ライフサイエンスコーパス: HSF

1 HSF binds to nmnat promoter and induces NMNAT expression

2 HSF is also required for metazoan development; however,

3 HSF is necessary for both the activation of PARP's enzym

4 HSF mediates the transcriptional response of eukaryotic

5 HSF showed increased Tyr 705 STAT3 phosphorylation compa

6 HSF-1 (heat shock transcription factor 1) and HSP70 were

7 HSF-1 activation was associated with an increase in occl

8 HSF-1 bound to and transactivated the Slug promoter inde

9 HSF-1 developmental activation requires binding of E2F/D

10 HSF-1 knockdown reduced the ability of Akt to induce Slu

11 HSFs expressed TGFBI and secreted TGFBIp (approximately

12 cantly decreased (25 microg/mL; P <or= 0.05) HSF attachment to collagen type I, whereas rTGFBIp did n

13 ative stress-responsive heat shock factor 1 (HSF-1) and expression of heat shock proteins, including

14 inase signaling control heat shock factor 1 (HSF-1), a conserved stress-activated transcription facto

15 Heat-shock factor 1 (HSF-1), a transcription factor for heat-shock proteins (

16 ative binding sites for heat shock factor 1 (HSF-1), nuclear factor 1 (NF-1), and one of two cyclic A

17 tasis network regulator heat shock factor 1 (HSF-1), the stress resistance and longevity transcriptio

18 conserved heat shock transcription factor-1 (HSF-1) is essential to cellular stress resistance and li

19 S-induced activation of heat shock factor-1 (HSF-1) resulted in cytoplasmic-to-nuclear translocation

20 , the binding sites for heat shock factor-1 (HSF-1), located in the Slug promoter.

21 ein 90 (hsp90) with the heat shock factor-1 (HSF-1), which induces the mRNA and protein levels of hsp

22 pared gene expression profiles of the HSF-1, HSF-6 and H9 lines.

23 There are 21 HSFs in Arabidopsis, and recent studies have established

24 ated with lower expression of most of the 21 HSFs and some of the HSPs in the mutant plants.

25 led that the expression of HSFA6b, a class A HSF, extensively increased with salinity, osmotic, and c

26 Class A HSFs can also interact weakly with TFIIB.

27 Here, we show that class A HSFs may activate transcription through direct contacts

28 pable of transcriptional activation (class A HSFs) or both, activation and repression (class B HSFs).

29 transcriptional activation domain of class A-HSFs.

30 ng and distinct functions of class A1 and A2 HSFs and may enable more precise use of HSFs in engineer

31 While investigating how HER2 activated HSF-1 independent of heat shock, we observed that HER2 a

32 sults provide strong evidence that activated HSF is stably bound to DNA in vivo and that turnover or

33 In addition, HSF-1 is needed for the effects of the DAF-2 insulin-lik

34 Additionally, HSF has no detectable role in the rapid HS repression of

35 bears a 32-bp deletion of its high-affinity HSF-binding site, yet retains its two low-affinity HSF s

36 nding site, yet retains its two low-affinity HSF sites.

37 study uncovered the existence of a novel Akt-HSF-1 signaling axis that leads to Slug upregulation and

38 were prospectively recruited and consumed an HSF diet for 8-wk followed by 8 wk of consumption of an

39 r 8-wk followed by 8 wk of consumption of an HSF diet with the addition of DHA and eicosapentaenoic a

40 These studies suggest that an HSF-1 decoy effectively dampens the HSP72/HSP25 response

41 minished luminescence in both HSF-1(+/+) and HSF-1(-/-) cardiomyocytes, suggesting that HSF-1 inhibit

42 ng the transcriptional regulators DAF-16 and HSF-1 in Caenorhabditis elegans), their relevance to mam

43 on in lin-14 was dependent on the DAF-16 and HSF-1 transcription factors, suggesting that the lin-4-l

44 tion of ethanol and identifies HSP-16.48 and HSF-1 as novel regulators of this pathway.

