ライフサイエンスコーパス: SIRT

1 SIRT mice showed increased mortality, impaired hepatocyt

2 SIRT-1 may be a key therapeutic target to treat arterial

3 SIRTs are interesting drug targets as they are considere

4 SIRTs mediate KSHV latency by epigenetically silencing a

5 hers previously demonstrated that sirtuin 1 (SIRT-1) regulates apoptosis and cartilage-specific gene

6 ions in the cellular deacetylase, sirtuin-1 (SIRT-1), contribute to vascular endothelial dysfunction

7 mitochondrial dysfunction via the sirtuin-1 (SIRT-1)/ peroxisome proliferator-activated receptor gamm

8 ice and mice homozygous for SIRT-1tm2.1Mcby (SIRT-1y/y), an allele carrying a point mutation that enc

9 andomly assigned to treatment (control, 263; SIRT, 267).

10 ele carrying a point mutation that encodes a SIRT-1 protein with no enzymatic activity (y/y mice).

11 Incubation with sirtinol, a SIRT-1 inhibitor, reduced EDD in both young and older mi

12 ge homeostasis requires enzymatically active SIRT-1 protein.

13 Patient images after SIRT were reconstructed using the same parameters and we

14 struction parameters for (90)Y imaging after SIRT imaging.

15 struction parameters for (90)Y imaging after SIRT imaging.

16 /CT was performed at baseline and 3 mo after SIRT to calculate percentage changes in maximum (18)F-FD

17 ed by (18)F-FDG PET/CT before and 3 mo after SIRT was identified as the only independent predictor of

18 Overall median survival after SIRT was 47 wk.

19 Overall median survival after SIRT was 60 wk.

20 lic parameters for predicting survival after SIRT.

21 uced forearm EDD was impaired (P = 0.01) and SIRT-1 protein expression was 37% lower in endothelial c

22 and so increased cellular NAD(+) levels and SIRT-1 activity that subsequently increases mitochondria

23 cantly increased the expression of HDACs and SIRTs.

24 histone deacetylases (HDACs), also known as SIRTs, whose activities are linked to the cellular metab

25 norUrsodeoxycholic acid (NorUDCA) attenuates SIRT protein expression, increases the acetylation of FX

26 ad transcription factor FOXO-1, activated by SIRT-1, was identified as the downstream molecule within

27 Deacetylation of FOXO3 by SIRT activation or SIRT1 or SIRT7 overexpression prevent

28 D was positively related to endothelial cell SIRT-1 protein expression (r = 0.44, P < 0.01).

29 e here report that miR-149 strongly controls SIRT-1 expression and activity.

30 l model demonstrate that mice with defective SIRT-1 also have defective cartilage, with elevated rate

31 VI5008), also inhibited the NAD(+)-dependent SIRT deacetylase enzymes.

32 wild-type (WT) mice and mice homozygous for SIRT-1tm2.1Mcby (SIRT-1y/y), an allele carrying a point

33 uble-strand break (DSB) repair pathways, how SIRTs play a central role in the crosstalk between DNA r

34 tudy supports the notion that multiple human SIRT proteins have evolutionarily conserved and nonconse

35 This study was undertaken to determine if SIRT-1 enzymatic activity plays a protective role in car

36 ition, chondrocyte apoptosis was elevated in SIRT-1 mutant mice as compared to their WT littermates.

37 The damaging phenotype in SIRT mice correlated with impaired farnesoid X receptor

38 Reductions in SIRT-1 may play an important role in vascular endothelia

39 ntly, NorUDCA restored liver regeneration in SIRT mice, which showed increased survival and hepatocyt

40 Mammalian SIRTs (SIRT1-7) differ in their cellular localization an

41 These mitochondrial SIRTs (mtSIRT) regulate multiple cellular and physiologi

42 e roles and functional relevance of mtSIRTs (SIRT -3, -4, -5) in cancers.

43 We found that: 1) three nuclear SIRT proteins (SIRT1, SIRT6, and SIRT7) show different s

44 ins; 4) SIRT1, but not the other two nuclear SIRT proteins, shows an in vitro deacetylase activity on

45 at controls the expression and activation of SIRT-1.

46 st in part via a NAD-dependent activation of SIRT-PGC1alpha axis, a well-established cascade, involve

47 the liver was improved with the addition of SIRT (68.8% v 78.7% in control v SIRT; P = .042).

