ライフサイエンスコーパス: HIF-1alpha

1 HIF-1alpha increased glycolytic enzymes and pyruvate deh

2 HIF-1alpha induces miR-210 expression, whereas miR-210 i

3 HIF-1alpha is a master regulator of gene expression and

4 HIF-1alpha is constitutively ubiquitinated by pVHL (von

5 HIF-1alpha pathway activation and increase in glycolysis

6 HIF-1alpha prolyl hydroxylation, which is prerequisite f

7 HIF-1alpha protein loss was correlated with the downregu

8 HIF-1alpha shRNA blocked albumin-induced changes in thes

9 HIF-1alpha was stabilized in Mvarphis following infectio

10 ream upregulated hypoxia inducible factor-1 (HIF-1alpha) expression.

11 also suppressed hypoxia-inducible factor-1 (HIF-1alpha) stabilization and decreased the transcriptio

12 stabilizing the regulatory subunit of HIF-1 (HIF-1alpha) in a murine breast cancer cell line, EMT6.

13 a-subunit of the transcription factor HIF-1 (HIF-1alpha), which interacts through its intrinsically d

14 e, we show that hypoxia inducible factor-1a (HIF-1alpha) controls the overexpression of the enzyme Cy

15 repression by hypoxia-induced factor 1alpha (HIF-1alpha) and increased heme-mediated protein degradat

16 tivation of hypoxia inducible factor 1alpha (HIF-1alpha) and posttranscriptionally by microRNA 199a2

17 endothelial hypoxia-inducible factor 1alpha (HIF-1alpha) controls glucose uptake in the hypothalamus

18 nd VEGF and hypoxia-inducible factor 1alpha (HIF-1alpha) expression in HT-29 xenografts initiated fro

19 hypoxia via hypoxia-inducible factor 1alpha (HIF-1alpha) might contribute to the augmentation of the

20 211 reduced hypoxia-inducible factor 1alpha (HIF-1alpha) protein levels and decreased cell growth dur

21 knockout of hypoxia-inducible factor 1alpha (HIF-1alpha) reversed the metabolic phenotype and impaire

22 tilizes the Hypoxia Inducible Factor 1alpha (HIF-1alpha) transcription factor and the JAK1/2-STAT3 (J

23 luding p53, hypoxia-inducible factor 1alpha (HIF-1alpha), NF-kappaB, and STAT proteins, and are the t

24 dition in a hypoxia inducible factor 1alpha (HIF-1alpha)-independent manner.

25 STAT3, and hypoxia-inducible factor 1alpha (HIF-1alpha).

26 tion factor hypoxia-inducible factor 1alpha (HIF-1alpha).

27 ligase for hypoxia-inducible factor 1alpha (HIF-1alpha).

28 ing through hypoxia-inducible factor-1alpha (HIF-1alpha) activation.

29 racted with hypoxia-inducible factor-1alpha (HIF-1alpha) and attenuated the latter's binding to promo

30 , including hypoxia-inducible factor-1alpha (HIF-1alpha) and plasminogen activator inhibitor-1 (PAI-1

31 tion factor hypoxia-inducible factor-1alpha (HIF-1alpha) is an essential mediator of IFN-gamma-depend

32 tion factor hypoxia inducible factor-1alpha (HIF-1alpha) is increased, the role of HIF-1alpha in pulm

33 lization of hypoxia inducible factor-1alpha (HIF-1alpha) mediates such metabolic reprogramming.

34 stabilized hypoxia-inducible factor-1alpha (HIF-1alpha) protein and promoted PrP(C) accumulation and

35 ibition and hypoxia-inducible factor-1alpha (HIF-1alpha) protein translation upregulation, in turn re

36 EBPbeta and hypoxia-inducible factor-1alpha (HIF-1alpha) signaling was assessed using selective inhib

37 involved in hypoxia-inducible factor-1alpha (HIF-1alpha) stabilization, including the phosphoinositid

38 tion factor hypoxia inducible factor-1alpha (HIF-1alpha) was recently shown to be critical for IFN-ga

39 ng required hypoxia inducible factor-1alpha (HIF-1alpha), downstream of NAD(P)H oxidase-4 (NOX4)-deri

40 Hypoxia-inducible factor-1alpha (HIF-1alpha), which accumulates in mammalian host organis

41 tion factor hypoxia-inducible factor-1alpha (HIF-1alpha).

