ライフサイエンスコーパス: HIF

1 HIF knockdown only affected glucose uptake and bone reso

2 HIF-1 promotes the transcription of an ADP ribosyltransf

3 HIF-1alpha activation in MCT-RVfib reflected increased D

4 HIF-1alpha activation lowered surface BCR, CD19 and B ce

5 HIF-1alpha deletion had no effect on the increase in nor

6 HIF-1alpha mediated changes in gene expression in CNS re

7 HIF-1alpha overexpression significantly increased CSC su

8 HIF-1alpha positively regulates Th17 differentiation, a

9 HIF-1alpha was stabilised in PC12 cells by all the PHD i

10 HIF-1alpha-mutated MDSCs significantly secrete various a

11 HIF-2alpha promoted protective phosphorylated TIE2 (p-TI

12 HIFs act to promote oxygen delivery (by stimulating eryt

13 ion factors like hypoxia-inducible factor 1 (HIF-1) and c-Myc, yet the impact of hypoxia on negative

14 he activation of hypoxia inducible factor 1 (HIF-1) and not HIF-2.

15 ay controlled by hypoxia-inducible factor 1 (HIF-1) that epigenetically activates pluripotency factor

16 heme oxygenase 1 hypoxia-inducible factor 1 (HIF-1), monocyte chemotactic protein 1, transforming gro

17 ric and Western blot measurements of HIF-1a, HIF-2a, VEGF (vascular endothelial growth factor), and e

18 ion of PHi markedly upregulates lung HIF-1a, HIF-2a, VEGF, and eNOS expression after ETX exposure.Con

19 esized that hypoxia inducible factor 1alpha (HIF-1alpha) in CNS respiratory centres is necessary for

20 The hypoxia-inducible factor 1alpha (HIF-1alpha) is critically involved in tissue regeneratio

21 esized that hypoxia inducible factor 1alpha (HIF-1alpha), an O(2) -sensitive transcription factor, is

22 report that hypoxia-inducible factor-1alpha (HIF-1alpha) is crucial for the enhancement of placental

23 seeded with hypoxia inducible factor-1alpha (HIF-1alpha)-mutated muscle-derived stem cells (MDSCs) to

24 r delivery of CSC overexpressing HIF-1alpha (HIF-CSC) significantly improved the blood flow recovery.

25 mRNAs (e.g. hypoxia-inducible factor 1alpha [HIF-1alpha], fibroblast growth factor 9 [FGF-9], and p53

26 lution and dioxygen bound to the PHD2.Fe.2OG.HIF-alpha substrate complex.

27 IRF-3, HIF-1, and CASP1 were exclusively upregulated in ECD kid

28 This study identifies CHD4 as a HIF coactivator and elucidates the fundamental mechanism

29 s PHD-2 activity, promoting EC survival in a HIF-dependent manner, and furthermore dephosphorylates p

30 regulates cryptic transcript expression in a HIF-dependent manner, causing immune activation and redu

31 SEMA5B is a HIF target gene highly expressed in RCC that promotes in

32 FCF has also been shown to affect HIF-1alpha and HER2, which are both known to play a cruc

33 Furthermore, both inhibition of PI3K/AKT/HIF-1alpha and attenuation of glycolysis significantly b

34 ll death in bladder cancer cells by PI3K/AKT/HIF-1alpha-mediated glycolysis promotion.

35 ediated by hypoxia-inducible factor 1 alpha (HIF-1alpha) and recombination signal-binding protein for

36 ncrease of hypoxia inducible factor 1 alpha (HIF-1alpha), but a reduction of HIF-2alpha protein expre

37 involving hypoxia inducible factor-1 alpha (HIF-1alpha), vascular endothelial growth factor (VEGF) a

38 of hypoxia-inducible factor 1 subunit alpha (HIF-1alpha) and phagosomal recruitment of mammalian targ

39 e limitations of the present study, although HIF-1alpha seems to possess a potential diagnostic value

40 HIF-deficient tumors, identifying FTO as an HIF-independent vulnerability of VHL-deficient cancers.

41 e hypoxia-inducible factors (HIFs) HIF-1 and HIF-2 and their downstream targets, including the proang

42 e hypoxia-inducible factors (HIFs) HIF-1 and HIF-2, transcription factors that are key regulators of

43 alterations in the balance of HIF-1alpha and HIF-2alpha activities can affect different aspects of cc

44 In summary, HIF-1alpha and HIF-2alpha play different but overlapping roles in osteo

45 eading to accumulation of the HIF-1alpha and HIF-2alpha transcription factors.