48 INTERPRETATION: Addition of SIRT to first-line FOLFOX chemotherapy for patients with

49 The addition of SIRT to FOLFOX-based first-line chemotherapy in patients

50 ty, preventing cathepsin-induced cleavage of SIRT 1 in EPCs and blunting SIPS and apoptotic cell deat

51 Because all of the components of SIRT are functional in many different organisms, it is r

52 ized Monte Carlo dosimetry in the context of SIRT was confirmed in this study.

53 Consistently, the effect of SIRT activators was reduced in the presence of NG-nitro-

54 6) B6D2F1 mice, aortic protein expression of SIRT-1 and eNOS phosphorylated at serine 1177 were lower

55 To elucidate the mechanism of SIRT inhibition by 27, we determined the 2.5 A crystal s

56 ection and studies investigating the role of SIRT as consolidation therapy after chemotherapy are nee

57 To further define the role of SIRT in metastatic colorectal cancer, careful patient se

58 Therefore, early use of SIRT in combination with chemotherapy in unselected pati

59 experiments revealed that the activation of SIRTs stimulated keratinocyte proliferation via endothel

60 Inhibitors of SIRTs can reactivate KSHV from latency.

61 re, we examined the effects of inhibitors of SIRTs, nicotinamide (NAM) and sirtinol, on KSHV reactiva

62 The role of SIRTs in cancer is extremely complex, with dichotomous f

63 After deacetylase inhibitor or SIRT activator treatment, ChIP showed, in fact, a signif

64 10 patients in the FOLFOX plus SIRT group and 11 patients in the FOLFOX alone group die

65 t-related deaths occurred in the FOLFOX plus SIRT group and three treatment-related deaths occurred i

66 The median survival time in the FOLFOX plus SIRT group was 22.6 months (95% CI 21.0-24.5) compared w

67 %) deaths in 554 patients in the FOLFOX plus SIRT group.

68 (37%) of 507 patients receiving FOLFOX plus SIRT).

69 e and 554 patients were assigned FOLFOX plus SIRT.

70 (54%) of 507 patients receiving FOLFOX plus SIRT.

71 FOLFOX (mFOLFOX6; control) or mFOLFOX6 plus SIRT (SIRT) plus or minus bevacizumab.

72 cans to optimize the reconstruction for post-SIRT imaging and clarify whether BPL leads to an improve

73 The Sirtuin family of proteins (SIRT) encode a group of evolutionarily conserved, NAD-de

74 ata suggest selective internal radiotherapy (SIRT) in third-line or subsequent therapy for metastatic

75 (90)Y after selective internal radiotherapy (SIRT) may allow for verification of treatment delivery b

76 3 mo after selective internal radiotherapy (SIRT).

77 e >/= 3 adverse events, including recognized SIRT-related effects, were reported in 73.4% and 85.4% o

78 tuin isoforms, silent information regulator (SIRT) 1, SIRT3, and SIRT6, play an essential role in the

79 00-fold improvement over previously reported SIRT inhibitors.

80 ls recovered 96 h after infection, restoring SIRT-1 and reducing HIV transcription to 20% of its high

81 There are seven SIRT isoforms in mammals, with diverse biological functi

82 nd 5) overexpression of any one of the seven SIRT proteins does not extend cellular replicative lifes

83 ipulated by increased expression of a single SIRT protein.

84 X (mFOLFOX6; control) or mFOLFOX6 plus SIRT (SIRT) plus or minus bevacizumab.

85 ) to transgenic mice that overexpress SIRT1 (SIRT).

86 nts and reverts NAFLD by inducing a sirtuin (SIRT)1- and SIRT3-dependent mitochondrial unfolded prote

87 lls, histone deacetylase (HDAC) and Sirtuin (SIRT) are two families responsible for removing acetyl g

88 new synthetic dinucleotides act as sirtuin (SIRT) inhibitors and show isoform selectivity for SIRT2

89 treating the cells with deacetylase sirtuin (SIRT) inhibitor nicotinamide or histone deacetylase (HDA

90 f the class III histone deacetylase sirtuin (SIRT)-1.

