ライフサイエンスコーパス: SIRT

1 SIRT mice showed increased mortality, impaired hepatocyt

2 SIRT was superior to (177)Lu-PSMA for the treatment of l

3 SIRT(oe) mice showed exacerbated parenchymal injury wher

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

5 SIRT-1's proviral activity is, we demonstrate, mediated

6 SIRTs are interesting drug targets as they are considere

7 SIRTs mediate KSHV latency by epigenetically silencing a

8 Sirtuin 1 (SIRT) mRNA levels were lower in PLAC when compared to DM

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

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

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

12 CPT1A, AMPK, PPARalpha, ACC, FAS, SREBP-1c, SIRT-1, and inflammatory/antioxidant markers were analyz

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

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

15 fter SIRT was achieved in 15 (52%) of the 29 SIRT patients and was predictive of survival.

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

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

18 ge homeostasis requires enzymatically active SIRT-1 protein.

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

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

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

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

23 EASL criteria, disease control at 6 mo after SIRT was achieved in 15 (52%) of the 29 SIRT patients an

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

25 Overall median survival after SIRT was 47 wk.

26 Overall median survival after SIRT was 60 wk.

27 lic parameters for predicting survival after SIRT.

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

29 O-1, PGC-1alpha, CPT1A, PPARalpha, AMPK, and SIRT-1 levels were higher in the livers of rats in the T

30 primarily released in an enveloped form, and SIRT-1 is required for this process.

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

32 clusion: The combination of (177)Lu-PSMA and SIRT is efficient and feasible for the treatment of adva

33 mo for combined sequential (177)Lu-PSMA and SIRT.

34 entional oncology techniques (PVE, TACE, and SIRT) in combination with other locoregional and systemi

35 (SIRTs), including HDACs 2, 7, 8, and 11 and SIRTs 4 and 6, repress KSHV ori-Lyt promoter activity.

36 cantly increased the expression of HDACs and SIRTs.

37 uming enzymes (NADases), including PARPs and SIRTs.

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

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

40 4-norursodeoxycholic acid) was tested in BDL/SIRT(oe) mice.

41 unced improvement in liver parenchyma in BDL/SIRT(oe) mice.

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

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

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

45 dentify randomized clinical trials comparing SIRT, as monotherapy or followed by sorafenib, with sora

46 Conclusion: SIRT as initial therapy for advanced HCC is noninferior

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

48 t inhibitor of class III histone deacetylase SIRTs (silent mating type information regulation 2 homol

49 Here, we show that the histone deacetylase, SIRT-1, is essential for autophagy and EV-D68 infection.

50 iously demonstrated that lysine deacetylase, SIRT-1, regulates DVL protein levels and its function, w

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

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

53 lls failed to show RV-induced TLR2-dependent SIRT-1 expression.

54 and this was associated with TLR2-dependent SIRT-1 expression.

55 Cotransfection of cells with NAT1 and either SIRT 1 or 2, but not SIRT3, significantly decreased NAT1

56 ing NAD(+) availability regulates endogenous SIRT activity, leading to increased resistance to oxidat

57 Median overall survival from the first SIRT was 18 mo (95% confidence interval [95%CI], 8-28 mo

58 RT and EBRT, leading to inflation of BED for SIRT and possible undertreatment.

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

60 hat DVL could potentially be a substrate for SIRT-1 mediated deacetylation.

61 Likewise, hepatocytes isolated from SIRT(oe) mice showed increased apoptosis in response to

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

63 However, SIRT family (1-7)-associated neurodegeneration has not b

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

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

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

67 apsigargin treatment or SERCA2A knockdown in SIRT-1 knockdown cells had no additional effect on EV-D6

68 reas a significant reduction was observed in SIRT(hep-/-) hepatocytes.

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

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

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

72 Increased SIRT activity was correlated with enhanced deacetylation

73 Pretreatment with quercetin, which increases SIRT-1 expression, normalized RV-induced IFN levels in C

74 Indeed, SIRTs have anti-inflammatory effects through a myriad of

75 against psychostimulant- and opioid-induced SIRT (1-7) expression in astrocytes.

76 Conclusion: First-line SIRT is safe and produced promising outcomes in patients

77 est that prospective trials using first-line SIRT should be considered.

78 included 22 patients treated with first-line SIRT.

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

80 epatocyte-specific SIRT1-KO (knockout) mice (SIRT(hep-/-) ) were subjected to bile duct ligation (BDL

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

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

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

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

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

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

87 The proviral activity of SIRT-1 does not require its deacetylase activity or func

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

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

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

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

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

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

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

95 tion, and additionally, through an effect of SIRT in the liver, peroxisome proliferator-activated rec

96 as to investigate the safety and efficacy of SIRT as first-line therapy in patients with uveal melano

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

98 Further, inhibition of SIRT-1 enhanced RV-induced IFN responses, and this was a

99 Inhibition of SIRT-1 in quercetin-pretreated COPD cells abolished the

100 Knockdown of SIRT-1 also decreases poliovirus and SARS-CoV-2 titers b

101 Knockdown of SIRT-1 inhibits autophagy and reduces EV-D68 extracellul

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

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

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

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

106 further information on the potential use of SIRT with (90)Y resin microspheres as first-line therapy

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

108 Inhibitors of SIRTs can reactivate KSHV from latency.

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

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

111 and METH, and opioids, such as morphine, on SIRT family (1-7) [class I, II, III and IV] expression a

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

113 sorafenib with SIRT (SIRveNIB and SARAH) or SIRT followed by sorafenib (SORAMIC), were included.