45 h polyubiquitinated protein accumulation and HSF activation.

46 ted in concurrent phosphorylation of Akt and HSF-1.

47 Together, E2F and HSF-1 directly regulate a gene network, including a spec

48 ncreases in concentrations after the HSF and HSF-DHA diets relative to the low-fat diet in the APOE3/

49 rsenite-induced activation of JNK2/c-Jun and HSF-1 pathways was also markedly elevated in p27 knock-o

50 e expression or function of JNK2, c-Jun, and HSF-1, but not JNK1, led to dramatic inhibition of arsen

51 l level specifically through JNK2/c-Jun- and HSF-1-dependent pathways upon arsenite exposure, which p

52 s enzymes regulated by insulin signaling and HSF-1 are required for tissue protection during infectio

53 ependent upon the HSFA1 clade of Arabidopsis HSFs, which cause a rapid and dynamic eviction of H2A.Z

54 Conversely, class B HSFs inhibit promoter activity through an active mechani

55 or both, activation and repression (class B HSFs).

56 -terminal regulatory region (CTR) of class B HSFs.

57 Our findings suggest this is because HSF-1 and DAF-16 together activate expression of specifi

58 We believe HSF-1 acts in heat-shock-inducible transcription and CYL

59 The positive association between HSF-1 and Slug was confirmed by immunohistochemical stai

60 nia, but were intact to parvocellular-biased HSF stimuli, regardless of generator location.

61 inding sites diminished luminescence in both HSF-1(+/+) and HSF-1(-/-) cardiomyocytes, suggesting tha

62 We show both HSFs bind to discontinuous heat shock element (HSE) sequ

63 One gene activated by HSF during heat stress encodes the enhancer of decapping

64 ck gene promoters and is regulated either by HSF binding or activation of preloaded HSF.

65 n occludin protein expression is mediated by HSF-1 activation and subsequent binding of HSF-1 to the

66 nse, from the top of its regulatory cascade (HSF-1) down to the execution stages delivered by HSP70,

67 BP-mediated acetylation of HSF, thus causing HSF to dissociate from the gene.

68 Rather than protecting cells, HSF-1 promotes their demise by activating components of

69 SF phosphorylation, and enhanced chromosomal HSF DNA binding to low affinity target promoters such as

70 he first time, that there are four consensus HSF sequence-binding elements (HSEs), the binding sites

71 In contrast, HSF is dispensable for establishing or maintaining Pol I

72 F) diet, and the HSF diet with 3.45 g DHA/d (HSF-DHA), each for 8 wk.

73 tion-dependent, but not heat shock-dependent HSF phosphorylation, and enhanced chromosomal HSF DNA bi

74 development and show that the developmental HSF-1 transcriptional program is distinct from the HSR.

75 arriers consuming a high-saturated fat diet (HSF diet) and, in addition, evaluated whether being over

76 4 promoters before heat shock and diminishes HSF binding during heat shock.

77 Once induced, HSFA2 becomes the dominant HSF and is able to form heterooligomeric complexes with

78 ter region and that downregulation of either HSF activates transcription of HIF-1alpha.

79 s also activated by overexpression of either HSFs.

80 riptional activity of Caenorhabditis elegans HSF-1 during larval development and show that the develo

81 tion of DHA and eicosapentaenoic acid (EPA) (HSF + DHA diet; 3.45 g DHA/d and 0.5 g EPA/d).

82 f E2F/DP to a GC-rich motif that facilitates HSF-1 binding to a heat-shock element (HSE) that is dege

83 mutant animals lacking the heat shock factor HSF-1.

84 -16 requires heat shock transcription factor HSF-1 and Hsp70/HSP-1.

85 O and heat shock factor transcription factor HSF-1 exert neuroprotective functions.

86 k response regulated by transcription factor HSF-1 has been implicated as an effector mechanism, the

87 ut the major heat shock transcription factor HSF-1 in several cancer cell lines using small interferi

88 suggest that heat-shock transcription factor HSF-1 is required for IIS to modulate longevity.

