ライフサイエンスコーパス: SIRT1

1 SIRT1 (Sir2) is an NAD(+)-dependent deacetylase that pla

2 SIRT1 and AMPK also act on sodium transport mechanisms t

3 SIRT1 deficiency in the epidermis inhibited the regenera

4 SIRT1 expression by T cells significantly associated wit

5 SIRT1 has been shown to promote progression of colorecta

6 SIRT1 increases the levels of the transcriptional coacti

7 SIRT1 is part of the E1-E2 DNA replication complex and i

8 SIRT1 is the proto member of the proteins in the mammali

9 SIRT1 is widely expressed in the brain; however, neurona

10 SIRT1 loss altered the production of many cytokines, inh

11 SIRT1 overexpression or PCAF silencing inhibited the int

12 SIRT1 protects against several complex metabolic and age

13 SIRT1 T530 phosphorylation is essential to prevent DNA b

14 SIRT1 was required to mediate the effects of 5-HT on mit

15 SIRT1, a NAD(+)-dependent deacetylase, is pivotal in reg

16 SIRT1, the most conserved mammalian NAD(+)-dependent pro

17 SIRT1-overexpressing (SIRT(oe) ) and hepatocyte-specific

18 SIRT1-regulated Akt, endothelial nitric oxide synthase a

19 ing type information regulation 2 homolog 1 (SIRT1), which deacetylates forkhead box o3 (FOXO3a), lea

20 g type information regulation 2 homologue 1 (SIRT1) content and activity (P < 0.001).

21 olstered via Silent information regulator 1 (SIRT1) and peroxisome proliferator-activated receptor-ga

22 HES1) and the protein deacetylase sirtuin 1 (SIRT1) at the Isl1 gene.

23 Sirtuin 1 (SIRT1) binds, deacetylates, and thereby inactivates HIF-

24 gher abundance of the deacetylase sirtuin 1 (SIRT1) correlated with lower acetylation occupancy and l

25 The class III NAD-sirtuin 1 (SIRT1) is an important negative regulator of inflammatio

26 The NAD(+)-dependent deacetylase Sirtuin 1 (SIRT1) is down-regulated in triple-negative breast cance

27 The NAD(+)-dependent deacetylase Sirtuin 1 (SIRT1) regulates cell metabolism, proliferation, and DNA

28 Sirtuin 1 (SIRT1) regulates liver regeneration and bile acid metabo

29 g with significant suppression of sirtuin 1 (SIRT1) signaling pathway in the liver.

30 In animal studies, sirtuin 1 (SIRT1) was associated with protection against inflammati

31 We investigated how Sirtuin 1 (SIRT1), a conserved mammalian NAD(+)-dependent protein d

32 Sirtuin 1 (SIRT1), an NAD(+) (nicotinamide adenine dinucleotide)-de

33 monstrates the beneficial role of Sirtuin 1 (SIRT1), an NAD(+) dependant deacetylase, in improved ins

34 Sirtuin 1 (SIRT1), an NAD(+)-dependent deacetylase, is a key regula

35 D+)-dependent deacetylase enzyme, Sirtuin 1 (SIRT1), can prevent activation of these pathways and pro

36 nergy sensing pathways, including sirtuin 1 (SIRT1), forkhead box O (FoxO), AMP-activated protein kin

37 S2 expression can be modulated by sirtuin 1 (SIRT1), the master metabolic sensor of the cell, belongi

38 and RA reduced HDAC1, HDAC4, and sirtuin 1 (SIRT1), which were involved in chromatin remodeling of t

39 th the metabolic sensing protein, Sirtuin 1 (SIRT1).

40 netic approaches to show that the sirtuin 1 (SIRT1)/FoxO1 signaling pathway in the hypothalamic arcua

41 NAD-dependent deacetylase sirtuin-1 (SIRT1) is a class III histone deacetylase that positivel

42 f nutrient and oxygen deprivation-sirtuin-1 (SIRT1), AMP-activated protein kinase (AMPK), and hypoxia

43 low-energy sensors, which include sirtuin-1 (SIRT1), AMP-activated protein kinase (AMPK), and hypoxia

44 nse to lipolytic stimulation in a sirtuin-1 (SIRT1)-dependent manner via a mechanism that requires so

45 3) SIRT1 activation prevented nuclear translocation of NF-k

46 apy, by reversing the expression of miR-34a, SIRT1, cyclin D1, and E-cadherin.