46 nd hypoxia-inducible factors (HIF-1alpha and HIF-2alpha)-can exert renoprotective effects by promotin

47 n of BMP4 (bone morphogenetic protein 4) and HIF-1alpha (hypoxia-inducible factor 1alpha), blocking t

48 However, antiangiogenic agents and HIF-2 inhibitors have limited efficacy in cancer therapy

49 Moreover, suppression of PI3K/AKT and HIF-1alpha attenuated Vitamin K2-increased glucose consu

50 cating that Vitamin K2 promotes PI3K/AKT and HIF-1alpha-mediated glycolysis in bladder cancer cells.

51 hich includes activation of SIRT1, AMPK, and HIF-2alpha, enhanced autophagic flux, reduced cellular s

52 tage of tumor TEMs compared with control and HIF-2alpha (fl/fl) /LysMcre mice.

53 rolyl-4-hydroxylase domain (PHD) enzymes and HIF-alpha asparagine hydroxylase factor inhibiting HIF (

54 y, our data identify enhanced glycolysis and HIF-1alpha activation as drivers of low-grade inflammati

55 atty acid palmitate increased glycolysis and HIF-1alpha expression, which culminated in IL-1beta indu

56 ve implicated HIF-1alpha as an inhibitor and HIF-2alpha as a promoter of aggressive tumour behaviours

57 f nuclear SerRS in inhibiting both c-Myc and HIF-1 may provide therapeutic opportunities to correct d

58 revents hypoxia-induced binding of c-Myc and HIF-1 to the VEGFA promoter, and activation of VEGFA exp

59 on of key transcriptional regulators MYC and HIF-1A.

60 y be related primarily to enhanced SIRT1 and HIF-2alpha signaling; this can explain the effects of SG

61 SphK2, and HIF-1alpha expression levels are elevated in metastatic

62 1 gene promoter, inducing Zta synthesis, and HIF-1alpha-stabilizing drugs can induce EBV reactivation

63 duced the survival of both HIF wild type and HIF-deficient tumors, identifying FTO as an HIF-independ

64 antly, DFO induced binding of p53 as well as HIF-1alpha to Zp in chromatin immunoprecipitation (ChIP)

65 cer cells under normoxia, CHD4 enrichment at HIF target gene promoters increased RNA polymerase II lo

66 -inducible transcription factors (alpha,beta-HIFs) which upregulate the expression of sets of genes t

67 FTO inhibition reduced the survival of both HIF wild type and HIF-deficient tumors, identifying FTO

68 f AMPK pathway mainly and activation of both HIF-1/REDD1 and Bnip3 pathways partially contribute to i

69 The TiPARP nuclear bodies recruit both HIF-1alpha and an E3 ubiquitin ligase HUWE1, which promo

70 S neurons (CNS-HIF-1alpha(-/-) ) by breeding HIF-1alpha floxed mice with mice expressing Cre-recombin

71 of which are at least partially mediated by HIF-1alpha.

72 cus on transcriptional responses mediated by HIF.

73 bFGF-p38 MAP kinase signaling, beta-catenin-HIF-1alpha expression, and the nuclear size.

74 ion of the HIF-2alpha gene in myeloid cells (HIF-2alpha(mye/-) ) markedly exacerbated APAP-induced li

75 In normal circumstances, HIF-1alpha protein turnover is rapid, and hyperglycemia

76 k, ventilation in hypoxia was blunted in CNS-HIF-1alpha(-/-) and significantly decreased in NTS-HIF-1

77 s constitutively deleted in CNS neurons (CNS-HIF-1alpha(-/-) ) by breeding HIF-1alpha floxed mice wit

78 S expression after ETX exposure.Conclusions: HIF augmentation improves lung structure and function, p

79 n of RBPJkappa with DNA sequences containing HIF-1alpha-binding sites.

80 In contrast, HIF-1alpha (fl/fl) /LysMcre mice had a significantly sma

81 n are distinct signals integrated to control HIF activity.

82 nsferase, TiPARP, which serves to deactivate HIF-1.

