ライフサイエンスコーパス: HIF-1alpha

1 HIF-1alpha (hypoxia-inducible factor 1alpha) directly bo

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

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

4 HIF-1alpha and HIF-2alpha have common as well as distinc

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

6 HIF-1alpha depletion from CD4(+) T cells reduced frequen

7 HIF-1alpha is detectable in GCF and saliva of periodonta

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

9 HIF-1alpha overexpression significantly increased CSC su

10 HIF-1alpha positively regulates Th17 differentiation, a

11 HIF-1alpha stabilization was detected in peripheral bloo

12 HIF-1alpha total amount in GCF were also higher in perio

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

14 HIF-1alpha, and its downstream proteins, glucose transpo

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

16 .IMPORTANCE Hypoxia inducible factor 1alpha (HIF-1alpha) and HIF-2alpha are transcription factors whi

17 es activate hypoxia-inducible factor 1alpha (HIF-1alpha) and this transcription factor can drive VEGF

18 nesis, with hypoxia-inducible factor 1alpha (HIF-1alpha) being a major contributor.

19 tion factor hypoxia-inducible factor 1alpha (HIF-1alpha) binds a hypoxia response element (HRE) locat

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

21 Hypoxia-inducible factor 1alpha (HIF-1alpha) is a major determinant in the enhanced funct

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

23 Hypoxia-inducible factor 1alpha (HIF-1alpha), a principal regulator of innate immunity to

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

25 ominantly a hypoxia-inducible factor 1alpha (HIF-1alpha)-dependent gene under hypoxia.

26 pression of hypoxia-inducible factor 1alpha (HIF-1alpha).

27 ker protein hypoxia-inducible factor-1alpha (HIF-1alpha) after 3 h of exposure to static hypoxia.

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

29 The hypoxia-inducible factor-1alpha (HIF-1alpha) promotes an adaptive transcriptional respons

30 e show that hypoxia-inducible factor-1alpha (HIF-1alpha), expressed in endothelial cells (ECs), is th

31 , activated hypoxia-inducible factor-1alpha (HIF-1alpha), proliferation and upregulation prolyl hydro

32 iation with hypoxia-inducible factor-1alpha (HIF-1alpha), vascular endothelial growth factor (VEGF-A)

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

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

35 d with elevated levels of acetyl-HIF-1alpha, HIF-1alpha, and aromatase in breast tissue of obese comp

36 (2)-mediated increases in acetyl-HIF-1alpha, HIF-1alpha, and aromatase.

37 teroids suggests that activation of the IL-4-HIF-1alpha-IL-13 axis might play a role in the developme

38 t of the interleukin 6 cytokine family, as a HIF-1alpha target gene, which directly inhibits the TGF-

39 KM2 up-regulates BMSC CXCL12 production in a HIF-1alpha-dependent fashion, which subsequently enhance

40 of HIF-1alpha via short interfering RNA or a HIF-1alpha inhibitor decreased their production.

41 s mitochondrial dynamics in cancer through a HIF-1alpha-regulated pseudohypoxic state.

42 ted SIRT1 levels, leading to elevated acetyl-HIF-1alpha and HIF-1alpha levels and enhanced aromatase

43 blocked PGE(2)-mediated increases in acetyl-HIF-1alpha, HIF-1alpha, and aromatase.

44 re associated with elevated levels of acetyl-HIF-1alpha, HIF-1alpha, and aromatase in breast tissue o

45 P-associated factor (PCAF), which acetylates HIF-1alpha, blocked PGE(2)-mediated increases in acetyl-

46 -145, that nuclear S1P, histone acetylation, HIF-1alpha expression, and TNBC tumor growth were all re

47 h hypoxic and pseudohypoxic stimuli activate HIF-1alpha and its target genes in ATM during diet-induc

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

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

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

51 parallel, hypoxia inducible factor-1 alpha (HIF-1alpha) activates RASSF1A transcription via HIF-bind

52 d increase hypoxia-inducible factor-1 alpha (HIF-1alpha) activation, thereby promoting neovasculariza

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

54 levels of hypoxia-inducible factor-1 alpha (HIF-1alpha) and the synthesis of extracellular matrix pr

55 ected with hypoxia-inducible factor-1 alpha (HIF-1alpha) by using electroporation method, specificall

56 Hypoxia-inducible factor-1 alpha (HIF-1alpha) is expressed as an adaptive response to hypo

57 cts of the hypoxia-inducible factor-1 alpha (HIF-1alpha) transcription factor on osteoclast formation

58 ies (ROS), hypoxia inducible factor 1 alpha (HIF-1alpha), and its target genes in the islets were exa

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

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

61 duction of hypoxia-inducible factor 1 alpha (HIF-1alpha).