47 entified the transcription factor FoxO1 as a SIRT1 target involved in transcriptional reprogramming o

48 increased cortical mtDNA and ATP levels in a SIRT1-dependent manner.

49 e metabolism in cells and animal models in a SIRT1-dependent manner.

50 t only demonstrates the essential roles of a SIRT1-miR-1185-1-CD24 axis in both colorectal cancer ste

51 ausing upregulated angiogenic pathways via a SIRT1-PGC-1alpha pathway.

52 al biogenesis and oxidative metabolism via a SIRT1/PGC-1alpha/PPARalpha-dependent pathway through an

53 When a SIRT1 activator (SRT2104) is injected into the mPFC or l

54 associated sEV release, and treatment with a SIRT1 agonist prevented this effect.

55 fatty acids (MUFAs) allosterically activate SIRT1 toward select peptide-substrates such as PGC-1alph

56 eart failure), but SGLT2 inhibitors activate SIRT1/PGC-1alpha/FGF21 signaling and promote autophagy.

57 Agents designed to activate SIRT1 might be developed as treatments for IBDs.

58 loops: voluntary food restriction activates SIRT1, promoting anxiety, hyperactivity, and addiction t

59 ting and exercising, thus further activating SIRT1.

60 EX527 attenuated secretion while activating SIRT1 by resveratrol-potentiated secretion.

61 , necessary to investigate how ATRAP affects SIRT1 protein expression to resolve ageing-associated ki

62 tiation factor RRN3, were up-regulated after SIRT1 inhibition.

63 expression in the ciRPTEC but did not alter SIRT1 mRNA expression.

64 ivity, possibly by activating PGC-1alpha and SIRT1, to improve physical endurance, strongly suggestin

65 At DNA damage sites, BRG1 and SIRT1 physically interact, whereupon SIRT1 deacetylates

66 nvolved in molecular regulation of CD24- and SIRT1-related cancer stemness networks, marking it a pot

67 Furthermore, CLOCK and SIRT1 are important for regulating cocaine reward and do

68 Intracellular proinflammatory cytokines and SIRT1 were measured in blood T, natural killer T-like ce

69 line, +/-1uM prednisolone and cytokines, and SIRT1 assessed using flow cytometry.

70 s associated with elevated HDAC1, HDAC4, and SIRT1 in colon adenocarcinomas.

71 type information regulation 2 homologs) and SIRT1 is an inhibitor of poly-ADP-ribose polymerase-1 (P

72 cose homeostasis, linking hyperglycaemia and SIRT1 downregulation.

73 rved between serum concentrations of MBL and SIRT1 (r = -0.30; P = 0.006).

74 odontal treatment on serum levels of MBL and SIRT1.

75 arameters, inflammatory biomarkers, MBL, and SIRT1 levels were measured at baseline and at post-treat

76 e also induced in hypertrophied muscles, and SIRT1 levels correlated with muscle mass, paired box pro

77 creased PAPR2 expression, deceased NAD+, and SIRT1, increased PGC-1alpha acetylation (inactive form),

78 on its canonical targets such as Notch1 and SIRT1, and on Ras/MAPK-dependent pathways.

79 strating a functional link between ORF4a and SIRT1 in mammalian cells.

80 s, including HDAC3, Rev-erb-alpha, PARP1 and SIRT1.

81 with significant effects for MTF2, PHF19 and SIRT1 (P<0.05).

82 in untreated PMDD LCLs with MTF2, PHF19 and SIRT1 all significantly decreased (P<0.05).

83 and reduced poly(ADP-ribose) polymerase and SIRT1 activities, respectively, affecting many associate

84 e debate on the relationship between RSV and SIRT1 has precluded the use of RSV as a therapeutic drug

85 anism between colorectal cancer stemness and SIRT1 remains to be further clarified.

86 quiring the catalytic AMPKalpha2 subunit and SIRT1, two known activators of PPARalpha.

