ライフサイエンスコーパス: HIF1alpha

1 HIF1alpha binds directly to the Il22 promoter, and SCFAs

2 HIF1alpha expression decreased and HIF2alpha expression

3 HIF1alpha expression was not associated with survival.

4 HIF1alpha has been termed a tumor-suppressor in clear ce

5 HIF1alpha is a common component of pathways involved in

6 HIF1alpha is induced in LPS-activated macrophages, where

7 HIF1alpha is therefore a key reprogrammer of metabolism

8 HIF1alpha itself induces the transcription of various ce

9 HIF1alpha stabilized by LSD1 cooperates with CBP and MTA

10 HIF1alpha, but not HIF2alpha, induced Warburg-like metab

11 HIF1alpha, SLC2A1, and VEGFA expression could be evaluat

12 HIF1alpha- and HIF2alpha-mediated regulation of gene exp

13 ate and lactate, hypoxia-inducible factor-1 (HIF1alpha), and the monocarboxylate transporters MCT1 an

14 n of MMPs-9, -13 and -14 expression, PARP-1, HIF1alpha, and increased collagen biosynthesis as well a

15 phy through hypoxia-inducible factor 1alpha (HIF1alpha) activation of SF3B1 and SF3B1-mediated splice

16 pression of hypoxia-inducible factor 1alpha (HIF1alpha) also required C/EBPbeta.

17 eracts with hypoxia-inducible factor 1alpha (HIF1alpha) and activates the HIF-1alpha-dependent transc

18 rthologs of Hypoxia inducible factor 1alpha (HIF1alpha) and Lactate dehydrogenase (LDH) are required

19 identified hypoxia-inducible factor 1alpha (HIF1alpha) as a key transcription factor to drive HK2 ge

20 ded to high hypoxia-inducible factor 1alpha (HIF1alpha) expression and glycolytic activity compared w

21 r (AhR) and hypoxia-inducible factor 1alpha (HIF1alpha) expression, which are differentially regulate

22 Hypoxia-inducible factor 1alpha (HIF1alpha) is a crucial hypoxic factor for chondrocyte g

23 Hypoxia-inducing factor 1alpha (HIF1alpha) is known to be hyperactivated in TNBCs.

24 of CD36 and hypoxia-inducible factor 1alpha (HIF1alpha) proteins as contributing factors for NAFLD.

25 lization of hypoxia-inducible factor 1alpha (HIF1alpha) to upregulate the VEGF.

26 pression of hypoxia-inducible factor 1alpha (HIF1alpha), glucose transporter 1 (SLC2A1; also known as

27 2alpha) and hypoxia-inducible factor 1alpha (HIF1alpha), were enriched in the DhMRs.

28 h levels of hypoxia-inducible factor 1alpha (HIF1alpha), which is known to promote glycolysis, stemne

29 tivation of hypoxia inducible factor 1alpha (HIF1alpha).

30 mediated by hypoxia-inducible factor 1alpha (HIF1alpha).

31 mulation of hypoxia-inducible factor-1alpha (HIF1alpha) and activation of NF-kappaB in tumor cells.

32 2 (HK2) and hypoxia-inducible factor-1alpha (HIF1alpha) and associated negatively with PFK-2b express

33 upregulated hypoxia-inducible factor-1alpha (HIF1alpha) caused by antiangiogenic treatment.

34 elevated by hypoxia-inducible factor-1alpha (HIF1alpha) in MDSC localized to tumors, compared with sp

35 lisation of hypoxia-inducible factor-1alpha (HIF1alpha) in tumours causes transcriptional changes in

36 nistically, hypoxia inducible factor-1alpha (HIF1alpha) mediated this functional re-programming of mo

37 cy triggers hypoxia-inducible factor-1alpha (HIF1alpha) stabilization in cultured Pink1(-/-) mouse em