42 regulating hypoxia-inducible factors-1alpha (HIF-1alpha) and -2alpha (HIF-2alpha) is well-studied.

43 ssing [HIF-1alpha-OE] or lacking HIF-1alpha [HIF-1alpha-knockout (KO)] in intestinal epithelial cells

44 cute colitis via a NTR1-prolyl hydroxylase 2/HIF-1alpha-miR-210 signaling pathway.

45 ng RNA); we describe its oncogenic role as a HIF-1alpha co-activator that regulates the HIF-1 transcr

46 YC-1 is a HIF-1alpha inhibitor, and we revealed that low-dose YC-1

47 Here we describe the efficacy of a HIF-1alpha inhibitor, Acriflavine, and demonstrate its p

48 e stress inhibits PHD activity to accumulate HIF-1alpha, which mediates albumin-induced profibrotic e

49 ings, levels of Hsp90 ATPase activity, Aha1, HIF-1alpha, PKM2, and aromatase were increased in the ma

50 colysis in endothelial cells via the ERK/Akt/HIF-1alpha pathway, thereby suggesting new therapeutic t

51 ilization of hypoxia-induced factor 1 alpha (HIF-1alpha).

52 or (VEGF), hypoxia-inducible factor 1-alpha (HIF-1alpha) and erythropoietin (EPO) were measured as po

53 ediated by hypoxia-inducible factor 1-alpha (HIF-1alpha) during these conditions.

54 In addition, an HIF-1alpha Cys(520) serine mutant is resistant to 2-AAPA

55 he change in VEGF (r = 0.492, P = 0.002) and HIF-1alpha (r = 0.388, P = 0.016).

56 ochemistry at 8 wk colocalized to RAM-11 and HIF-1alpha.

57 ular endothelial growth factor (VEGF)-A, and HIF-1alpha in the ischemic muscles.

58 ng to the Akt/p70S6K/S6 axis activation, and HIF-1alpha protein translation, as well as malignant tra

59 maintains the endothelial Notch activity and HIF-1alpha stability via targeting F-box and WD-40 domai

60 cologically or genetically increases CA, and HIF-1alpha and hypoxic gene signature expression correla

61 s associated with reduced levels of CDK6 and HIF-1alpha, as well as pronounced changes in cell cycle

62 nergistic action of intratumoral hypoxia and HIF-1alpha activation.

63 idazole-/HIF-1alpha immunohistochemistry and HIF-1alpha/2alpha Western blot/messenger RNA analysis of

64 ATMIN in hypoxia is mediated by both p53 and HIF-1alpha in an oxygen dependent manner.

65 in the superficial zone (SZ), while PHD3 and HIF-1alpha (target of PHD2) are mainly expressed in the

66 PKM2 and HIF-1alpha were shown to co-localize in the nucleus of s

67 1, Hsp90 ATPase activity, levels of PKM2 and HIF-1alpha, and aromatase expression in LFS stromal cell

68 r, mechanisms underlying ASS1 repression and HIF-1alpha turnover are not known.

69 echanism for Parkin in tumor suppression and HIF-1alpha regulation.

70 ng a transient ternary complex with TAZ1 and HIF-1alpha and competing for a shared binding site throu

71 s, and decreases the level of PGK1, VEGF and HIF-1alpha in vitro and in vivo.

72 of histone and DNA demethylation, as well as HIF-1alpha stability, mediate these effects.

73 Because HIF-1alpha has been shown to regulate the microRNA miR-1

74 on assays showed lack of association between HIF-1alpha and PKM2 in NP cells.

75 by which CITED2 displaces the tightly bound HIF-1alpha from their common cellular target.

76 IMP)-1 and collagen-I, which were blocked by HIF-1alpha shRNA.

77 strated that ASS1 silencing is controlled by HIF-1alpha and Arg starvation-reactivated ASS1 is associ

78 t of the negative regulation of cyclin D1 by HIF-1alpha, which promotes proliferation of ovarian canc

79 scription of WNT11 is regulated primarily by HIF-1alpha.

80 (FAD), a metabolic cofactor of LSD1, causing HIF-1alpha downregulation in later stages of hypoxia.