87 d a significant positive correlation between SIRT1 expression and muscle fiber cross-sectional area i

88 occurring form of DBC1, which does not bind SIRT1 and is dynamically regulated, thus contributing to

89 ster modulators of mitochondrial biogenesis, SIRT1 and PGC-1alpha.

90 In addition, blocking SIRT1 by EX527 attenuated secretion while activating SIR

91 Interestingly, both SIRT1 overexpression and hepatocyte-specific SIRT1 deple

92 translated region) and could be inhibited by SIRT1 via histone deacetylation.

93 P4 secretion from adipocytes is regulated by SIRT1 and requires early autophagic components.

94 fection, the acetylated Lys129 is removed by SIRT1, which promptly inactivates OTUD3 and thus allows

95 ared with stable patients and controls (%CD8 SIRT1 T cells: 17 +/- 10; 37 +/- 10; 30 +/- 10) (mean +/

96 Central SIRT1 is required for MCH-induced weight gain through it

97 Chemical SIRT1 activators (SIRT1720 and resveratrol) suppressed t

98 Conclusion: SIRT1 expression is increased during human and murine ch

99 e data identify the evolutionarily conserved SIRT1-FoxO1 axis as a regulator of resting CD8(+) memory

100 Consistently, SIRT1 KO embryos display reduced Mat2a expression and hi

101 By contrast, SIRT1 serum levels increased (1.06 +/- 1.03 to 1.66 +/-

102 of methyltransferase DNMT3b and deacetylase SIRT1 may explain the observed p66(Shc)-related epigenet

103 gy sensor mTOR, NAD(+)-dependent deacetylase SIRT1, hypoxia-inducible factor HIF1alpha, oxidative str

104 ependent on the NAD(+)-dependent deacetylase SIRT1.

105 e response of the protein lysine deacetylase SIRT1 to small-molecule activators.

106 BOS is associated with decreased SIRT1 in peripheral blood proinflammatory T, NK, and NKT

107 al Th1 subset, inducing a lactate-dependent, SIRT1-mediated deacetylation/degradation of T-bet transc

108 We determined SIRT1 expression in livers from patients with cholestati

109 Moreover, AMPK-directed SIRT1 phosphorylation is required for energy starvation-

110 The cells respond by downregulating SIRT1, AMPK, and HIF-2alpha, thus leading to an impairme

111 atic activity decreased significantly during SIRT1 overexpression or activation by resveratrol.

112 ibitors may be related primarily to enhanced SIRT1 and HIF-2alpha signaling; this can explain the eff

113 on analysis indicates that pyruvate enhances SIRT1 binding at histone gene promoters where it reduces

114 1 specifically in the intestinal epithelium (SIRT1 iKO, villin-Cre+, Sirt1(flox/flox) mice) and contr

115 y of the histone deacetylase sirtuin family (SIRT1, SIRT2, SIRT3, SIRT5 and SIRT6) using both recombi

116 e, as well as to analyze the requirement for SIRT1 in autophagy regulation by HO-1.

117 oplasmic translocation of p53 resulting from SIRT1-mediated deacetylation of p53.

118 Intestinal tissues from SIRT1 iKO mice given antibiotics, however, did not have

119 upon replication stress and cells harboring SIRT1 that cannot be phosphorylated exhibit a high preva

120 Hepatic SIRT1 overexpression corrects defective autophagy, resto

121 negative regulator of inflammation; however, SIRT1 activity following lung transplant has not been st

122 Consistent with neuronal hypoexcitability, SIRT1 knockout reduces mitochondrial density and express

123 We show that impaired SIRT1, FoxO3a, AMPK, and PPAR-alpha signaling are respon

124 mal tubule to determine the role of ATRAP in SIRT1 protein expression.

125 In fact, WT mice show a decrease in SIRT1 activity during liver regeneration, coincidentally

126 FoxO1 is proteasomally degraded in SIRT1-deficient CD8(+)CD28(-) T cells, and inhibiting it

127 llating genes under CR show an enrichment in SIRT1 targets in the liver.