62 ization of Hypoxia Inducible Factor-1 alpha (HIF-1alpha).

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

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

65 genome expression analysis, we found that an HIF-1alpha transcriptional footprint is preferentially u

66 Exposure of infected macrophages to an HIF-1alpha stabilizer significantly reduced recovery of

67 to test the involvement of microRNA-126 and HIF-1alpha in a model of replicative endothelial senesce

68 rd to the interplay between microRNA-126 and HIF-1alpha, transfection with a microRNA-126 inhibitor d

69 s, leading to elevated acetyl-HIF-1alpha and HIF-1alpha levels and enhanced aromatase gene transcript

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

71 Levels of ADAMTS-1, VEGF-A, and HIF-1alpha in GCF and serum were quantified by enzyme-li

72 nt correlation between ADAMTS-1, VEGF-A, and HIF-1alpha levels in the GCF and clinical periodontal pa

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

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

75 GCF and salivary samples were collected; and HIF-1alpha, VEGF, and TNF-alpha levels were measured by

76 31, VEGF, VEGF receptor II, phosphor-ERK and HIF-1alpha.

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

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

79 ation of HIF-1 and suggests that hypoxia and HIF-1alpha stabilization can be uncoupled in cancer.

80 d lysosomal associated protein 2 (LAMP2) and HIF-1alpha levels and modified cytokine production.

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

82 1 gene promoter, inducing Zta synthesis, and HIF-1alpha-stabilizing drugs can induce EBV reactivation

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

84 antly inhibited the expression of astrocytic HIF-1alpha, and the downstream genes GLUT-1, EPO, and VE

85 Both HIF-1alpha and HIF-2alpha are required for the clear cel

86 Relevant to this, binding sites for both HIF-1alpha and ERalpha overlap in SNAT2's cis-regulatory

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

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

89 increased lung metastatic tumours, caused by HIF-1alpha-dependent endothelial cell death and increase

90 e that induction of BZLF1 gene expression by HIF-1alpha requires phosphorylated, wild-type p53 as a c

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

92 cles released by these cells failed to carry HIF-1alpha.

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

94 After sepsis challenge, HIF-1alpha but not HIF-2alpha expression was rapidly ind

95 th WT and MT p53 proteins bind and chaperone HIF-1alpha to stabilize its binding at its downstream DN

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

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

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

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

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

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

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

103 with a microRNA-126 inhibitor downregulated HIF-1alpha expression in early passage endothelial cells

104 n, and was attenuated in the setting of dual HIF-1alpha and HIF-2alpha knockdown.

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

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

107 deletion of VHL in CD4 T cells would elevate HIF-1alpha and increase Th17 differentiation.

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

109 delineate the essential role of endothelial HIF-1alpha in driving the vascular repair program.

110 n LC3-II to the phagosome, whereas enhancing HIF-1alpha reduced phagosomal decoration.

111 Hypoxia-inducible factors (HIFs), especially HIF-1alpha and HIF-2alpha, are key mediators of the adap

112 enescent endothelial cells failed to express HIF-1alpha, and the microvesicles released by these cell

113 ges were also the major cell type expressing HIF-1alpha during infection and that infection-induced V

114 f the hypoxia-inducible transcription factor HIF-1alpha is necessary for chondrocyte survival by unid

115 reby the oxygen-sensing transcription factor HIF-1alpha orchestrated epithelial barrier integrity, se

116 d by the oxygen-sensing transcription factor HIF-1alpha, which is degraded under normoxic conditions

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

118 via hypoxia-inducible transcription factors HIF-1alpha and HIF-2alpha, regulates TEM function in the

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

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

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

122 GCF HIF-1alpha and TNF-alpha total amounts in gingivitis gro

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

124 GCF HIF-1alpha, VEGF, and TNF-alpha total amounts were posit

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

126 P and CP groups had significantly higher GCF HIF-1alpha, VEGF, and TNF-alpha total amounts than gingi

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

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

129 are mediated mainly by two isoforms of HIF, HIF-1alpha and HIF-2alpha.

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

131 d a preserved ERK1/2 phosphorylation, higher HIF-1alpha and Glut1 levels, and substantially increased

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

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

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

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

136 dative stress in MeHg-induced alterations in HIF-1alpha levels.

137 idants, reversed the MeHg-induced decline in HIF-1alpha protein levels and the decrease in cell proli

138 icantly blocked the MeHg-induced decrease in HIF-1alpha expression (p < 0.05).

139 The decrease in HIF-1alpha modulated a couple key angiogenic and anti-an

140 in the absence of a significant decrease in HIF-1alpha mRNA levels.