114 SIRT1-overexpressing (SIRT(oe) ) and hepatocyte-specific SIRT1-KO (knockout) m

115 proteins with NADase activity (e.g., PARPs, SIRTs, CD38).

116 10 patients in the FOLFOX plus SIRT group and 11 patients in the FOLFOX alone group die

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

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

119 %) deaths in 554 patients in the FOLFOX plus SIRT group.

120 (37%) of 507 patients receiving FOLFOX plus SIRT).

121 e and 554 patients were assigned FOLFOX plus SIRT.

122 (54%) of 507 patients receiving FOLFOX plus SIRT.

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

124 of liver resection and transplantation post SIRT.

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

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

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

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

129 3 mo after selective internal radiotherapy (SIRT).

130 in 149 of 515 patients (28.9%) who received SIRT and 249 of 575 (43.3%) who received sorafenib only

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

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

133 00-fold improvement over previously reported SIRT inhibitors.

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

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

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

137 ipulated by increased expression of a single SIRT protein.

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

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

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

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

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

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

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

145 lass III histone deacetylase (HDAC)-sirtuin (SIRT) family, that act as cellular sensors to regulate e

146 ter metabolism alongside increasing sirtuin (SIRT) signalling and mitochondrial biogenesis in rodent

147 focus from the function of nuclear sirtuin (SIRT)6 to that of cytoplasmic SIRT6, which deacetylates

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

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

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

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

152 ylation of NAT1 was enhanced by the sirtuin (SIRT) inhibitor nicotinamide but not by the histone deac

153 ies, we attributed this activity to Sirtuin (SIRT)1; however, the inhibitors used in this previous st

154 sfunction (p = 4.18E-08), while the sirtuin (SIRTs) signalling pathway was activated (p = 8.89E-06) w

155 Sirtuins (SIRT) exhibit deacetylation or ADP-ribosyltransferase ac

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

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

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

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

160 Sirtuins (SIRTs) are NAD(+)-dependent deacylases that play a key r

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

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

163 Sirtuins (SIRTs), a family of NAD-dependent protein deacylases, pl

164 Sirtuins (SIRTs), central regulators of the aging process, decreas

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

166 l histone deacetylases (HDACs) and sirtuins (SIRTs), including HDACs 2, 7, 8, and 11 and SIRTs 4 and

167 , poly-ADP-ribose polymerases, and sirtuins (SIRTs).

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

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

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

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

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

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

174 ibition of fatty acid synthase; non-specific SIRT inhibition; and activation of protein phosphatase t

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

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

177 Our data show that SIRT-1, through its translocation to the cytosol, is cri

178 om prospective clinical trials suggests that SIRT combined with chemotherapy might improve outcomes o

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

180 Nevertheless, recent findings show that SIRTs, specifically SIRT6, are also necessary for mounti

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

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

183 ch makes this protein a unique member of the SIRT family.

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

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

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

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

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

189 luding selective internal radiation therapy (SIRT) and TACE.

190 A) and selective internal radiation therapy (SIRT) for the treatment of liver metastases of castratio

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

192 iCCA), selective internal radiation therapy (SIRT) has been suggested as promising in nonrandomized s

193 Selective internal radiation therapy (SIRT) has been tested as salvage therapy, but no data ex

194 hip of selective internal radiation therapy (SIRT) in patients with metastatic colorectal cancer (mCR

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

196 ed for selective internal radiation therapy (SIRT) over sorafenib in patients with advanced hepatocel

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

198 Selective internal radiation therapy (SIRT) with yttrium-90 ((90)Y) resin microspheres is an e

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

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

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

202 on, 411 of 635 (64.7%) patients allocated to SIRT and 522 of 608 (85.8%) allocated to sorafenib compl

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

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

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

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

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

208 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

209 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)

210 3.4% and 85.4% of patients in control versus SIRT.

211 firming that quercetin exerts its effect via SIRT-1.

212 TLR2 may limit RV-induced IFN responses via SIRT-1.

213 howed exacerbated parenchymal injury whereas SIRT(hep-/-) mice evidenced a moderate improvement after

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

215 u-PSMA alone (n = 31) or in combination with SIRT (n = 5) were retrospectively analyzed.

216 r chemotherapy alone or the combination with SIRT.

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

218 Median OS with SIRT, whether or not followed by sorafenib, was noninfer

219 analysis, whether overall survival (OS) with SIRT, as monotherapy or followed by sorafenib, is noninf

220 ing 1,243 patients, comparing sorafenib with SIRT (SIRveNIB and SARAH) or SIRT followed by sorafenib

221 ompared with data from patients treated with SIRT and chemotherapy in MISPHEC.

222 tases of colorectal cancer were treated with SIRT.

223 astases from breast cancer were treated with SIRT.

224 ignificantly higher in patients treated with SIRT: median 21.7 months (95% CI: 14.1; not reached) ver

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

226 udies have assumed equivalence between (90)Y SIRT and EBRT, leading to inflation of BED for SIRT and

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