128 This increase in SIRT1 was abrogated by the addition of exogenous pyruvat

129 t the importance of methionine metabolism in SIRT1-mediated mESC maintenance and embryonic developmen

130 An 80% reduction in SIRT1 levels was observed in patients with diabetes, bot

131 o the human setting, we noted a reduction in SIRT1 mRNA in kidney biopsies obtained from individuals

132 ed as a major serine phosphorylation site in SIRT1 in obese, but not lean, mice, and this phosphoryla

133 respond to various human sirtuins, including SIRT1, SIRT2, SIRT3 and SIRT5.

134 n that DBC1 regulates its targets, including SIRT1, by protein-protein interaction.

135 Treatment options that increase SIRT1 may improve graft survival.

136 panied by decreased OLT damage and increased SIRT1/LC3B expression, whereas adjunctive inhibition of

137 ansport, or inhibition of enolase, increased SIRT1 protein levels in normal human epidermal keratinoc

138 activity and increased NAD(+), which induced SIRT1-dependent autophagy in both OXPHOS-competent and O

139 Moreover, ORF4a inhibited SIRT1-mediated modulation of NF-kappaB signaling, demons

140 iomarker PAT2 and the adipogenesis inhibitor SIRT1.

141 The mammalian homologue of SIR2 is SIRT1, an NAD-dependent histone deacetylase.

142 In keratinocytes, SIRT1 knockdown inhibited EMT, cell migration, and TGF-b

143 Together, these data suggest that KRAS, SIRT1 and BCL6 are coordinately over-expressed in eutopi

144 tions of MCH are compromised in mice lacking SIRT1 specifically in POMC neurons.

145 PBMs from healthy controls had lower SIRT1 and SIRT7 and readily formed p-FOXO3 and underwent

146 es, mediates the downregulation of mammalian SIRT1 protein during senescence and in vivo ageing.

147 n; however, neuronal substrates that mediate SIRT1 action on depressive behaviors remain largely unkn

148 llow-up analyses showed cancer cell-mediated SIRT1 loss induced NF-kappaB signaling in cachectic musc

149 AAV-Cre-mediated SIRT1 knockdown in the medial prefrontal cortex (mPFC) o

150 ne (LDN) abrogates hyperinsulinemia-mediated SIRT1 repression and prevents NF-kappaB p65 nuclear tran

151 Thus, ATRAP likely mediates SIRT1 protein abundance in ciRPTEC.

152 We also directly monitored SIRT1 and SIRT2 activity in HEK293T cells with an mCherr

153 Moreover, SIRT1 iKO mice with defective gut microbiota developed m

154 y, likely through inactivation of the NAD(+)-SIRT1-caveolin-1 axis, which limits an important fuel so

155 Expression of nonglycosylatable SIRT1 in the liver abrogated metabolic flexibility, resu

156 In senescence, nuclear SIRT1 is recognized as an autophagy substrate and is sub

157 oneogenesis and ketogenesis is activation of SIRT1 (sirtuin-1) and its downstream mediators: PGC-1alp

158 The activation of SIRT1 (through its effects to promote gluconeogenesis an

159 Activation of SIRT1 by SRT1720 reduced Alizarin red staining by a thir

160 The activation of SIRT1, AMPK, and HIF-2alpha enhances autophagy, a lysoso

161 ypoxia mimicry, which includes activation of SIRT1, AMPK, and HIF-2alpha, enhanced autophagic flux, r

162 apoptotic form of FOXO3 and the activity of SIRT1 and particularly SIRT7 regulate this process in vi

163 ctivates the histone deacetylase activity of SIRT1.

164 equences of depleting breast cancer cells of SIRT1.

165 cytosolic ubiquitin-mediated degradation of SIRT1.

166 Mice with intestinal deletion of SIRT1 (SIRT1 iKO) had abnormal activation of Paneth cell

167 Here we show that selective deletion of SIRT1 in forebrain excitatory neurons causes depression-

168 ice with intestinal epithelial disruption of SIRT1, we found this protein to prevent intestinal infla

169 ATPase domain of BRG1 and the ZnF domain of SIRT1 interact with poly-ADP ribose (PAR) in response to

170 nce pathways, suggesting a downregulation of SIRT1 may be responsible for perpetuating vascular calci

171 pairment was attributed to downregulation of SIRT1 signaling and mTOR was not implicated.