81 Of interest, we found that in CLL cells, HIF-1alpha is transcriptionally regulated after cocultur

82 cribing epigenetic regulation of chromosomal HIF-1alpha turnover in gene activation that bears import

83 Under hypoxic conditions, HIF-1alpha levels are greatly increased in glioma stem-l

84 In contrast, HIF-1alpha-OE mice showed increased miR-210 expression a

85 Compared with controls, HIF-1alpha and Kv1.5 protein expression were decreased i

86 A in hypoxic conditions leads to a decreased HIF-1alpha mediated transcriptional response and correla

87 levels, increased VHL binding, and decreased HIF-1alpha stability.

88 uppression in NP cells resulted in decreased HIF-1alpha enrichment on target promoters and lower expr

89 n negatively regulated by miR-210, decreases HIF-1alpha, and triggers apoptosis of triple negative br

90 ulates the development of colitis, decreases HIF-1alpha/PHD2 interaction, stabilizes and increases HI

91 teasomal complex, driven by PHD2, to degrade HIF-1alpha in situ.

92 ofoundly inhibits human Treg differentiation HIF-1alpha dependent, suggesting that targeting HIF-1alp

93 Here we show that human CITED2 displaces HIF-1alpha by forming a transient ternary complex with T

94 otective effects are dependent on downstream HIF-1alpha expression.

95 we found that PD184161 blocked AngII-driven HIF-1alpha protein induction in a dose-dependent manner.

96 Silencing either HIF-1alpha or PKM2 suppressed aromatase expression in LF

97 IP5 acts by enhancing HIF-1alpha hydroxylation and thus pVHL-dependent degrada

98 ion and NF-kappaB activation while enhancing HIF-1alpha levels and the expression of M2 marker Argina

99 In addition, exercise/HIF-1alpha downregulates the expression of TXNIP, a well

100 tified RAB20 and TXNIP as two novel exercise/HIF-1alpha-regulated genes in skeletal muscle.

101 However, whether and to what extent HIF-1alpha expressed by myeloid cells contributes to the

102 s at the ASS1 promoter, thereby facilitating HIF-1alpha-proteasomal complex, driven by PHD2, to degra

103 ent suggesting that the transcription factor HIF-1alpha may influence IL-22 expression.

104 rk (PTK6), via the hypoxia-inducible factors HIF-1alpha and HIF-2alpha.

105 own of hypoxia-induced transcription factors HIF-1alpha and HIF-2alpha alone or in combination failed

106 Mice deficient for HIF-1alpha in their myeloid cell compartment had a more

107 vel, oxygen-independent ubiquitin ligase for HIF-1alpha: hypoxia-associated factor (HAF; encoded by S

108 Furthermore, HIF-1alpha messenger RNA levels vary significantly withi

109 ation and the expression of its target genes HIF-1alpha, IL-8, BCL-2, and BCL-XL through the accumula

110 In establishing a novel glycolysis-HIF-1alpha feed-forward mechanism in hypoxic tumor cells

111 ycolysis, but also identifies the NAC1-HDAC4-HIF-1alpha axis as a novel molecular pathway that promot

112 In this study, we identified the NAC1-HDAC4-HIF-1alpha axis as an important pathway in regulating gl

113 Clinical implication of the NAC1-HDAC4-HIF-1alpha pathway is suggested by the results showing t

114 poxia-inducible transcription factors (HIFs) HIF-1alpha and HIF-2alpha are known to contribute to the

115 However, HIF-1alpha is not recognized and ubiquitinated by pVHL i

116 Our results suggest that the HSPA1L/HIF-1alpha/GP78 axis has a crucial role in PrP(C) accumu

117 roxyl dioxygenase enzymes, which hydroxylate HIF-1alpha and HIF-2alpha to destabilize HIF by binding

118 e, albumin reduced the level of hydroxylated HIF-1alpha, indicating an inhibition of the activity of

119 ted in association with a decline in hypoxic HIF-1alpha protein expression downstream of silenced NOX

120 romatin immunoprecipitation assay identified HIF-1alpha binding to NMDA-NR1 promoter during hypoxia.

121 activity of the transcription factor CREB in HIF-1alpha-deficient Mvarphis drove IL-10 production in

122 e HIF-1alpha locus, leading to a decrease in HIF-1alpha mRNA and a reduction in HIF-1alpha stabilisat

123 PASMCs from patients with PAH, decreases in HIF-1alpha expression and activity underlie augmented pu

124 RENCA cells deficient in HIF-1alpha failed to undergo EMT changes upon VHL knocko

125 This increase in HIF-1alpha levels is functionally important, as macropha

126 ophages results in a synergistic increase in HIF-1alpha protein levels.