83 eries from AD-HIES patients showed decreased HIF-1alpha expression and revealed abnormal organization

84 IH increases HIF-1alpha and decreases HIF-2alpha protein levels.

85 n signals for dioxgen availability-dependent HIF-alpha degradation via the ubiquitin proteasome syste

86 tion was not sufficient to induce detectable HIF activity in the kidney endothelium, in vitro experim

87 MCT-RVfib manifest a DNMT1-HIF-1alpha-PDK-mediated, chamber-specific, metabolic mem

88 nd the viral regulatory protein HBx to drive HIF-signalling.

89 er, RNA-seq analysis identified dysregulated HIF-1alpha target genes that are relevant to cell prolif

90 emphysema lung samples exhibited reduced EC HIF-2alpha expression.Conclusions: Here, we demonstrate

91 We also discover ectopic HIF binding sites in repeat regions which are normally m

92 KT/mTOR pathway and its downstream effectors HIF-1alpha and VEGF-A in cell lines, xenografts, and tra

93 thelial PAS domain protein 1 (EPAS1 encoding HIF-2alpha), inhibited both distinct and overlapping tra

94 nducible factor (HIF) genes, HIF1A (encoding HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1

95 with emphysema were measured for endothelial HIF-2alpha expression.Measurements and Main Results: EC

96 usly reported that deficiency of endothelial HIF-2 exacerbated renal ischemia-reperfusion injury, whe

97 ue protective role for pulmonary endothelial HIF-2alpha and how decreased expression of this endogeno

98 beta subunits of HIF1 and HIF2 and enhances HIF-driven transcriptional programs to promote breast ca

99 d that hypoxia in IHs is regulated by EPAS1 (HIF-2alpha) instead of HIF-1alpha, and also that propran

100 hypoxia inducible factors (HIFs; especially HIF-2alpha); these enzymes and transcription factors are

101 opose new research areas that may facilitate HIF isoform-specific inhibition as a novel therapeutic s

102 f drugs that target the transcription factor HIF or HIF-responsive growth factors, such as VEGF, for

103 t depletion of the hypoxia-inducible factor (HIF) genes, HIF1A (encoding HIF-1alpha) and endothelial

104 anscription factor hypoxia-inducible factor (HIF) in the regulation of innate immunity.

105 poxia, but whether hypoxia-inducible factor (HIF) is involved is unknown.

106 ed effects of five hypoxia-inducible factor (HIF) prolyl hydroxylases (PHD) inhibitors on PC12 cells

107 eld has focused on hypoxia-inducible factor (HIF) signaling and reactive oxygen species (ROS).

108 ial metabolism and hypoxia inducible factor (HIF) signaling due to iron depletion.

109 ence suggests that hypoxia-inducible factor (HIF) signaling plays a fundamental and pivotal role in t

110 Oxygen regulates hypoxia-inducible factor (HIF) transcription factors to control cell metabolism, e

111 als that stabilize hypoxia inducible factor (HIF), including desferrioxamine, cobalt chloride, and di

112 iptional regulator hypoxia-inducible factor (HIF), which controls a wide range of oxygen responsive t

113 endent on mTOR and hypoxia-inducible factor (HIF)1alpha.

114 d up-regulation of hypoxia-inducible factor (HIF-1alpha), its translocation and binding to the long n

115 Hypoxia inducible factor (HIFs) signaling contributes to malignant cell behavior i

116 inase (AMPK), and hypoxia-inducible factors (HIF-1alpha and HIF-2alpha)-can exert renoprotective effe

117 Hypoxia-inducible factors (HIFs) and the HIF-dependent cancer hallmarks angiogenesi

118 Hypoxia-inducible factors (HIFs) are critical regulators of the mammalian response

119 activation of the hypoxia-inducible factors (HIFs) HIF-1 and HIF-2 and their downstream targets, incl

120 e activity of the hypoxia-inducible factors (HIFs) HIF-1 and HIF-2, transcription factors that are ke

121 es on the role of hypoxia-inducible factors (HIFs) in hypertension, type 2 diabetes (T2D), and cognit

122 , is repressed by hypoxia-inducible factors (HIFs), reducing FA oxidation (FAO).

123 hypoxia involves hypoxia inducible factors (HIFs), which are stabilized by low oxygen availability a

124 regulators called hypoxia-inducible factors (HIFs).

125 and activation of hypoxia-inducible factors (HIFs).

126 ia is mediated by hypoxia-inducible factors (HIFs).