89 ole that the heat shock transcription factor HSF-1 played in determining a stimulatory phenotype of C

90 required the heat-shock transcription factor HSF-1, RNA polymerase II, and ENY-2, a factor that binds

91 Caenorhabditis elegans transcription factor HSF-1, which regulates the heat-shock response, also inf

92 S, HSP70, and the HSP70 transcription factor HSF-1.

93 GAGA-associated factor (GAF) and HS factor (HSF) regulate.

94 Thus, a humidity sensitive factor (HSF) appears to function at an early point in the ssi4 s

95 ne strictly controlled by heat shock factor (HSF) 1.

96 ing domain and either the heat shock factor (HSF) activation domain or a potent subdomain of VP16.

97 shock and hypoxia through heat shock factor (HSF) and hypoxia-inducible factor 1alpha in vivo.

98 There are 21 heat shock factor (HSF) homologs in Arabidopsis (Arabidopsis thaliana), of

99 Heat shock factor (HSF) is a conserved and highly potent transcription acti

100 Heat-shock factor (HSF) is the master transcriptional regulator of the heat

101 ription, translation, and heat-shock factor (HSF) oligomerization, as well as the role of heat-shock

102 We discovered that heat shock factor (HSF) proteins 2 and 4-which previously have been implica

103 ence of several potential Heat Shock Factor (HSF) responsive elements (HSE) in the human RANKL gene p

104 ing truncated versions of heat shock factor (HSF) showed that deletion of either one of two activatin

105 ranscriptional activator, heat shock factor (HSF), and poly(ADP-ribose) polymerase (PARP).

106 We show that heat shock factor (HSF), the transcription activator of hsp70, is localized

107 taining binding sites for heat shock factor (HSF)-1, activator protein (AP)-2, and AP-1 transcription

108 no significant change in heat shock factor (HSF)-1, but a more than twofold increase in HSF2 and -4

109 e factor (HIF)-1alpha and heat shock factor (HSF)-1.

110 ock proteins (HSPs) via a heat shock factor (HSF)-dependent mechanism.

111 nal coregulators of yeast heat-shock factor (HSF).

112 fore examined the role of heat shock factor (HSF-1), a master transcriptional regulator of stress-ind

113 Heat shock transcription factor (HSF) and the promoter heat shock element (HSE) are among

114 Heat shock transcription factor (HSF) is an evolutionarily conserved protein that mediate

115 y conserved heat-shock transcription factor (HSF) strongly influences yeast prion formation and strai

116 ng motif of heat shock transcription factor (HSF), -764G, was significantly associated with sustained

117 enes of the heat shock transcription factor (HSF), including genes encoding proteins thought to be im

118 ng the heat-shock (HS) transcription factor (HSF)-1 that enhances immunity in the invertebrate Caenor

119 e decoy for heat-shock transcription factor (HSF)-1, based on the sequence of the porcine heat-shock

120 way and the heat shock transcription factor (HSF-1) influence the amount of aggregation that occurs,

121 le that the heat shock transcription factor, HSF-1, and its downstream effectors played as common gen

122 Enhancing stress responsive factors HSF-1 or DAF-16 suppresses misfolding of these metastabl

123 encoding heat stress transcription factors (HSF genes) and heat shock proteins (HSP genes) is reduce

124 Heat shock factors (HSFs) are principal regulators of plant responses to sev

125 Heat shock factors (HSFs) are the master regulators of transcription under p

126 ponse in eukaryotes, the heat shock factors (HSFs), have undergone large-scale gene amplification in

127 demonstrating a role for heat shock factors (HSFs).

128 riptionally regulated by heat shock factors (HSFs).