38 Hypoxia-inducible factor-1alpha (HIF1alpha) transcriptionally regulates numerous key aspe

39 GM-CSF in a hypoxia-inducible factor-1alpha (HIF1alpha)- and a NF-kappaB-dependent manner to recruit

40 sorin is preferentially induced in GSCs by a HIF1alpha/STAT3 co-activator complex and stabilizes Notc

41 , the HIF1alpha acetylation that occurs in a HIF1alpha methylation-dependent manner is inhibited by t

42 induced filaggrin (Flg) gene expression in a HIF1alpha- and HIF2alpha-dependent manner, suggesting th

43 lung adenocarcinoma by uniquely targeting a HIF1alpha/LEO1-mediated cell metabolism pathway.

44 essing Il1r1 for conversion into DATPs via a HIF1alpha-mediated glycolysis pathway, which is required

45 rial reactive oxygen species, which activate HIF1alpha signaling supporting metastasis of NCLX-null t

46 hat hIAPP misfolded protein stress activates HIF1alpha/PFKFB3 signaling, this increases glycolysis di

47 Additionally, HIF1alpha is critical for the maturation of dendritic ce

48 Our data reveal a novel EML4-ALK-HIF1alpha-HK2 cascade to enhance glucose metabolism in E

49 Levels of hypoxia-inducible factor 1 alpha (HIF1alpha) mRNA, a target of MIR122, were increased in l

50 ion factor hypoxia inducible factor 1 alpha (HIF1alpha), targeting it for eventual proteasomal degrad

51 ion factor hypoxia-inducible factor 1-alpha (HIF1alpha) is required for dmPGE2-enhanced CXCR4 upregul

52 ulation of hypoxia-inducible factor 1-alpha (HIF1alpha), and deletion of both Hif1a and Kif3a did not

53 LSD1-induced hypoxia-inducible factor alpha (HIF1alpha) demethylation has recently been proposed, the

54 olic switching and a complex interplay among HIF1alpha, ATF4, and p53.

55 Cultured principal cells exhibited an HIF1alpha-dependent increase of Sdf1 transcription in re

56 breast cancer cells to EGFR inhibitors in an HIF1alpha- and a methylation-specific manner, suggesting

57 A, B1, and E2F, and repression of p21 in an HIF1alpha-dependent manner, leading to cell proliferatio

58 was increased during hypoxic exposure in an HIF1alpha-dependent manner.

59 m by which tumors support angiogenesis in an HIF1alpha-independent manner.

60 of MSLC in the perivascular niche through an HIF1alpha-dependent process.

61 = 0.005) and MCT 1 (R = 0.85, P = 0.032) and HIF1alpha expression (R = 0.83, P = 0.043).

62 gulation of TRIM29 is dependent upon ATM and HIF1alpha and occurs through increased transcription of

63 alpha, as well as overexpression of cJUN and HIF1alpha, were positively correlated with vessel densit

64 mainly by increasing expression of cJUN and HIF1alpha.

65 ompanied by the formation of MTA1, HSP90 and HIF1alpha complex under hypoxic condition but not under

66 hese data also define a role for hypoxia and HIF1alpha in enhancement of hematopoietic transplantatio

67 controlling the feedback between IGFBP2 and HIF1alpha.

68 lta19/Delta19 mice, PHD levels were low, and HIF1alpha protein levels were increased.

69 influencing histone and DNA methylation, and HIF1alpha hydroxylation.

70 re was no correlation between HIF1A mRNA and HIF1alpha protein expression in ccRCC (R = 0.02), reflec

71 l, DNA-damage and -repair responses, p53 and HIF1alpha.

72 post-translational modifications (PTMs) and HIF1alpha-induced tumor angiogenesis remains to be eluci

73 ients like the aryl hydrocarbon receptor and HIF1alpha, which also interact with hsp90 through their

74 peutic efficacy by inhibiting DNA repair and HIF1alpha pathway activation in tumor cells.

75 d as a translational activator of TWIST1 and HIF1alpha.