127 e chromatin remodeling system is involved in HIF-1alpha degradation at the ASS1 promoter.

128 The reduction in HIF-1alpha levels by indolepyruvate, following LPS or tr

129 Reduction in HIF-1alpha protein stability led to attenuation of the b

130 crease in HIF-1alpha mRNA and a reduction in HIF-1alpha stabilisation.

131 Increased HIF-1alpha activates the JAK1/2-STAT3 axis and enhances

132 PD184161 also increased HIF-1alpha binding to von Hippel-Lindau tumor suppressor

133 1 expression levels correlate with increased HIF-1alpha expression and poor colorectal cancer patient

134 a/PHD2 interaction, stabilizes and increases HIF-1alpha transcriptional activity, and promotes intest

135 Deletion of IPMK in mouse brain increases HIF-1alpha/VEGF levels and vascularization.

136 on, whereas Glrx ablation by siRNA increases HIF-1alpha protein and expression of downstream angiogen

137 serine mutant is resistant to 2-AAPA-induced HIF-1alpha stabilization.

138 n switch assay shows that GSSG-ester-induced HIF-1alpha contains reversibly modified thiols, and MS c

139 own of LncHIFCAR impairs the hypoxia-induced HIF-1alpha transactivation, sphere-forming ability, meta

140 nhibitor, indicated that PD184161 influenced HIF-1alpha protein stability.

141 The mtDNA depleted cells, with inhibited HIF-1alpha, showed upregulation of glycolytic pathway ge

142 r silencing of HIF-1alpha (small interfering HIF-1alpha) attenuated miR-210 expression in response to

143 Three major HIF isoforms, HIF-1alpha, HIF-2alpha, and HIF-3alpha, are present in t

144 K477R HIF-1alpha mutation and specific cancer-associated Parki

145 n that was significantly reduced in NTR1-KO, HIF-1alpha-KO mice, and wild-type mice pretreated intrac

146 nctionally important, as macrophages lacking HIF-1alpha are defective for IFN-gamma-dependent control

147 control of infection in vivo as mice lacking HIF-1alpha in the myeloid lineage are strikingly suscept

148 ce overexpressing [HIF-1alpha-OE] or lacking HIF-1alpha [HIF-1alpha-knockout (KO)] in intestinal epit

149 Furthermore, inhibition of the macrophage HIF-1alpha-PDK1 axis suppresses systemic inflammation, s

150 tion constants <100 nM, which induced marked HIF-1alpha intracellular stabilization.

151 rate-limiting role for FAD in LSD1-mediated HIF-1alpha regulation.

152 moxic conditions, BACH2 was able to modulate HIF-1alpha degradation by suppressing prolyl hydroxylase

153 ticular cartilage progenitors via modulating HIF-1alpha signaling.

154 Moreover, HIF-1alpha protein translation was upregulated via activ

155 f conventional AMPK signalling or the mTORC1-HIF-1alpha axis, but contributed to the activation of be

156 rovide evidence of involvement of the mTORC1-HIF-1alpha pathway in burn-induced metabolic derangement

157 e identified a critical function for Mvarphi HIF-1alpha in tempering IL-10 production following infec

158 ulum of H. capsulatum The absence of myeloid HIF-1alpha did not alter immune cell recruitment to the

159 In this study, we demonstrated that myeloid HIF-1alpha-deficient mice exhibited elevated fungal burd

160 erefore we name it LncHIFCAR (long noncoding HIF-1alpha co-activating RNA); we describe its oncogenic

161 Notably, HIF-2alpha, not HIF-1alpha, expression was induced by GR signaling, and

162 t specifically increases HIF-2alpha, but not HIF-1alpha, accumulation in multiple STS subtypes.

163 inal transactivation domain (C-TAD), but not HIF-1alpha-N-terminal-(N)-TAD or HIF-2alpha-TAD.

164 rtension was dependent on HIF-2alpha but not HIF-1alpha.

165 iated with decreased oxidative stress (Nox2, HIF-1alpha, hydrogen peroxide, hydroxynonenal), and fibr

166 rch endothelia exhibited elevated ROS, NOX4, HIF-1alpha, and glycolytic enzyme and PDK1 expression, s

167 udy, we examined whether NT activates a NTR1-HIF-1alpha-miR-210 cascade using in vitro (NCM460-NTR1 c

168 associated with a strong decrease in nuclear HIF-1alpha levels as well as reduction in the proliferat

169 stimulus for angiogenesis, increased nuclear HIF-1alpha and HIF-2alpha, and expression of WNT11.