129 Heat stress factors (HSFs) are a class of transcription factors that are synt

130 rol of the heat shock transcription factors (HSFs) and their interactions with heat shock promoters r

131 Plant heat shock transcription factors (HSFs) are capable of transcriptional activation (class A

132 Heat stress transcription factors (HSFs) are central regulators of the heat stress response

133 sis A-type heat-shock transcription factors (HSFs), and identified HSFA1D, HSFA2, and HSFA3 as key fa

134 EB2A), two heat shock transcription factors (HSFs), and several zinc finger proteins.

135 ontrol of heat stress transcription factors (HSFs).

136 ns (>or=1.5 mg/mL) of horse spleen ferritin (HSF) or its iron-free variant (HSAF).

137 Human corneal fibroblasts (HSFs) were used for in vitro studies, and New Zealand Wh

138 scription (STAT)3 pathway in HS fibroblasts (HSFs) derived from post-burn HS skin.

139 thors report that human scleral fibroblasts (HSFs) express TGFBI and that its protein product, TGFBIp

140 In normal human skin fibroblasts (HSFs), fluorescent glycosphingolipid analogues are endoc

141 Human seminal fluid (HSF) is a complex mixture of reacting glandular metaboli

142 ture signal transduction and a mechanism for HSF and HSP activation.

143 We identify that the requirement for HSF-1 in this phenotype was IL2 neuron-specific and requ

144 Consistent with a more global role for HSF and Snf1 in activating gene expression in response t

145 blasts, while mutations in binding sites for HSF-1, NF-1, and octamer binding proteins (Oct-1) increa

146 element, which is a key regulatory step for HSF function.

147 Approximately 165 in vivo targets for HSF have been identified in S. cerevisiae using chromati

148 ngs reveal a previously unsuspected role for HSFs in control of VEGF and other genes activated by can

149 g DNA-binding dynamics, the presence of free HSF during homeostasis and the initial phase of the heat

150 tem using low versus high spatial frequency (HSF) sinusoidal gratings, respectively, in Experiment 2.

151 that HSF2 and HSF4 displace each other from HSF/HSE complexes in the HIF-1alpha promoter so that HIF

152 s, and reveal a requirement for autophagy in HSF-1-regulated functions in the heat-shock response, pr

153 poral biochemical and biophysical changes in HSF from infertile men with spinal cord injury compared

154 iomyocytes, deteriorated cardiac function in HSF-1(-/-) mice, and decreased survival.

155 MDR1 promoter activity was higher in HSF-1(-/-) cardiomyocytes, whereas a mutant MDR1 promote

156 -binding activity of NF-kappaB was higher in HSF-1(-/-) mice.

157 agonist, verapamil, increased Dox loading in HSF-1(-/-) cardiomyocytes, deteriorated cardiac function

158 gp and lowering Dox loading were observed in HSF-1(-/-) mouse hearts.

159 ) mutation showed increased activity only in HSF-1(+/+) cardiomyocytes.

160 LV) dysfunction was significantly reduced in HSF-1(-/-) mice.

161 n of either one of two activating regions in HSF led to the diminished histone displacement and corre

162 TGFBIp plays an inhibitory role in HSF attachment to collagen type I in vitro through inter

163 , Bcl-Xl, and c-Myc were also upregulated in HSF, and knockdown of STAT3 by small interfering RNA att

164 use of fluid-phase cell attachment assays in HSFs, human foreskin fibroblasts (HFFs), and human corne

165 r abrogated FN and Col1A2 gene expression in HSFs indicating involvement of STAT3 in ECM production.

166 (Col1A2) and fibronectin 1 (FN), was seen in HSFs.

167 STAT3 target gene, SOCS3, was upregulated in HSFs and showed increased STAT3 binding on its promoter

168 ransducer glycoprotein 130 is upregulated in HSFs by quantitative real-time reverse-transcriptase-PCR

169 onversely, constitutively active Akt induced HSF-1 phosphorylation and Slug expression.

170 ll molecule inhibitors prevented HRG-induced HSF-1 activation and Slug expression.