127 inase (AMPK), and hypoxia inducible factors (HIFs; especially HIF-2alpha); these enzymes and transcri

128 Hypoxia-inducible transcription factors (HIFs) directly dictate the expression of multiple RNA sp

129 ing hypoxia-inducible transcription factors (HIFs), but it is still an outstanding question why cell

130 First, HIF-1alpha was constitutively deleted in CNS neurons (CN

131 N), and an E3 ubiquitin ligase component for HIF destruction called von Hippel-Lindau.

132 The selectivities of many HIs for HIF hydroxylases and possible off-target effects in cell

133 Our results indicated a role for HIF-1alpha in down-regulating mitochondrial metabolism w

134 GCF HIF-1alpha levels in G-AgP reduced at 1 and 3 months pos

135 At baseline all clinical parameters and GCF HIF-1alpha, VEGF, and TNF-alpha levels were significantl

136 treatment on gingival crevicular fluid (GCF) HIF-1alpha, VEGF, and TNF-alpha levels in generalized ag

137 We used pan-genomic HIF-binding and transcriptomic data to identify a novel

138 n displayed significantly increased gingival HIF-1alpha protein levels and bone regeneration, as comp

139 tion of the hypoxia-inducible factors (HIFs) HIF-1 and HIF-2 and their downstream targets, including

140 vity of the hypoxia-inducible factors (HIFs) HIF-1 and HIF-2, transcription factors that are key regu

141 nhibit the CRL2(VHL) complex leading to high HIF-1alpha protein levels and a metabolic shift to glyco

142 g in Enz resistance via altering the hypoxia HIF-1alpha signals.

143 Hypoxia/HIF-1alpha- and extracellular adenosine/A2 adenosine rec

144 motivated by the need to prevent the hypoxia/HIF-1alpha-driven accumulation of extracellular adenosin

145 To identify HIF transcriptional targets in IEC, chromatin immunoprec

146 using human ccRCC cell lines have implicated HIF-1alpha as an inhibitor and HIF-2alpha as a promoter

147 discusses the range of evidence implicating HIFs in beta cell dysfunction, diabetes pathogenesis, an

148 ration of exogenous IL-6 ameliorated AILI in HIF-2alpha(mye/-) mice.

149 ation of UBXN7, with concomitant increase in HIF-1alpha protein levels, reduction in oxidative phosph

150 ated virus that expressed Cre-recombinase in HIF-1alpha floxed mice.

151 Phi IL-6 expression were markedly reduced in HIF-2alpha(mye/-) mice compared to wild-type mice post-A

152 itin ligase that targets proteins, including HIF-1alpha, for proteasomal degradation.

153 ties were decreased accompanied by increased HIF-1alpha and erythropoietin levels in the kidneys of K

154 se control in people with diabetes increases HIF-1alpha protein and has wide-ranging benefits, some o

155 IH increases HIF-1alpha and decreases HIF-2alpha protein levels.

156 t effects of different methods of increasing HIF-1alpha, even within the same tissues.

157 pha asparagine hydroxylase factor inhibiting HIF (FIH).

158 reversed the effect of HIF-2alpha knockdown; HIF-2alpha siRNA increasing osteoclast formation in 3D.

159 an parasite, Toxoplasma gondii, both lacking HIF.

160 induction of ATG9A was lost in cells lacking HIF-1.

161 Likewise, HIF-1alpha failed to activate transcription from Zp when

162 ylase inhibitor (PHi) therapy increases lung HIF expression, preserves lung growth and function, and

163 inistration of PHi markedly upregulates lung HIF-1a, HIF-2a, VEGF, and eNOS expression after ETX expo

164 o the mammary fat pads of syngeneic LysMcre, HIF-1alpha (fl/fl) /LysMcre, or HIF-2alpha (fl/fl) /LysM

165 Macrophage HIF-1alpha-deficient tumors also responded significantly

166 numbers of proangiogenic TEMs in macrophage HIF-1alpha-deficient tumors presented significantly less

167 Glycolysis is the main HIF-regulated pathway that drives bone resorption.

168 sed approach identified autophagy as a major HIF-1-targeted pathway in IEC.

169 ndamental mechanism underlying CHD4-mediated HIF transactivation in breast tumors.

