ライフサイエンスコーパス: HIF

1 HIF (hypoxia-inducible factor)-1alpha is a major determi

2 HIF activation was achieved by conditional deletion of t

3 HIF proteins were induced remarkably under low oxygen co

4 HIF-1 also mediates increased flux through the serine sy

5 HIF-1alpha increased glycolytic enzymes and pyruvate deh

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

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

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

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

10 Hypoxia-inducible factor 1 (HIF-1) has been recognized as an important mediator of t

11 hanisms by which hypoxia-inducible factor 1 (HIF-1) mediates adaptive metabolic responses to hypoxia,

12 nt was driven by hypoxia-inducible factor 1 (HIF-1), followed the downregulation of E-cadherin, and p

13 synergizes with hypoxia-inducible factor-1 (HIF-1) to promote tumor progression.

14 es hypoxia-inducible transcription factor-1 (HIF-1)-dependent endothelial cell glycolysis, which is c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

29 Three major HIF isoforms, HIF-1alpha, HIF-2alpha, and HIF-3alpha, are present in the intestine

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

31 dentified hypoxia-inducible gene 2 (HIG2), a HIF-1 target, as a new inhibitor of ATGL.

32 y upregulated in colon tumor epithelium in a HIF-2alpha-dependent manner.

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

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

35 Systemic administration of a HIF-prolyl hydroxylase inhibitor replicated the Phd2-def

36 PT2385, a HIF-2alpha-specific inhibitor, had preventive and therap

37 uces the expression of ADORA2A by activating HIF-2alpha.

38 upstream of the AKT/mTOR pathway, activating HIF-target genes, notably vascular endothelial growth fa

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

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

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

42 Deletion of VEGF-A, an HIF target gene, in CD8(+) T cells accelerated tumorigen

43 eviously unsuspected role for PD184161 as an HIF-1 inhibitor in VSMC under nonhypoxic conditions.

44 t PD184161, a potent MEK1/2 inhibitor, is an HIF-1 blocker in Ang II-treated VSMC.

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

46 or HIF isoforms, HIF-1alpha, HIF-2alpha, and HIF-3alpha, are present in the intestine.

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

48 onfirmed an anticorrelation between AMPK and HIF-1 activities and the association of metabolic states

49 eloped two signatures consisting of AMPK and HIF-1 downstream genes, respectively, to quantify the ac

50 By applying the AMPK and HIF-1 signatures to The Cancer Genome Atlas patient tran

51 by Idh1 and Fasn, supported by glutamine and HIF-2alpha increments.

52 group of tumours associated with hypoxia and HIF signalling.

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

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

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

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

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

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

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

60 uggest new and important connections between HIF proteins and PlGF pathways in the regulation of plac

61 In blood cancers, the synergism between HIF overexpression and stabilization within the hypoxic

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

63 The potentiation of YAP1 activity by HIF-2alpha was not via canonical signaling mechanisms su

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

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

66 PT2385 is a first-in-class HIF-2alpha antagonist.

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

68 which we extracted a core circuit containing HIF-1, AMPK, and ROS.

69 We investigated whether PHD3 controls HIF-1 transcriptional activity in nucleus pulposus (NP)

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

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

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

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

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

75 tion, in part by triggering oxygen dependent HIF-2alpha degradation in astrocytic precursors.

76 cal approach had no effect on PHD3-dependent HIF-1 activity.

77 arious cancer cells upon oxygen deprivation, HIF-1 activation down-modulates LD catabolism mediated b

78 otic steps can support energy demand despite HIFs degradation.

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

80 palmitoyltransferase 1A (CPT1A), as a direct HIF target gene.

81 heavily pretreated ccRCC, validating direct HIF-2alpha antagonism for the treatment of patients with

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

83 er, these data identify Phd2 as the dominant HIF-hydroxylase in neutrophils under normoxic conditions

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

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

86 as a direct response to increased epithelial HIF-2alpha signaling.