172 t in GSD-Ia is mediated by downregulation of SIRT1/FoxO3a/AMPK/PPAR-alpha signaling.

173 The detrimental effects of SIRT1 during cholestasis were validated in vivo and in v

174 ic hepatitis patients had high expression of SIRT1 and SIRT7 and failed to induce p-FOXO3 and apoptos

175 Fine-tuning expression of SIRT1 is essential to protect the liver from cholestatic

176 y, we tested whether increased expression of SIRT1 protein in sensory neurons prevents and reverses e

177 ablish nutrient-dependent O-GlcNAcylation of SIRT1, within its N-terminal domain, as a crucial determ

178 ish that nutrient-dependent glycosylation of SIRT1 is essential to gate its functions and maintain ph

179 fasted-to-refed transition, glycosylation of SIRT1 modulates its interactions with various transcript

180 the regulation of the protein homeostasis of SIRT1 and suggests a potential strategy to stabilize SIR

181 SIRT1 catalytic activity, the homeostasis of SIRT1 at the protein level is poorly understood.

182 tudy also reveals that hyperglycosylation of SIRT1 is associated with aging and high-fat-induced obes

183 the PGR positive cells reveal an increase of SIRT1 expression in the endometrium compared to control

184 Inhibition of SIRT1 by selisistat EX527 blunted UA-induced angiogenic

185 expression, whereas adjunctive inhibition of SIRT1 signaling diminished HO-1-mediated hepatoprotectio

186 Conversely, inhibition of SIRT1 via Sirtinol and siRNA increased RUNX2 by over 50%

187 tent agonists of PARP1 through inhibition of SIRT1.

188 he decrease, but not complete inhibition, of SIRT1 exerted by norUDCA treatment correlated with prono

189 While knockout of SIRT1 increased EV release with enlarged late endolysoso

190 nt increased both mRNA and protein levels of SIRT1 in podocytes and that puerarin led to SIRT1-mediat

191 itis expressed significantly lower levels of SIRT1 mRNA than controls.

192 Higher levels of SIRT1 protein were localized to cortical and hippocampal

193 of MBL and CRP and increased serum levels of SIRT1.

194 They find that loss of SIRT1 activity drives senescence-associated sEV release,

195 ch-clamp recordings demonstrate that loss of SIRT1 decreases intrinsic excitability and spontaneous e

196 -lysosome pathway contributes to the loss of SIRT1 during ageing of several tissues related to the im

197 Of note, loss of SIRT1 glycosylation discomposed these interactions resul

198 There was a loss of SIRT1 in T, NK-like, and NK cells in BOS patients compar

199 Loss of SIRT1 was associated with increased T, NKT-like, and NK

200 However, the mechanisms of SIRT1 regulation remain to be elucidated.

201 ith inhibition of FXR, whereas modulation of SIRT1 by NorUDCA associated with restored FXR signaling.

202 st-known endogenous allosteric modulators of SIRT1 and characterize a LD-nuclear signaling axis that

203 growth driven by neuronal overexpression of SIRT1.

204 Mechanistically, phosphorylation of SIRT1 at Ser-164 substantially inhibited its nuclear loc

205 her these studies highlight the potential of SIRT1 activation as a therapeutic strategy in progressiv

206 iet to determine the biological relevance of SIRT1 during cholestasis.

207 se metabolism and highlight the relevance of SIRT1/FoxO1 pathway in obesity.

208 ether, these data support a critical role of SIRT1 in inflammation and insulin resistance in hyperins

209 However, the role of SIRT1 in the multi-step process leading to transformatio

210 h SIRT1 activity is altered, and the role of SIRT1 in tumor metabolism is unknown.

211 This study aimed to determine the role of SIRT1 in vascular smooth muscle cell (vSMC) calcificatio

212 es is characterized by marked suppression of SIRT1 and AMPK, leading to a diminution in autophagic fl

213 ne supplementation increases the survival of SIRT1 KO newborn mice.

214 mitochondria and unexpectedly is a target of SIRT1 deacetylation.

215 ux through a mechanism distinct from that of SIRT1.