170 nt role in the intracellular accumulation of HIF-1alpha of hypoxic nasopharyngeal carcinoma cells and

171 and inactivation result in the activation of HIF-1alpha and aerobic glycolysis in response to oxidati

172 s, ADI-PEG20 inhibited hypoxic-activation of HIF-1alpha and HIF-2alpha, leading to decreased inducibl

173 D3 silencing decreased hypoxic activation of HIF-1alpha C-terminal transactivation domain (C-TAD), bu

174 nd Akt-dependent translational activation of HIF-1alpha protein.

175 ted with the stabilization and activation of HIF-1alpha under oxidative stress.

176 tabilization and transcriptional activity of HIF-1alpha and strengthening adaptive response of cells

177 57BL/6 mice exhibited substantial amounts of HIF-1alpha in acute cutaneous lesions.

178 4 in the nuclei results in an attenuation of HIF-1alpha acetylation, enhancing the stabilization and

179 PHD3 is a transcriptional coactivator of HIF-1alpha in nucleus pulposus cells independent of the

180 A complex comprised of HIF-1alpha and PKM2 was recruited to the aromatase promo

181 on of a novel feedback circuit consisting of HIF-1alpha/miR-210/HIF-3alpha.

182 e (CAM) assay, associated with a decrease of HIF-1alpha and VEGF expression within tumors.

183 ibits the proteasome-mediated degradation of HIF-1alpha by preventing PHDs from interacting with HIF-

184 3 promoted ubiquitination and degradation of HIF-1alpha in partial mtDNA-depleted cells.

185 ation and thus pVHL-dependent degradation of HIF-1alpha.

186 ation and thus pVHL-dependent degradation of HIF-1alpha.

187 essing the oxygen-independent degradation of HIF-1alpha.

188 ylases, enzymes promoting the degradation of HIF-1alpha.

189 mice with pulmonary endothelial deletion of HIF-1alpha exposed to hypoxia.

190 Deletion of HIF-1alpha in neutrophils or dendritic cells did not alt

191 ctly binds to the oxygen-dependent domain of HIF-1alpha and inhibits the proteasome-mediated degradat

192 ction between the protein binding domains of HIF-1alpha and p300.

193 Through allosteric enhancement of HIF-1alpha release, CITED2 activates a highly responsive

194 IPMK deletion elicits a major enrichment of HIF-1alpha protein and thus VEGF.

195 Hypoxia and expression of HIF-1alpha and HIF-2alpha are characteristic features of

196 enic factor GAX, and decreased expression of HIF-1alpha and proangiogenic factors NF-kappaB and VEGFR

197 PET data with pimonidazole and expression of HIF-1alpha in arthritic ankles.

198 n of NMDA-NR1, suggesting that expression of HIF-1alpha is necessary for the upregulation of NMDA-NR1

199 atients and correlate with the expression of HIF-1alpha target genes, including CXCR4, thus further e

200 M YC-1 reduced hypoxia-induced expression of HIF-1alpha targets involved in anaerobic glycolysis.

201 inent induction in the nuclear expression of HIF-1alpha, which transcriptionally activates the CXCR4

202 hese results hint toward a novel function of HIF-1alpha as a potential pharmacological target to impr

203 gests that KDM4A can enhance the function of HIF-1alpha by increasing the total available protein to

204 We investigated the function of HIF-1alpha in the host response to Histoplasma capsulatu

205 Inactivation of HIF-1alpha impairs chemotaxis and cell adhesion to strom

206 vated protein kinase (AMPK) independently of HIF-1alpha.

207 an E3 ligase component and an indication of HIF-1alpha hydroxylation.

208 lar oxygen levels, resulting in induction of HIF-1alpha.

209 IP5 reinstates the interaction of HIF-1alpha and pVHL.

210 We further identify lysine 477 (K477) of HIF-1alpha as a major ubiquitination site for Parkin.

211 Endothelium-specific knockdown of HIF-1alpha impairs the ability of POMC neurons to adapt

212 his study, we demonstrate that the levels of HIF-1alpha are directly controlled by the repressive chr

213 ignificantly increased the protein levels of HIF-1alpha, tissue inhibitor of metalloproteinase (TIMP)

214 Furthermore, loss of HIF-1alpha in CD8(+) T cells reduced tumor infiltration

215 al change in TAZ1 that increases the rate of HIF-1alpha dissociation.