87 Intestinal epithelial HIF-2alpha-overexpressing mice demonstrated that neutrop

88 s-associated colon cancer models, epithelial HIF-2alpha was essential in tumor growth.

89 tumors; however, the function of epithelial HIF-2alpha as a critical link in the progression of infl

90 rated an important role for tumor epithelial HIF-2alpha in colon tumors; however, the function of epi

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

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

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

94 hand, knockdown of hypoxia-inducible factor (HIF) beta in the VHL-deficient CC-RCC had a protective e

95 ole for intestinal hypoxia-inducible factor (HIF) in hepatic steatosis.

96 Hypoxia-inducible factor (HIF) is a key transcriptional factor in the response to

97 udied O2 "sensor," hypoxia-inducible factor (HIF) is regarded as an important regulator of hypoxia-in

98 anscription factor hypoxia-inducible factor (HIF) that increases lactate efflux as a result of enhanc

99 in, a component of hypoxia-inducible factor (HIF) ubiquitination machinery, and consequently suppress

100 ion is through the hypoxia-inducible factor (HIF), a transcription factor complex stabilized under lo

101 ein 4 (GATA-4) and hypoxia-inducible factor (HIF)-1alpha and -2alpha in response to angiotensin II an

102 ylase (PHD)-3 as a hypoxia inducible factor (HIF)-1alpha cofactor is controversial and remains unknow

103 Over-activation of hypoxia inducible factor (HIF)-1alpha has been implicated in the progression of CK

104 obustly stabilizes hypoxia-inducible factor (HIF)-1alpha in primary monocytes.

105 tivated mTORC1 and hypoxia-inducible factor (HIF)-1alpha, which paralleled dysfunction, morphological

106 ific deficiency in hypoxia inducible factor (HIF)-2alpha, an oxygen labile transcription factor.

107 s those abrogating hypoxia inducible factor (HIF)/vascular endothelial growth factor signaling, are i

108 hypothesized that hypoxia-inducible factor (HIF)1alpha promotes proliferation and spreading of ATII

109 rapeutics, such as hypoxia-inducible factor (HIF-1) inhibitors and hypoxia-activated prodrugs.

110 iption factors and hypoxia-inducible-factor (HIF)-1 gene signature.

111 ible factor family of transcription factors (HIF).

112 fluctuations, and hypoxia-inducible factors (HIFs) are central mediators of these cellular responses.

113 Hypoxia inducible factors (HIFs) are centrally involved in the modulation of cellul

114 stabilization of hypoxia-inducible factors (HIFs) are hallmark features of inflammation and solid tu

115 r stabilizing the hypoxia-inducible factors (HIFs) are the most prevalent molecular features of clear

116 Hypoxia inducible factors (HIFs) are ubiquitously expressed transcription factors i

117 as activators of hypoxia-inducible factors (HIFs) in the liver.

118 re dependent upon hypoxia-inducible factors (HIFs), a family of essential transcriptional activators

119 hat interact with hypoxia-inducible factors (HIFs), transcription factors that are activated by recep

120 ogram mediated by hypoxia-inducible factors (HIFs).

121 by hypoxia-inducible transcription factors (HIFs), and their effects appear to be dependent on the c

122 regulating hypoxia signalling and feedback (HIF-3alpha, KDM3A, SLC2A1, EGLN-3).

123 pport the role of the PHD3 as a cofactor for HIF-1, independent of PKM2-JMJD5.-Schoepflin, Z.

124 lts uncover an lncRNA-mediated mechanism for HIF-1 activation and establish the clinical values of Ln

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

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

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

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

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

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

131 As (lncRNAs) have been implicated in hypoxia/HIF-1-associated cancer progression through largely unkn

132 of the CXCL1-CXCR2 signaling axis identified HIF-2alpha-dependent neutrophil recruitment as an essent

133 Together, our studies identify HIF control of fatty acid metabolism as essential for cc

134 the treated cells, there was no decrease in HIF-1 binding to hypoxia response elements.