170 Redox-mediated HIF-1alpha inactivation also decreased the expression of

171 ult in the suppression of succinate-mediated HIF-1alpha activation, imposing a consequent reduction o

172 In normoxic control mice, HIF-1alpha deletion in the CNS or NTS did not affect ven

173 In primary neurons, HIF-1alpha was stabilised by FG4592 (30 uM) and DMOG (10

174 ryotes and prokaryotes where they act on non HIF substrates.

175 f hypoxia inducible factor 1 (HIF-1) and not HIF-2.

176 lpha(-/-) and significantly decreased in NTS-HIF-1alpha(-/-) compared to control mice (P < 0.0001).

177 cence showed that HIF-1alpha deletion in NTS-HIF-1alpha(-/-) was restricted to glutamatergic neurons.

178 as deleted in NTS neurons in adult mice (NTS-HIF-1alpha(-/-) ) by microinjecting adeno-associated vir

179 Increased activation of HIF-1alpha in ATM of obese visceral adipose tissue resul

180 ll development because genetic activation of HIF-1alpha in murine B cells led to reduced repertoire d

181 e Western Blot data showed the activation of HIF-1alpha, but not Notch, ERK1/2, (PI3K)AKT, and P38 pa

182 d suggest that alterations in the balance of HIF-1alpha and HIF-2alpha activities can affect differen

183 cies and demonstrated therapeutic benefit of HIF-1alpha-stabilizing drugs.

184 Binding of HIF-1 to the ATG9A promoter, the only transmembrane comp

185 ive cell lines are reactivated by classes of HIF-1alpha-stabilizing drugs.

186 omotes the ubiquitination and degradation of HIF-1alpha.

187 Conditional deletion of HIF-1alpha in glutamatergic neurons of the nucleus tract

188 ith macrophage-specific targeted deletion of HIF-1alpha, we demonstrate the critical role of HIF-1alp

189 isoform through binding the PAS-B domain of HIF-2alpha.

190 S1P specifically binds to the PAS domains of HIF-1alpha.

191 steoclasts in 3D gels reversed the effect of HIF-2alpha knockdown; HIF-2alpha siRNA increasing osteoc

192 matous lungs exhibit decreased expression of HIF-2alpha (hypoxia-inducible factor-2alpha)-regulated g

193 The extent of HIF-alpha substrate prolyl hydroxylation, which signals

194 that discriminates between the inhibition of HIF-alpha prolyl-4-hydroxylase domain (PHD) enzymes and

195 d suppression of HIF1A or drug inhibition of HIF-associated glycolytic pathways selectively impairs b

196 Inhibition of HIF-PHD by roxadustat leads to increased EPO production,

197 s regulated by EPAS1 (HIF-2alpha) instead of HIF-1alpha, and also that propranolol-induced apoptosis

198 The intersection of HIF biology with diabetes is a complex area in which man

199 Knockdown of HIF-1alpha did not affect osteoclast differentiation but

200 orphometric and Western blot measurements of HIF-1a, HIF-2a, VEGF (vascular endothelial growth factor

201 ndings reveal a new fundamental mechanism of HIF regulation in breast cancer, which has clinical rele

202 Here, we report a deactivation mechanism of HIF-1 and several other oncogenic transcription factors.

203 fatty acids as a physiological modulator of HIF, defining a mechanism for lipoprotein regulation tha

204 mice was paralleled by increased numbers of HIF-1alpha+ monocytes, suggesting that CMH enhances mono

205 ions; and examines the differing outcomes of HIF-targeting approaches in these conditions.

206 Hence, the pharmacological prevention of HIF-1alpha degradation by prolyl hydroxylase (PHD) under

207 mplexes, and is enriched at the promoters of HIF target genes, including vascular endothelial growth

208 tor 1 alpha (HIF-1alpha), but a reduction of HIF-2alpha protein expression in lymphatic endothelial c

209 This Review summarizes the regulation of HIF isoforms and their impact in various PH subtypes, as

210 work demonstrates that dynamic regulation of HIF-1alpha is essential for normal B cell development.

211 fatty acids are an independent regulator of HIF.

212 approaches confirmed the regulatory role of HIF-1alpha in BACE1-AS/BACE1 in Tat-mediated amyloidosis

213 These studies reveal an oncogenic role of HIF-1alpha in ccRCC initiation and suggest that alterati

214 -1alpha, we demonstrate the critical role of HIF-1alpha-derived from macrophages in regulating ATM ac

215 both accelerate growth via stabilization of HIF-alpha subunits.