216 t binding and facilitates the recruitment of HIF-1alpha and p300 cofactor to the target promoters.

217 /-) mice showed significant up-regulation of HIF-1alpha in circulating and liver-infiltrating immune

218 e contribution of KDM4A to the regulation of HIF-1alpha is most robust in conditions of mild hypoxia.

219 ndence of LSD1 activity to the regulation of HIF-1alpha stability.

220 tational SS involve epigenetic regulation of HIF-1alpha through specific miRs contributing to increas

221 4, thus further emphasizing the relevance of HIF-1alpha expression to CLL pathogenesis.

222 alpha (HIF-1alpha) is increased, the role of HIF-1alpha in pulmonary artery smooth muscle cells (PASM

223 r therapy and highlights the significance of HIF-1alpha-targeting molecules.

224 HIF-1alpha inhibitor PX-478 or silencing of HIF-1alpha (small interfering HIF-1alpha) attenuated miR

225 Silencing of HIF-1alpha in NG108 cells leads to a significant decreas

226 atpenin A5 antagonizes the stabilization of HIF-1alpha and reduces hypoxic gene expression in transf

227 Chemical stabilization of HIF-1alpha by Dimethyloxalylglycine (DMOG) also signific

228 nes suggested that normoxic stabilization of HIF-1alpha explains the persistent expression of hypoxic

229 cell dissemination through stabilization of HIF-1alpha in RCC.

230 Moreover, pharmacologic stabilization of HIF-1alpha in the liver stimulated HMGCR degradation via

231 ned GLUT1 as a critical downstream target of HIF-1alpha mediating high glucose-induced matrix express

232 targets the 3' untranslated region (UTR) of HIF-1alpha mRNA.

233 t hypoxic IL-22 upregulation is dependent on HIF-1alpha.

234 h significantly altered mTOR, but not Akt or HIF-1alpha, activation and only minor AMPKalpha phosphor

235 of caspase-1, in vivo knockdown of NLRP3, or HIF-1alpha other than IL-1beta-neutralizing antibodies a

236 and in vivo (transgenic mice overexpressing [HIF-1alpha-OE] or lacking HIF-1alpha [HIF-1alpha-knockou

237 In PASMCs derived from patients with PAH, HIF-1alpha expression is decreased, and MLCK activity, M

238 We conclude that compromised PASMC HIF-1alpha expression may contribute to the increased to

239 tionally, we performed ex vivo pimonidazole-/HIF-1alpha immunohistochemistry and HIF-1alpha/2alpha We

240 Furthermore, Glrx overexpression prevents HIF-1alpha stabilization, whereas Glrx ablation by siRNA

241 arkin interacts with HIF-1alpha and promotes HIF-1alpha degradation through ubiquitination, which in

242 IP5 promotes HIF-1alpha prolyl hydroxylation and thus pVHL-dependent

243 creased levels of the Hsp90 client proteins, HIF-1alpha, and PKM2 were found in LFS stromal cells.

244 cooperatively mediated by various putatively HIF-1alpha-dependent mechanisms, comprising attenuated p

245 isoform of PHDs in renal tubules, to reduce HIF-1alpha level significantly attenuated albumin-induce

246 analysis demonstrated that YC-1 + GI reduced HIF-1alpha expression and pimonidazole accumulation in t

247 These miRs regulate HIF-1alpha-regulated apoptotic, angiogenic, and immune p

248 Similar upregulation of renal HIF-1alpha and TGF-beta expression was observed in NOX4

249 53 is induced as part of MtRS and it renders HIF-1alpha inactive by physical interaction.

250 Exogenously provided FAD restores HIF-1alpha stability, indicating a rate-limiting role fo

251 was specific to nonhypoxic activators, since HIF-1alpha induction by hypoxia (1% O2) was unaffected u

252 Therefore, Glrx ablation stabilizes HIF-1alpha by increasing GSH adducts on Cys(520) promoti

253 undescribed function for NQO1 in stabilizing HIF-1alpha, a master transcription factor of oxygen home

254 which may be due to its inhibition on STAT3/HIF-1alpha/VEGF signalling in HepG2 cells.