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

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

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

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

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

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

141 AngII increases HIF-1 transcriptional activity by modulating specific si

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

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

144 nd colleagues report a role for MUC1-induced HIF expression in rewiring ribose synthesis, which drive

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

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

147 ocyte antigen-G(+) pcEVT, and that an intact HIF complex is required for this process.

148 experiments with mouse models of intestinal HIF-2alpha or Yes-associated protein 1 (YAP1) overexpres

149 These results suggest that intestinal HIF-2alpha could be a viable target for hepatic steatosi

150 or without obesity revealed that intestinal HIF-2alpha signaling was positively correlated with body

151 Intestine HIF-2alpha inhibition markedly reduced intestine and ser

152 Mechanistically, intestine HIF-2alpha regulates ceramide metabolism mainly from the

153 c disorders that were dependent on intestine HIF-2alpha.

154 her, our findings provide a new insight into HIF-mediated hypoxia response regulation by coupling the

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

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

157 Deletion analyses of the two key HIF isoforms found that HIF-1alpha, but not HIF-2alpha,

158 Three major HIF isoforms, HIF-1alpha, HIF-2alpha, and HIF-3alpha, ar

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

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

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

162 A luciferase assay to monitor HIF-1 activity demonstrated that the overexpression of U

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

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

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

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

167 icated that gene targets of PI3K-Akt but not HIF were enriched in early transcriptional responses to

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

169 HIF isoforms found that HIF-1alpha, but not HIF-2alpha, was essential for the effector state in CD8(

170 ), which we previously identified as a novel HIF-1 activator, increased the radioresistance of cancer

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

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

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 In CKD mice, activation of HIF-2alpha at the beginning of CKD significantly aggrava

176 d that during chronic hypoxia, activation of HIF-2alpha may overcome the bone marrow retention signal

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

178 oughput RNA sequencing (RNA-seq) analysis of HIF-2alpha-overexpressing mice in conjunction with data

179 l and promising field for the application of HIF inhibitors in clinical practice.

180 4 in the nuclei results in an attenuation of HIF-1alpha acetylation, enhancing the stabilization and

181 Those expression changes of HIF proteins in the process of in-vitro syncytialization

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

183 D stages revealed significant correlation of HIF-target genes with eGFR in glomeruli and tubulointers

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

185 3 promoted ubiquitination and degradation of HIF-1alpha in partial mtDNA-depleted cells.

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

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

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

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

190 by inhibiting ATGL, HIG2 acts downstream of HIF-1 to sequester FAs in LDs away from the mitochondria

191 Although the effect of HIF activation in chronic kidney disease (CKD) has been

192 n this study, we investigated the effects of HIF activation in the developing renal stroma, which als

193 is study aimed to investigate the effects of HIF-2alpha activation on renal fibrosis according to the

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

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

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

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

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

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

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

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

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

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

204 reover, we detected no direct interaction of HIF-2alpha with YAP1.

205 osteolytic lesion formation, irrespective of HIF-1 Conversely, silencing or pharmacologic inhibition

206 with poor clinical outcome, irrespective of HIF-1 In addition, LOX was expressed by tumor cells in t

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

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

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

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

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

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

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

214 ndau protein (pVHL), a negative regulator of HIF, and that treatment with the c-src inhibitor PP2 res

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

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

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

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

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

220 cubation (3 kPa) caused (i) stabilization of HIF-2alpha and up-regulation of hypoxia-regulated genes

221 ity by stabilizing the regulatory subunit of HIF-1 (HIF-1alpha) in a murine breast cancer cell line,

222 erexpression of HIFs, specific inhibition of HIFs might represent a new powerful treatment strategy.

223 es are associated with the overexpression of HIFs, specific inhibition of HIFs might represent a new

224 Here we seek to address the role of HIFs in myeloid trafficking during inflammation in a mou

225 undergoing pharmacological stabilization of HIFs retained their constitutive ability for early metas

226 nhibition and VHL deficiency is dependent on HIF activation.