216 Targeting of HIF and its downstream targets in angiogenesis and metab

217 l exploitation of the intricate interplay of HIFs, angiogenesis, and metabolism in breast cancer cell

218 This Review presents a brief overview of HIFs; discusses the range of evidence implicating HIFs i

219 iew discusses the pathophysiological role of HIFs, angiogenesis, and metabolism in breast cancer and

220 nhibitors, and investigated their effects on HIF-dependent transcriptional regulation, erythropoietin

221 HBx had no significant impact on HIF expression or associated transcriptional activity un

222 erformed in Caco-2 IECs using HIF-1alpha- or HIF-2alpha-specific antibodies.

223 that target the transcription factor HIF or HIF-responsive growth factors, such as VEGF, for the tre

224 eic LysMcre, HIF-1alpha (fl/fl) /LysMcre, or HIF-2alpha (fl/fl) /LysMcre mice and evaluated the tumor

225 intramuscular delivery of CSC overexpressing HIF-1alpha (HIF-CSC) significantly improved the blood fl

226 geting this newly identified TR4/lincRNA-p21/HIF-1alpha/VEGF-A signaling with Bex, an FDA-approved dr

227 nsitivity via modulating the TR4/lincRNA-p21/HIF-1alpha/VEGF-A signaling.

228 preclinical HIs, categorizing them into pan-HIF-alpha hydroxylase (broad spectrum), PHD-selective, a

229 Pharmacologic HIF hydroxylase inhibitors (HIs) are effective for the t

230 Here, we show that pharmacological HIF-2alpha inhibition with PT2385, at doses similar to t

231 The discovery of the PHD-HIF-pVHL system revolutionized our fundamental understan

232 matory effects generated by endothelial PHD2/HIF-1 signaling.

233 Physiologically, HIF-dependent genes contribute to the aforementioned mai

234 2 (pyruvate kinase M2), phosphorylated PKM2, HIF-1alpha (hypoxia-inducible factor-1alpha), and lactat

235 we demonstrated that (a) elevated placental HIF-1alpha by AT(1) -AA or LIGHT upregulates CD73 and AD

236 nced adenosine underlies increased placental HIF-1alpha in an angiotensin receptor type 1 receptor ag

237 hrough upregulated ADORA2B induces placental HIF-1alpha expression, which creates a positive feedback

238 Whether antenatal or postnatal HIF (hypoxia-inducible factor) augmentation can preserve

239 These findings identify FTO as a potential HIF-independent therapeutic target for the treatment of

240 Although transiently protective, prolonged HIF activity drives distinct pathological responses in d

241 that anti-inflammatory macrophages promoted HIF-associated vascularization and expression of the imm

242 genes, and tobacco smoke decreases pulmonary HIF-2alpha concentrations.

243 (2)S produced by the infected WT mice reduce HIF-1alpha levels, thereby suppressing glycolysis and pr

244 pan- over PHD-selective HIs likely reflects HIF hydroxylase independent off-target effects.

245 ecause the prolyl hydroxylases that regulate HIF stability are oxygen- and iron-dependent enzymes, ou

246 CRL2(VHL) ligase complex regulates HIF-1alpha protein levels under aerobic (normoxia) or an

247 n 1 (STC1) and its transcriptional regulator HIF-1alpha as limiting factors for HSPC proliferation.

248 ises the exciting possibility that restoring HIF-2alpha pathways in lymphedema could mitigate long-te

249 Second, HIF-1alpha was deleted in NTS neurons in adult mice (NTS

250 n levels were reduced uniformly by selective HIF-1alpha inhibitor CAY10585.

251 linical status of pan- and isoform-selective HIF inhibitors, and propose new research areas that may

252 Here, we showed HIF-1alpha target genes are enriched in TP53-mutated ver

253 These findings indicate that some HIF-1alpha-stabilizing drugs may be helpful as part of a

254 This stage-specific HIF suppression is required for normal B cell developmen

255 In conclusion, the PHD inhibitors stabilise HIF-1alpha in normoxia, induce autophagy, and protect ce

256 at 100 uM except for DMOG, which stabilised HIF-1alpha at 1 and 2 mM.