216 ation studies identified genetic variants of SIRT1 linked to major depressive disorders.

217 , or inhibition of enolase, was dependent on SIRT1.

218 This effect on SIRT1 activity was not observed in DBC1 KO mice.

219 mechanism exerts spatiotemporal control over SIRT1 functions by constituting a previously unknown mol

220 ic mouse that is inducible and overexpresses SIRT1 protein in neurons (nSIRT1OE Tg).

221 ffects were abolished in mice overexpressing SIRT1 fed a high-fat diet.

222 required for energy starvation-induced PABP1-SIRT1 association, PABP1 deacetylation, and poly(A)RNA n

223 We propose SIRT1 inhibition can break this cycle and provide a pote

224 The NAD+-dependent protein SIRT1 deacetylates RECQL4 in vitro and in cells thereby

225 B site within the SIRT1 promoter and reduced SIRT1 levels.

226 ely, these findings help explain how reduced SIRT1 expression, by disrupting lysosomal function and g

227 we demonstrated that ATRAP knockdown reduced SIRT1 protein expression in the ciRPTEC but did not alte

228 We demonstrate that reduced SIRT1 levels are associated with elevated levels of acet

229 These findings suggest that reduced SIRT1-mediated deacetylation of HIF-1alpha contributes t

230 rmine the mechanistic basis by which reduced SIRT1 expression influences processes related to certain

231 We discovered that reducing SIRT1 levels decreased the expression of one particular

232 effects involved oxidative stress reduction, SIRT1-mediated mitochondrial function promotion, and pAK

233 espite this, if/how nutrient inputs regulate SIRT1 interactions, stability, and therefore downstream

234 -induced changes in microRNA levels regulate SIRT1 and insulin-like growth factor 1 signalling.

235 creased in obese individuals, down-regulated SIRT1 levels, leading to elevated acetyl-HIF-1alpha and

236 nd oxidative stress, an effect that required SIRT1.

237 alpha-secretase (ADAM10), MINT2, FE65, REST, SIRT1, BIN1, and ABCA7, among others.

238 mice corrects defective autophagy, restores SIRT1/FoxO3a/AMPK/PPAR-alpha signaling and rectifies met

239 Remarkably, phosphorylated S164-SIRT1 and CK2 levels were also highly elevated in liver

240 s are down-regulated by the metabolic sensor SIRT1.

241 Mice with intestinal deletion of SIRT1 (SIRT1 iKO) had abnormal activation of Paneth cells start

242 Sirtuin1 (SIRT1) deacetylase delays and improves many obesity-rela

243 300 at Lys-566 and deacetylated by sirtuin1 (SIRT1).

244 gest that hyperinsulinemia induces sirtuin1 (SIRT1) repression and stimulates NF-kappaB p65 nuclear t

245 in situ and is deacetylated by the sirtuins SIRT1 and 2.

246 Sirtuins (SIRT1-7) are NAD-dependent proteins with the enzymatic a

247 SIRT1 overexpression and hepatocyte-specific SIRT1 depletion correlated with inhibition of FXR, where

248 pressing (SIRT(oe) ) and hepatocyte-specific SIRT1-KO (knockout) mice (SIRT(hep-/-) ) were subjected

249 d suggests a potential strategy to stabilize SIRT1 to promote productive ageing.

250 ough there is strong interest in stimulating SIRT1 catalytic activity, the homeostasis of SIRT1 at th

251 Targeting SIRT1 by RNAi led to elevated H3 lysine 9 acetylation on

252 pair through interaction with OGG1, and that SIRT1 indirectly modulates BER of 8-oxoG by controlling

253 fatty acid oxidation in hepatocytes and that SIRT1 signaling was potentially involved in the process.