227 on of PKM2 and JMJD5 levels had no effect on HIF-1 activity in NP cells.

228 er cell metabolism, with an initial focus on HIF-mediated effects, and will highlight how these metab

229 eason, recent investigations have focused on HIF-targeting therapeutic agents, with encouraging precl

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

231 ediating cell proliferation after hypoxia or HIF-2alpha activation in CRC are unclear.

232 D), but not HIF-1alpha-N-terminal-(N)-TAD or HIF-2alpha-TAD.

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

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

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

236 I (AngII), a vasoactive hormone, as a potent HIF-1 activator in vascular smooth muscle cells (VSMC).

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

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

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

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

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

242 get promoters and lower expression of select HIF-1 targets.

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

244 wth factors, are essential for cell-specific HIF-1 regulation.

245 Myeloid specific HIFs are crucial for aspects of myeloid cell function, i

246 n the scratch wound assay of cell spreading, HIF stabilization accelerated, whereas HIF1alpha shRNA d

247 Importantly, we show that GCs stabilize HIF protein in intact human liver tissue and isolated he

248 ur data support a model for GCs to stabilize HIF through activation of c-src and subsequent destabili

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

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

251 -1alpha dependent, suggesting that targeting HIF-1alpha could be a strategy to foster iTreg different

252 dence, we discuss the potential of targeting HIFs as a strategy to overcome these instances of AA the

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

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

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

256 These studies demonstrate that HIF-2alpha is a novel regulator of neutrophil recruitmen

257 Here we demonstrate that HIF-2alpha upregulates multiple myeloma PC CXCL12 expres

258 Our previous work demonstrates that HIF-2alpha is essential for CRC growth and progression.

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

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

261 al stromal cells in vitro We also found that HIF-2alpha strongly induced expression of the chemokine

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

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

264 Our findings indicate that HIF-2alpha increases cancer cell growth by up-regulating

265 These results indicate that HIF-mediated induction of Insig-2 and degradation of HMG

266 Here, we report that HIF-2alpha robustly increases YAP1 expression and activi

267 suggest, contrary to previous reports, that HIF pathways in myeloid cells during inflammation and hy

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

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

270 The HIF target vascular endothelial growth factor promoted A

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

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

273 te in the venous milieu, orchestrated by the HIF-induced NLRP3 inflammasome complex, is a key determi

274 BAF complex containing BRG1 that dampens the HIF transcriptional signature.

275 ulation of angiogenesis as downstream of the HIF signaling pathway precedes hyperinsulinemia.

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 ough genome-scale integrated analysis of the HIF-alpha network, we identified the major protein kinas

279 a HIF-1alpha co-activator that regulates the HIF-1 transcriptional network, crucial for cancer develo

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

281 We found that the HIF-1 inhibitor acriflavine (ACF) decreased survival and

282 ic analyses of patient tissues show that the HIF-1 signature is highly correlated with the expression

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

284 f cancer cells, gene networks triggering the HIF-1-mediated reprogramming and molecular mechanisms li

285 We show here how hypoxic response via the HIF transcription factors in one large vascular bed, tha

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

287 ioxidant, reduced glutathione (GSH), through HIF-1-mediated metabolic reprogramming.

288 ed bone marrow hypoxia, which contributed to HIF-dependent BMX upregulation.

289 hereby impairing PHD activity and leading to HIF activation.

290 In addition to HIFs, multiple histone demethylases are altered in their

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

292 In conclusion, late-stage renal tubular HIF-2alpha activation has protective effects on renal fi

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

294 and radioresistant phenotypes through UCHL1-HIF-1-mediated metabolic reprogramming including the act

295 y-deficient mutant (UCHL1 C90S), upregulated HIF-1 activity by stabilizing the regulatory subunit of

296 s infiltrating tumors are thought to utilize HIF transcription factors during adaptation to the hypox

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

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

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

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