171 Additionally, this aptamer inhibits HSF-induced transcription in vitro in the complex milieu

172 starvation is dependent on the Snf1 kinase, HSF-dependent heat shock induction of CUP1 is Snf1-indep

173 imply a similar regulatory role of mammalian HSFs in the complex etiology of prion disease.

174 t in the rat lens, among the three mammalian HSFs, expression of HSF1 and HSF2 is largely fetal, wher

175 orhabditis elegans, we engineered a modified HSF-1 strain that increased stress resistance and longev

176 RCF3 is a negative regulator of most HSFs, including HSFA1a, HSFA1b, and HSFA1d.

177 expression of wild-type or dominant negative HSF-1, we demonstrated that HSF-1 acts in multiple tissu

178 ress resistance controlled by HSF1 and a new HSF-FoxM1 connection that mediates cellular thermotolera

179 s were noncytotoxic and did not alter normal HSF morphology or proliferation.

180 ant negative rabs, we showed that, in normal HSFs, LacCer recycling was rapid (t1/2 approximately 8 m

181 Compared with normal HSFs, EEs in NPFs showed high cholesterol levels and an

182 molecules also induce AP-1 activity, but not HSF-1, and elicit no effect on clusterin expression leve

183 a FOXO transcriptional factor DAF-16 but not HSF-1.

184 to associate with Pol II, and acetylation of HSF by CBP has been implicated in inhibiting the DNA-bin

185 Pol II to direct CBP-mediated acetylation of HSF, thus causing HSF to dissociate from the gene.

186 ork opens the possibility that activation of HSF-1 could be used to boost immunity to treat infectiou

187 Here, we report that the activity of HSF-1 is regulated by IIS.

188 ed in inhibiting the DNA-binding activity of HSF.

189 moter region inhibited HS-induced binding of HSF-1 to the occludin promoter region and subsequent pro

190 y HSF-1 activation and subsequent binding of HSF-1 to the occludin promoter, which initiates a series

191 er, this is not a consequence of a change of HSF diffusibility, as shown here directly by fluorescenc

192 Considering that several coinducers of HSF-1 are currently in clinical trials, this work opens

193 at altering the homeostatic concentration of HSF can lead to large changes in the stress response wit

194 enes that function under the dual control of HSF-1 and DAF-16 transcription factors.

195 ophagosomal organelles, whereas depletion of HSF-1 potentiated both starvation- and rapamycin-induced

196 F depletion also delayed the dissociation of HSF from hsp70 and hsp26, and a similar delay was observ

197 fter photobleaching show a rapid exchange of HSF at chromosomal loci under non-heat-shock conditions

198 Co-expression of HSF-1 or HSF-2 with the RANKL gene promoter-luciferase r

199 ence of the transcriptionally active form of HSF-1 was detected at the same time point, this was not

200 The canonical function of HSF-1 is to regulate a network of genes encoding molecul

201 This genome-wide identification of HSF target genes provides novel insights into the role o

202 on was evaluated by RT-PCR and immunoblot of HSF lysates and culture supernatants.

203 Our findings establish the importance of HSF in prion initiation and strain determination and imp

204 In contrast, a robust increase of HSF-1 DNA binding activity is observed in all cancer cel

205 es NMNAT indirectly through the induction of HSF.

206 Such an endogenous inhibition of HSF-1 and Hsp27 in turn results in p53 mutation with gai

207 ptamer interferes with normal interaction of HSF with its DNA element, which is a key regulatory step

208 Knockdown of HSF-1 expression by siRNA reduced Slug expression and HR

209 Knockdown of HSF-1 increased the LC3 lipidation associated with forma

210 Also, lack of HSF-1 enhances nuclear factor kappaB (NF-kappaB) DNA bin

211 Thus, because high levels of HSF-1 are attributed to poor prognosis of cancer, system

212 eat-shock stress through increased levels of HSF-1.