255 nd hypoxia-inducible factor-1 alpha subunit [HIF-1alpha]).

256 ed that low-dose YC-1 (10 microM) suppressed HIF-1alpha expression, and induced hypoxia-dependent apo

257 significant up-regulation of miR-122 target HIF-1alpha is seen.

258 Targeting HIF-1alpha or de novo pyrimidine biosynthesis, in combin

259 astasis, which can be inhibited by targeting HIF-1alpha with RNA interference or the small-molecule i

260 -1alpha dependent, suggesting that targeting HIF-1alpha could be a strategy to foster iTreg different

261 ptosis in several glioma cell lines, targets HIF-1alpha-mediated pathways, and decreases the level of

262 activation of PHD2 and its principal targets HIF-1alpha and HIF-2alpha.

263 ha function requires NO production, and that HIF-1alpha and iNOS are linked by a positive feedback lo

264 lusion, we are the first to demonstrate that HIF-1alpha is a key regulator of glucose metabolism in s

265 Finally, we demonstrate that HIF-1alpha is crucial for control of infection in vivo a

266 We found that HIF-1alpha function requires NO production, and that HIF

267 lyses of the two key HIF isoforms found that HIF-1alpha, but not HIF-2alpha, was essential for the ef

268 We show here that HIF-1alpha links pathways for oxygen sensing and feedbac

269 The present study tested the hypothesis that HIF-1alpha mediates albumin-induced profibrotic effect i

270 Together, these data illustrate that HIF-1alpha is required for optimal innate leishmanicidal

271 In summary, our results show that HIF-1alpha activates INSIG-2 transcription, leading to a

272 Here we show that HIF-1alpha is important for glucose metabolism and insul

273 Here we show that HIF-1alpha-PDK1-mediated metabolic changes occur in mild

274 The HIF-1alpha and CITED2 transactivation domains bind to TA

275 eted or inactive, H3K9me3 accumulates at the HIF-1alpha locus, leading to a decrease in HIF-1alpha mR

276 MtRS induces tumor growth independent of the HIF-1alpha pathway.

277 a concomitant decrease in expression of the HIF-1alpha targets VEGF-A, glucose transporter-1, and la

278 The activation of the HIF-1alpha-24S-HC axis ultimately leads to the induction

279 the bone environment, yet down-regulates the HIF-1alpha pathway in chondrocytes, thereby promoting th

280 ved restenosis indicators by suppressing the HIF-1alpha/calpains/MMP2/TGF-beta1 pathway.

281 These data demonstrate that the HIF-1alpha/VEGF-A axis is an essential aspect of tumor i

282 Pretreatment of NCM460-NTR1 cells with the HIF-1alpha inhibitor PX-478 or silencing of HIF-1alpha (

283 Our studies showed even though HIF-1alpha is accumulated in the treated cells, there wa

284 itization of the P-Rex1/Rac1 pathway through HIF-1alpha-mediated transcriptional induction of CXCR4.

285 In contrast to HIF-1alpha, HIF-2alpha was not required for hypoxic phag

286 showed that upon treatment with triptolide, HIF-1alpha protein accumulated in pancreatic cancer cell

287 lish the functions of Parkin to ubiquitinate HIF-1alpha and inhibit cancer metastasis.

288 Using HIF-1alpha-deficient CD4 T cells, we show that hypoxic I

289 Circulating EPC and levels of VEGF, HIF-1alpha and EPO were significantly higher after exerc

290 on of invasion by nonpigmented melanomas via HIF-1alpha protein destabilization.

291 ng GSH adducts on Cys(520) promoting in vivo HIF-1alpha stabilization, VEGF-A production, and revascu

292 cytokine expression in macrophages, whereas HIF-1alpha levels were reduced.

293 type 1 collagen expressions associated with HIF-1alpha activation.

294 arvation-reactivated ASS1 is associated with HIF-1alpha downregulation.

295 hanistically, LncHIFCAR forms a complex with HIF-1alpha via direct binding and facilitates the recrui

296 contractility was inversely correlated with HIF-1alpha activity.

297 rkin expression is inversely correlated with HIF-1alpha expression and metastasis in breast cancer.

298 pha by preventing PHDs from interacting with HIF-1alpha.

299 Parkin interacts with HIF-1alpha and promotes HIF-1alpha degradation through u

300 involved in a positive-regulative loop with HIF-1alpha, and has a major action on ccRCC progression