76 This was a heart-specific phenomenon, as HIF1alpha protein accumulated predominantly in the myoca

77 K pathway, as well as other factors, such as HIF1alpha, Myc and MITF, are among those that control th

78 F1 and its receptor, CXCR4, were found to be HIF1alpha-regulated genes in ATII cells and were up-regu

79 ntagonized by LSD1 and the interplay between HIF1alpha protein methylation and other PTMs in regulati

80 Transcript 4 (DDIT4) acts as a link between HIF1alpha and mTOR signalling and regulation of adult st

81 e effect of LSD1 on the relationship between HIF1alpha post-translational modifications (PTMs) and HI

82 utant form of Spry2 (3P/3A-Spry2) that binds HIF1alpha, but not pVHL, we show that WT-Spry2, but not

83 These findings argue that both HIF1alpha and HIF2alpha exert protumorigenic functions d

84 ters SLC4A4 and SLC4A9, which rely upon both HIF1alpha and HIF2alpha activity for their expression.

85 cancerous cells is downregulated further by HIF1alpha-mediated induction of miR-224-5p, making the c

86 This effect is mediated by HIF1alpha-mediated increased lipid synthesis, accumulati

87 otion of intracellular glucose metabolism by HIF1alpha stabilization is required for cell proliferati

88 (ASS1) by either promoter methylation or by HIF1alpha is associated with increased metastasis and po

89 revealed that the signature was regulated by HIF1alpha and TP53 and included nine HIF1alpha-regulated

90 In established ccRCC, HIF1alpha has been implicated as a renal tumor suppresso

91 critical inflammatory cell type, Th17 cells, HIF1alpha acts via the retinoic acid-related orphan rece

92 This study aimed to clarify HIF1alpha and HIF2alpha expression patterns during cytot

93 In CGNPs cultured under normoxic conditions, HIF1alpha is posttranslationally stabilized in a manner

94 Conventional HIF1alpha or Notch signaling routes prevalent in solid t

95 WT-Spry2, but not the 3P/3A-Spry2 decreases HIF1alpha protein levels.

96 as a prototype, we show that Spry2 decreases HIF1alpha stability and enhances the ubiquitylation of H

97 LSD1 demethylates HIF1alpha at lysine (K) 391, which protects HIF1alpha ag

98 Importantly, the MAOA-dependent HIF1alpha/VEGF-A/FOXO1/TWIST1 pathway was activated in h

99 ition of angiogenesis is mediated by an EGFR-HIF1alpha-VEGF-dependent mechanism.

100 owed that specific down-regulation of either HIF1alpha or TWIST1 inhibited the ability of CPEB2B to i

101 tivity to glycolysis inhibitors and elevated HIF1alpha expression.

102 PDH availability in TEM resulted in elevated HIF1alpha expression.

103 poor prognosis, silencing of Spry2 elevated HIF1alpha protein levels.

104 though lower copy numbers of HIF1A (encoding HIF1alpha, located at 14q23.2) was associated with worse

105 We now demonstrate that endogenous HIF1alpha is detectable in exosomes and that LMP1 signif

106 idylinositol 3 kinase-AKT pathway to enhance HIF1alpha protein synthesis.

107 d expression of the Hypoxia Inducible Factor HIF1alpha, lactate dehydrogenase LDH5, glucose transport

108 deacetylase SIRT1, hypoxia-inducible factor HIF1alpha, oxidative stress-inducible factor NRF2, and t

109 fect of hypoxia-induced transcription factor HIF1alpha activation on classical dendritic cell (cDCs)

110 ed the stability of the transcription factor HIF1alpha and reprogrammed cell metabolism to a glycolyt

111 The hypoxia-inducible transcription factor HIF1alpha drives expression of many glycolytic enzymes.

112 of the hypoxia-sensing transcription factor HIF1alpha.