213 with experiments showing that the number of HSF molecules in a HeLa cell is roughly 100 times greate

214 In addition, overexpression of HSF-2 in SAKA-T cells resulted in a 5-fold increase in t

215 mportantly, it also eliminates preloading of HSF on HSP82 and SSA4 promoters before heat shock and di

216 nosis of cancer, systemic down-regulation of HSF-1 before chemotherapy is a potential therapeutic app

217 nes provides novel insights into the role of HSF in growth, development, disease, and aging and in th

218 tems was demonstrated by testing the role of HSF-1, the central regulator of heat shock gene expressi

219 This regulation occurs at an early step of HSF-1 activation via two HSF-1 regulators, DDL-1 and DDL

220 cose availability, expression of a subset of HSF targets by glucose starvation was dependent on Snf1

221 d in cytoplasmic-to-nuclear translocation of HSF-1 and binding to its binding motif in the occludin p

222 TGF-beta1 treatment of HSF significantly increased mRNA and protein levels of S

223 he regulation occurs through interactions of HSFs with general transcription factors (GTFs), as has b

224 le is known about the upstream regulators of HSFs.

225 d A2 HSFs and may enable more precise use of HSFs in engineering stress tolerance in the future.

226 showing the dependence of these processes on HSF.

227 lowing initiation in the presence of Tet(on)-HSF and Tet(on)-VP16(A2).

228 Activation by Tet(on)-HSF but not by Tet(on)-VP16(A2) required the GAGA elemen

229 ate-limiting step in the presence of Tet(on)-HSF was release of Pol II paused about 20 to 40 nucleoti

230 Co-expression of HSF-1 or HSF-2 with the RANKL gene promoter-luciferase reporter p

231 transcriptional activation induced by HRG or HSF-1 overexpression.

232 of animals exposed to hormetic heat shock or HSF-1 overexpression.

233 is elegans following hormetic heat stress or HSF-1 overexpression.

234 trol the expression of HSFA1 genes and other HSF genes under heat stress.

235 tly interacted with HSF-1 and phosphorylated HSF-1 at S326.

236 Plant HSFs of subgroup B lack a conserved sequence motif prese

237 er by HSF binding or activation of preloaded HSF.

238 ses suggest that DDL-1/2 negatively regulate HSF-1 activity by forming a protein complex with HSF-1.

239 ng that in addition to chaperone regulation, HSF-1 has a prominent role in cytoskeletal integrity, en

240 Recruitment of the master regulator, HSF, is first detected within 20 s of gene activation; t

241 bers are master regulators for the remaining HSFs.

242 g in response times when participants report HSF information of the hybrid stimulus in the presence o

243 gned to a low-fat diet, a high-fat high-SFA (HSF) diet, and the HSF diet with 3.45 g DHA/d (HSF-DHA),

244 Upon heat shock, HSF triggers these PARP activities mechanistically by di

245 ple model system to investigate how a single HSF is activated by multiple stresses.

246 st Saccharomyces cerevisiae encodes a single HSF protein that responds to heat stress and glucose sta

247 nding on the presence or absence of specific HSF(s).

248 Targeted HSF-1 knock-down by siRNA transfection inhibited the HSF

249 SF and Snf1 kinase interact in vivo and that HSF is a direct substrate for phosphorylation by Snf1 ki

250 ession in stromal/osteoblast cells, and that HSF may play an important role in modulating RANKL gene

251 We demonstrate that HSF and Snf1 kinase interact in vivo and that HSF is a d

252 nses similar to mammals, we demonstrate that HSF-1 altered sensitivity to both alcohol and nicotine.

253 ominant negative HSF-1, we demonstrated that HSF-1 acts in multiple tissues to regulate longevity.

254 In the present work, we have discovered that HSF-1 ablation induced the multidrug resistance gene, MD

255 We find that HSF-1, like the transcription factor DAF-16, is required

256 , and Enterococcus faecalis, indicating that HSF-1 is part of a multipathogen defense pathway.