257 hydroxylation, which signals for subsequent HIF-alpha degradation, may thus be a manifestation of th

258 In summary, HIF-1alpha and HIF-2alpha play different but overlapping

259 croenvironment within keloid tumors and that HIF-1alpha blockade could be a novel avenue of treatment

260 lpha stabilization in hepatic MPhis and that HIF-2alpha subsequently reprograms hepatic MPhis to prod

261 The results indicate that HIF-1alpha is a necessary signal for VAH and the previou

262 criptomic and proteomic analyses reveal that HIF-1alpha regulates glycolysis while HIF-2alpha regulat

263 lysis of transductional events revealed that HIF-1alpha upregulated Kdm5b and Kdm6b expression, where

264 We show that HIF activity is high in human and murine bone marrow pro

265 We previously showed that HIF-1alpha binds the BZLF1 gene promoter, inducing Zta s

266 Immunofluorescence showed that HIF-1alpha deletion in NTS-HIF-1alpha(-/-) was restricte

267 These findings suggest that HIF-2alpha is an important mediator of lymphatic health.

268 Our study suggests that HIF-2alpha normally promotes healthy lymphatic homeostas

269 We found, unexpectedly, that HIF-1alpha-stabilizing drugs only induce reactivation wh

270 We report that HIFs fail to bind CpG dinucleotides that are methylated

271 The HIF prolyl hydroxylase domain enzymes (PHDs) are Fe(II)-

272 rosis by upregulating HE4 and activating the HIF-1alpha/HE4/NF-kappaB signaling pathway.

273 Hypoxia-inducible factors (HIFs) and the HIF-dependent cancer hallmarks angiogenesis and metaboli

274 305M mutant mice suggests a function for the HIF-2alpha PAS-B domain beyond heterodimerization with H

275 rognosis, implying an important role for the HIF/NICI/SLC2A3 axis in this malignancy.

276 tosine indeed causes steric hindrance in the HIF binding pocket.

277 -dependent dioxygenase family, including the HIF proline hydroxylase (PHD, alias EGLN), and an E3 ubi

278 biology, highlighting the importance of the HIF pathway as a potential therapeutic target in osteoly

279 hat act as hypoxia-sensing components of the HIF system: prolyl-hydroxylation signals for dioxgen ava

280 omas (ccRCC), leading to accumulation of the HIF-1alpha and HIF-2alpha transcription factors.

281 the first report implicating the role of the HIF-1alpha/lncRNABACE1-AS/BACE1 axis in Tat-mediated ind

282 and ITGA5, causes further suppression of the HIF-1alpha/LOX/ITGA5/FN1 axis.

283 Genetic deletion of the HIF-2alpha gene in myeloid cells (HIF-2alpha(mye/-) ) ma

284 t PP2A (protein phosphatase 2) regulates the HIF (hypoxia-inducible factor)/PHD-2 (prolyl hydroxylase

285 of these are small molecules that target the HIF-2 isoform through binding the PAS-B domain of HIF-2a

286 tor of VEGFR-Notch signaling circuit through HIF-1alpha and RBPJkappa in EC sprouting angiogenesis.

287 nhanced recruitment of HIF1alpha, leading to HIF target gene transcription.

288 ata demonstrate that APAP treatment leads to HIF-2alpha stabilization in hepatic MPhis and that HIF-2

289 Finally, we observed lipid signaling to HIF and changes in target gene expression in developing

290 Mechanistically, REDD1 loss triggers HIF-dependent activation of a lipid storage pathway invo

291 pomorphic ventilatory phenotype in untreated HIF-2alpha S305M mutant mice suggests a function for the

292 on (ChIP) was performed in Caco-2 IECs using HIF-1alpha- or HIF-2alpha-specific antibodies.

293 e 12p13.31 which is regulated by hypoxia via HIF-1 promoter-binding in multiple cell types.

294 ing results in renal and other cancers where HIF-2 is considered to be driving growth.

295 ntly up-regulating glycolytic genes, whereas HIF-2alpha primarily up-regulated the angiogenesis trans

296 ta uncover a novel epigenetic basis by which HIF target gene expression is amplified in kidney cancer

297 l that HIF-1alpha regulates glycolysis while HIF-2alpha regulates genes associated with lipoprotein m

298 We have shown SphK2 is associated with HIF-1alpha in protein complexes, and is enriched at the

299 PAS-B domain beyond heterodimerization with HIF-1beta.

300 rs and Burkitt lymphomas were incubated with HIF-1alpha-stabilizing drugs: the iron chelator deferoxa