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

142 L-4-dependent, hypoxia-mediated increases in HIF-1alpha and T(C)2 cell differentiation were shown to

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

144 MeHg induced a significant reduction in HIF-1alpha protein by activating proline hydroxylase (PH

145 2alpha were determined, as were responses in HIF-1alpha-deficient OT-1 cells.

146 , HIF-1alpha protein levels were restored in HIF-1alpha stabilizer-treated senescent endothelial cell

147 binds, deacetylates, and thereby inactivates HIF-1alpha.

148 Thus, inappropriate HIF-1alpha signalling results in skeletal dysplasia caus

149 l as several transcription factors including HIF-1alpha.

150 tein response and autophagy genes, including HIF-1alpha, NFkB, PERK, and SQSTM1/p62.

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

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

153 villous explants demonstrated that increased HIF-1alpha resulting from ADORA2B activation facilitates

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 played a neuroprotective role via increasing HIF-1alpha expression in response to MeHg toxicity.

158 xia inducible transcription factor isoforms, HIF-1alpha and HIF-2alpha, and pulmonary hypoxia to inve

159 gene activation include c-MYC, KRAS, c-KIT, HIF-1alpha, PDGF-A and hTERT.

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

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

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

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

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

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

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

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

168 Of note, HIF-1alpha protein levels were restored in HIF-1alpha st

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

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

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

172 The absence of HIF-1alpha impaired the survival and proliferation of pr

173 Since the absence of HIF-1alpha is detrimental to host control of infection,

174 ected mice inhibited nuclear accumulation of HIF-1alpha and HIF-2alpha protein in immune cell types a

175 orter assay despite inducing accumulation of HIF-1alpha and transcription from another HRE-containing

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

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

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

179 Thus, therapeutic activation of HIF-1alpha-dependent vascular repair may represent a nov

180 l of infection, we asked if large amounts of HIF-1alpha protein, exceeding those induced by H. capsul

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

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

183 This p53-induced chaperoning of HIF-1alpha increases synthesis of HIF-regulated genes an

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

185 KDM8/PKM2 complex serves as a coactivator of HIF-1alpha to upregulate glycolytic genes.

186 that reduced SIRT1-mediated deacetylation of HIF-1alpha contributes to the elevated levels of aromata

187 Compound deficiency of HIF-1alpha and HIF-2alpha led to humoral defects after h

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

189 Constitutive deletion of HIF-1alpha in CNS neurons in transgenic mice tended to b

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

191 h pulmonary endothelium-specific deletion of HIF-1alpha or HIF-2alpha, to characterise their roles in

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

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

194 the present study, we analyzed the effect of HIF-1alpha in human macrophages infected with this fungu

195 le of this activation, we tested efficacy of HIF-1alpha inhibitor echinomycin in TP53-mutated AML sam

196 V life cycle by regulating the expression of HIF-1alpha and HIF-2alpha proteins.IMPORTANCE Hypoxia in

197 cine and CoCl(2) increased the expression of HIF-1alpha and target genes, including angiogenic and ce

198 -A expression, we analyzed the expression of HIF-1alpha during infection.

199 ime PCR was used to detect the expression of HIF-1alpha mRNA.

200 rial respiration and occurs independently of HIF-1alpha.

201 Here we describe induction of HIF-1alpha and HIF-2alpha during the differentiation of

202 Pharmacologic inhibition of HIF-1alpha or genetic manipulation to reduce HIF-1alpha

203 ell proliferation, whereas the inhibition of HIF-1alpha significantly increased the decline in cell p

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

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

206 Knockdown of HIF-1alpha expression via short interference RNA decreas

207 ng hypoxia increased the expression level of HIF-1alpha compared to static hypoxia.

208 hort interference RNA decreased the level of HIF-1alpha expression in MEK2-deficient BMDMs and decrea

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

210 Overexpression of HIF-1alpha significantly attenuated the decline in MeHg-

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

212 y CHX, MeHg promoted the degradation rate of HIF-1alpha.

213 ved the islets survival through reduction of HIF-1alpha and ROS production and suppression of apoptos

214 betes or its complications via regulation of HIF-1alpha have not currently proven to be clinically us

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

216 and IL-17 since targeted down regulation of HIF-1alpha via short interfering RNA or a HIF-1alpha inh

217 the nucleus are linked to the regulation of HIF-1alpha/2alpha functions associated with breast cance

218 impaired claudin-1 barrier via repression of HIF-1alpha/claudin-1 signaling, which was restored by tr

219 er there is a requirement for restriction of HIF-1alpha signalling in the other regions of the growth

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

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

222 To investigate the role of HIF-1alpha in MeHg-induced neurotoxicity, cobalt chlorid

223 aim of this study was to explore the role of HIF-1alpha in response to acute MeHg exposure in rat bra

224 -1alpha, we demonstrate the critical role of HIF-1alpha-derived from macrophages in regulating ATM ac

225 )) mice, which displayed higher stability of HIF-1alpha.