254 Here, we demonstrate that SIRT1 dose-dependently regulates cellular glutamine meta

255 Herein, we demonstrate that SIRT1 inhibition, both genetically and pharmacologically

256 The results demonstrate that SIRT1 is a member of, and can regulate, the HPV16 replic

257 We demonstrate that SIRT1-deficient mESCs are hypersensitive to methionine r

258 s provide in vivo and in vitro evidence that SIRT1 in the epidermis regulates cell migration, redox r

259 Here, we provide evidence that SIRT1, the most conserved mammalian NAD(+)-dependent pro

260 Furthermore, we also found that SIRT1 can regulate levels of adenylated hTR through PARN

261 We found that SIRT1 was highly expressed in livers from cholestatic pa

262 ays, allow us to propose the hypothesis that SIRT1 may actually play a crucial causal role in overloa

263 We hypothesized that SIRT1 expression is decreased in proinflammatory lymphoc

264 Recent work indicates that SIRT1 and orthologous sirtuins coactivate the oestrogen

265 tivates its expression, but we observed that SIRT1 repressed LEF1 protein and mRNA expression, ultima

266 Here we report that SIRT1 signaling regulates colorectal cancer stemness by

267 These findings demonstrate the key role that SIRT1 plays in preventing calcification in a diabetic en

268 ng with the well-known regulatory roles that SIRT1 plays in modulating both anabolic and catabolic pa

269 evelopmental Cell, Latifkar et al. show that SIRT1 controls lysosomal acidification and its loss enha

270 Moreover, we show that SIRT1 levels are required for OGT-mediated regulation of

271 Our data showed that SIRT1 protein expression was reduced in ATRAP-deficient

272 These results suggest that SIRT1 in mPFC excitatory neurons is required for normal

273 These observations suggest that SIRT1 phosphorylation modulates the distribution of repl

274 Mechanistically, we suggest that SIRT1 promotes progression of ABA, in part through its i

275 educed MERS-CoV replication, suggesting that SIRT1 is a proviral factor for MERS-CoV.

276 We demonstrate for the first time that SIRT1 is a proviral factor for MERS-CoV replication and

277 We also demonstrate for the first time that SIRT1 is a proviral factor for MERS-CoV replication and

278 In addition, the SIRT1-PABP1 association is not specific to energy starva

279 lanocortin (POMC) neuronal activity, and the SIRT1/FoxO1 pathway regulates the inhibitory effect of M

280 g gene editing technology (CRISPR/Cas9), the SIRT1 gene was removed from cervical cancer cells.

281 s IIa specific inhibitor MC1568, but not the SIRT1 specific inhibitor EX-527.

282 -HT(2A) receptor-mediated recruitment of the SIRT1-PGC-1alpha axis, which is relevant to the neuropro

283 l function and metabolic homeostasis via the SIRT1/SIRT5 axis, which underlies hydralazine's prolonge

284 actor, which bound to a CREB site within the SIRT1 promoter and reduced SIRT1 levels.

285 oaches, we demonstrated that LDN can bind to SIRT1 and increase its deacetylase activity.

286 es the S1-like domain and no longer binds to SIRT1.

287 SIRT1 in podocytes and that puerarin led to SIRT1-mediated deacetylation of NF-kappaB and suppressio

288 ts, but SGLT2 inhibitors may also upregulate SIRT1, PGC-1alpha, and FGF21 by a direct effect on the h

289 vent NAD depletion (theophylline) upregulate SIRT1 and reduce proinflammatory cytokine expression in

290 All treatments upregulated SIRT1 and inhibited IFNgamma and TNFalpha production by

291 We found that when SIRT1 was inhibited by either chemical or genetic manipu

292 nocyte adhesion and AoSMC migration, whereas SIRT1 activation prevented immune cell recruitment and c

293 RG1 and SIRT1 physically interact, whereupon SIRT1 deacetylates BRG1 at lysine residues 1029 and 1033

294 Here, we sought to determine whether SIRT1 also plays a role in regulating aromatase expressi

295 d may be dependent upon the context in which SIRT1 activity is altered, and the role of SIRT1 in tumo

296 activity-based anorexia (ABA) models, while SIRT1 activation accelerates ABA phenotypes.

297 man aortic smooth muscle cells (AoSMCs) with SIRT1 activators (SRT1720 and resveratrol) inhibit both

298 o enhance acetylation or cotransfection with SIRT1 to inhibit acetylation.

299 was reduced in chondrocytes transfected with SIRT1 siRNA or treated with nicotinamide (NAM), a sirtui

300 wing lung transplant and that treatment with SIRT1 activators (resveratrol, curcumin) and agents that