257 We conclude from these results that HSF-1 inhibition and depletion of Hsp27 is a trigger, at

258 xpression, indicating an essential role that HSF-1 plays in Akt-induced Slug upregulation.

259 The results also show that HSF-1 is required for C. elegans immunity against Pseudo

260 These data further suggest that HSF-2 is a downstream target of b-FGF to induce RANKL ex

261 d HSF-1(-/-) cardiomyocytes, suggesting that HSF-1 inhibits MDR1 activity in the heart.

262 The HSF-1 defense response is independent of the p38 MAPK/PM

263 ficant increases in concentrations after the HSF and HSF-DHA diets relative to the low-fat diet in th

264 APOE3/E3 and APOE3/E4 individuals after the HSF-DHA diet relative to the low-fat diet.

265 ose starvation was dependent on Snf1 and the HSF carboxyl-terminal activation domain.

266 iet, a high-fat high-SFA (HSF) diet, and the HSF diet with 3.45 g DHA/d (HSF-DHA), each for 8 wk.

267 int to DDL-1/2 as a link between IIS and the HSF-1 pathway.

268 viously characterized NF-kappaB aptamer, the HSF aptamer does not simply mimic DNA binding, but rathe

269 tein expression; which were abolished by the HSF-1 inhibitor quercetin.

270 ock-down by siRNA transfection inhibited the HSF-1-induced increase in occulin expression and junctio

271 P kinase activation occurs downstream of the HSF but either upstream of EDS1 or on a separate branch

272 Interestingly, approximately 30% of the HSF direct target genes are also induced by the diauxic

273 Although induction of the HSF target gene CUP1 by glucose starvation is dependent

274 Site-directed mutagenesis of the HSF-1 binding motif in the occludin promoter region inhi

275 we compared gene expression profiles of the HSF-1, HSF-6 and H9 lines.

276 domain plus a flanking linker region on the HSF (DL) is essential for the RNA binding.

277 Because the plasma FA response to the HSF + DHA diet was correlated with BMI in APOE4 carriers

278 In response to the HSF + DHA diet, there were significant BMI x genotype in

279 phavbeta5 expression and localization to the HSF cell surface.

280 Ip were used to assess TGFBIp binding to the HSF surface.

281 ha and that a critical balance between these HSF is required to maintain HIF-alpha expression in a re

282 HSF in a manner distinct from DNA binding to HSF.

283 imply mimic DNA binding, but rather binds to HSF in a manner distinct from DNA binding to HSF.

284 We selected an RNA aptamer that binds to HSF with high specificity.

285 These data point to HSF-1 as an important factor regulating clusterin expres

286 ted cells; and that the dampened response to HSF activation in decoy-treated, injured cells was accom

287 eta5 functionally blocked rTGFBIp binding to HSFs.

288 al promoters in strains expressing truncated HSF also correlated with the extent of histone displacem

289 at an early step of HSF-1 activation via two HSF-1 regulators, DDL-1 and DDL-2.

290 revealed that HSFA1b and HSFA7b are the two HSFs responsible for heat induction of miR398.

291 ionalization of the four Arabidopsis A1-type HSFs in diverse abiotic stress responses.

292 While HSF is essential for cell viability in Saccharomyces cer

293 While HSFs are central in heat stress responses, their role in

294 he identity of factors that collaborate with HSF in governing noninduced heat-shock gene expression i

295 1 activity by forming a protein complex with HSF-1.

296 The interaction of ILS with HSF-1 could represent an important molecular strategy to

297 irst time, that Akt directly interacted with HSF-1 and phosphorylated HSF-1 at S326.

298 Reagents that interfere with HSF function would be useful for both basic studies and

299 pressed chromatin state that interferes with HSF-1 binding and suppresses transcription initiation in

300 ified loci are heat-inducibly bound by yeast HSF, and the target genes encode proteins that have a br

301 the direct transcriptional targets of yeast HSF, representing nearly 3% of the genomic loci.