226 duced early, but not later, stabilization of HIF-1alpha.

227 By examining the 5' UTRs of HIF-1alpha, FGF-9, and p53 mRNAs and using fluorescence

228 decreased, indicating a broad dependence on HIF-1alpha for development of the sympathetic nervous sy

229 Abrogation of either STC1 or HIF-1alpha alleviated HSPC suppression by AML.

230 f phosphatase and tensin homolog (PTEN) over HIF-1alpha expression and CSC accumulation are de-regula

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

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

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

234 1 axis, which was restored via pharmacologic HIF-1alpha stabilization ex vivo.

235 and triple mutation on ERK phosphorylation, HIF-1alpha expression, and IL-1beta production.

236 2 (pyruvate kinase M2), phosphorylated PKM2, HIF-1alpha (hypoxia-inducible factor-1alpha), and lactat

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

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

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

240 Knockdown of placental HIF-1alpha in vivo suppressed the accumulation of adenos

241 at placental hypoxia induces ROS production, HIF-1alpha stabilization, and sFLT1 up-regulation; these

242 Here we show that prolonged HIF-1alpha signalling in chondrocytes leads to skeletal

243 We conclude that RASSF1A-HIF-1alpha forms a feedforward loop driving hypoxia sign

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

245 HIF-1alpha or genetic manipulation to reduce HIF-1alpha expression reduced the hypoxia-enhanced diffe

246 ide donor, prevented ROS production, reduced HIF-1alpha protein levels, and diminished sFLT1 producti

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

248 se, which inversely proportionally regulates HIF-1alpha and IL-1beta expression independent of ERK ac

249 ry role in the KSHV life cycle by regulating HIF-1alpha and HIF-2alpha expression.

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

251 tient biopsy analysis identified a repressed HIF-1alpha/claudin-1 axis, which was restored via pharma

252 Collectively, these studies reveal HIF-1alpha's critical role in maintaining barrier and hi

253 Salivary HIF-1alpha concentrations in gingivitis group were signi

254 gingival crevicular fluid (GCF) and salivary HIF-1alpha, VEGF, and TNF-alpha levels in periodontal he

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

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

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

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

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

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

261 enesis, despite their inability to stabilize HIF-1alpha.

262 of esophageal epithelial-targeted stabilized HIF-1alpha.

263 kinase M2), phosphorylated PKM2, succinate, HIF-1alpha (hypoxia-inducible factor-1alpha), lactate, a

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

265 nt of human neutrophils with IL-4 suppressed HIF-1alpha-dependent hypoxic survival and limited proinf

266 mental hypoxia or HIF1A knockdown suppressed HIF-1alpha-dependent claudin-1 expression and epithelial

267 By suppressing HIF-1alpha and other oncogenic transcription factors, Ti

268 he ability of the protein to bind its target HIF-1alpha.

269 ors (MSTFs) (KLF2, KLF4, NRF2, YAP/TAZ/TEAD, HIF-1alpha, NF-kappaB, AP-1, and others).

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

271 Therefore, we hypothesized that HIF-1alpha promotes the high muscle healing capacity of

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

273 These data indicate that HIF-1alpha is a target of miRNA-126 in protective and re

274 We also observed that HIF-1alpha activated the expression of paired box (Pax)7

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

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

277 Using a hypoxia-tracer, we show that HIF-1alpha nuclear translocation occurred both in hypoxi

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

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

280 so extended previous studies by showing that HIF-1alpha in retinal neurons and HIF-2alpha in Muller g

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

282 We verified that HIF-1alpha protein is more strongly expressed in keloid

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

284 he expression of glycolytic enzymes, and the HIF-1alpha inhibitor (FIH) inhibits HIF-1 activity.

285 ole in maintaining barrier and highlight the HIF-1alpha/claudin-1 axis as a potential therapeutic tar

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

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

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

289 In hypoxic cells, this HIF-1alpha-induced p53 is transcriptionally inefficient

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

291 hyperresponsiveness and inflammation through HIF-1alpha activation.

292 Unlike HIF-1alpha, dose-dependent coexpression of ORF34 stabili

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

294 Here we demonstrate a novel pathway where HIF-1alpha transcriptionally upregulates both WT and MT

295 etected in corneal epithelial cells, whereas HIF-1alpha protein stabilization was observed in infiltr

296 Moreover, while HIF-1alpha inhibition reduced tube formation and wound h

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

298 parsely and without spatial association with HIF-1alpha, arguing for an importance of hypoxia-indepen

299 ylated, wild-type p53 as a coactivator, with HIF-1alpha binding recruiting p53 to Zp.IMPORTANCE EBV,

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