression of key lipogenic enzymes

85 e, we show that miR-33b also cooperates with SREBP1 in regulating glucose metabolism by targeting pho