91 Silent information regulator or sirtuin (SIRT) enzymes are beta-nicotinamide adenine dinucleotide

92 scent substrate was devised for the sirtuin (SIRT) class of human protein deacetylases comprised of a

93 Members of the sirtuin (SIRT) family of NAD-dependent deacetylases promote longe

94 One such factor is the sirtuin (SIRT) family of nicotinamide adenine dinucleotide (NAD(+

95 At least seven Sir2 homologs, sirtuins (SIRT) 1 to 7 have been identified in mammals.

96 The sirtuins (SIRT 1-7) comprise a family of NAD(+)-dependent protein-

97 Sirtuins (SIRTs 1-7), or class III histone deacetylases (HDACs), a

98 Sirtuins (SIRTs) are critical enzymes that govern genome regulatio

99 Sirtuins (SIRTs) are NAD-dependent deacylases, known to be involve

100 Sirtuins (SIRTs) catalyze the NAD(+)-dependent deacetylation of N(

101 Sirtuins (SIRTs), class III histone deacetylases, are well charact

102 s (HDACs) and the NAD(+) dependent sirtuins (SIRTs) in the DNA damage response (DDR).

103 atency, the role of class III HDAC sirtuins (SIRTs) in KSHV latency remains unclear.

104 The role of sirtuins (SIRTs) was then investigated by using resveratrol and a

105 The sirtuins (SIRTs) have gained preeminence for their roles in the re

106 ilent information regulator genes (sirtuins [SIRTs]) 6 and 7 were significantly high in HBECs from as

107 of SIRT1 deacetylase, but not the other six SIRT proteins; 4) SIRT1, but not the other two nuclear S

108 local administration of natural or synthetic SIRT activators, in fact, significantly accelerated skin

109 ific integrase mediated repeated targeting" (SIRT), an attP attachment site for the phage phiC31 inte

110 Our results indicate that SIRTs regulate KSHV latency by inhibiting different stag

111 We confirmed the SIRT-RELB-SIRT3 adaptation link to mitochondrial bioener

112 However, the SIRT-deacetylated peptide is readily cleaved by trypsin,

113 genesis due to a decreased activation of the SIRT-1/PGC-1alpha pathway, suggesting that mitochondrial

114 be the final recipients and effectors of the SIRT-NO-HDAC signaling cascade.

115 cells are characterized by activation of the SIRT/FOXO/SOD2 axis of the mitochondrial unfolded protei

116 trypsin, and a microtiter plate assay of the SIRTs has been devised using the fluorescent substrate a

117 We found that one of the SIRTs, SIRT1, binds to the RTA promoter to mediate KSHV

118 cades, selective internal radiation therapy (SIRT) has become a real alternative in the treatment of

119 sphere selective internal radiation therapy (SIRT) is a valuable treatment in unresectable hepatocell

120 adding selective internal radiation therapy (SIRT) using yttrium-90 resin microspheres to standard fl

121 ation (selective internal radiation therapy [SIRT]) has emerged as a valuable therapeutic option in u

122 ation (selective internal radiation therapy [SIRT]) is a valuable therapeutic option for unresectable

123 Among these, SIRT -3, -4, and -5 are located in the mitochondria and

124 oxaliplatin) or FOLFOX plus single treatment SIRT concurrent with cycle 1 or 2 of chemotherapy.

125 Selective internal radiation treatment (SIRT) via intrahepatic arterial administration of (90)Y

126 We used SIRT to generate a series of six mutations in the Drosop

127 addition of SIRT (68.8% v 78.7% in control v SIRT; P = .042).

128 ite were similar (68.1% v 76.4% in control v SIRT; P = .113).

129 sis was 12.6 v 20.5 months in control versus SIRT (hazard ratio, 0.69; 95% CI, 0.55 to 0.90; P = .002

130 ite was 10.2 v 10.7 months in control versus SIRT (hazard ratio, 0.93; 95% CI, 0.77 to 1.12; P = .43)

131 3.4% and 85.4% of patients in control versus SIRT.

132 cy of combining first-line chemotherapy with SIRT using yttrium-90 resin microspheres in patients wit

133 eostasis in vivo, by investigating mice with SIRT-1 mutations to characterize their cartilage.

134 astases from breast cancer were treated with SIRT.

135 tases of colorectal cancer were treated with SIRT.

136 ions (25 HCC patients, 41 tumors) with (90)Y SIRT (7 glass spheres, 20 resin spheres) and the posttre

137 f hepatic toxicity associated with the (90)Y SIRT treatment.