113 alpha-subunits of hypoxia-inducible factors (HIF1alpha and HIF2alpha) promote transcription of genes

114 the hypoxia-inducible transcription factors, HIF1alpha and HIF2alpha, leading to expression of a gene

115 discovered a mid-gestational requirement for HIF1alpha for proliferation of hypoxic CMs, involving me

116 ession of regulatory DNA trans-factors (e.g. HIF1alpha and TWIST1).

117 Global HIF1alpha chromatin immunoprecipitation (ChIP) analysis

118 a novel feed-forward mechanism of glycolysis-HIF1alpha signaling.

119 On the other hand, HIF1alpha stabilization stimulated glycolysis in bone th

120 double knockouts of HIF1alpha and HIF2alpha (HIF1alpha/2alpha dKO) generated with the MyoD(Cre) syste

121 When its levels were high, HIF1alpha interacted with the Cd36 promoter to augment e

122 However, HIF1alpha and HIF2alpha differentially regulated cell pr

123 However, HIF1alpha negatively regulates adult muscle regeneration

124 However, HIF1alpha/2alpha dKO produced with the tamoxifen-inducib

125 In other malignancies, however, HIF1alpha has an established tumor-promoting role.

126 In addition, HSP90alpha, HIF1alpha, and VEGF expression were also found positivel

127 Active RhoC elevated HSP90alpha, HIF1alpha, VEGF expression, and angiogenesis in the huma

128 but not 3P/3A-Spry2 results in a decrease in HIF1alpha-sensitive glucose uptake.

129 position; these increases were eliminated in HIF1alpha null cells.

130 Increases in HIF1alpha and HIF2alpha protein levels due to silencing

131 gh glycolytic metabolism drives increases in HIF1alpha to enhance TEM function during hypoxia.

132 Inhibition of NOX activity resulted in HIF1alpha destabilization and reduced levels of cyclin D

133 iochemical assays and in cells, resulting in HIF1alpha accumulation.

134 ts on key proangiogenesis factors, including HIF1alpha, VEGFR, and MMP-2/MMP-9.

135 mediators of cell stress pathways, including HIF1alpha, ATF4, and p53, are key to normal development

136 glycolysis that occurs in sepsis, including HIF1alpha and mTOR, and mediators of endotoxin tolerance

137 tly to the Il22 promoter, and SCFAs increase HIF1alpha binding to the Il22 promoter through histone m

138 drial superoxide dismutase (SOD2), increases HIF1alpha (hypoxia-inducible factor-1), reduces endothel

139 that hypoxic glycolysis, in turn, increases HIF1alpha transcriptional activity and stimulates tumor

140 Indeed, HIF1alpha interacting with beta-catenin displaced TCF4 f

141 LSD1 also directly suppresses PHD2-induced HIF1alpha hydroxylation, which has a mutually dependent

142 vate and KLF6 deficiency attenuate inducible HIF1alpha expression in macrophages.

143 Moreover, DDB2 inhibits HIF1alpha in HNSCC cells.

144 It inhibits HIF1alpha in both normoxia and hypoxia by reducing mRNA

145 onizing the crosstalk between PTMs involving HIF1alpha protein degradation.

146 a metabolic vulnerability in a subset of low HIF1alpha/low MEIS1-expressing MLL-rearranged leukemia c

147 -MRI and with histopathologic hypoxia marker HIF1alpha and gene expression of Wnt target GLUL, pharma

148 was induced by hypoxia, whereas HAF-mediated HIF1alpha degradation was SUMOylation independent.

149 ually dependent interplay with Set9-mediated HIF1alpha methylation.

150 gulates hypoxia signaling through modulating HIF1alpha chromatin-binding, leading NEPC to exhibit hig

151 Moreover, HIF1alpha or HIF2alpha overexpression in CC-RCCVHL cells

152 and thereby promotes activation of the mTOR-HIF1alpha pathway.

153 upregulates aerobic glycolysis via the mTOR/HIF1alpha pathway and neutralizes fumarate-induced prote

154 rcuit involving the mTOR complex 1 (mTORC1), HIF1alpha and inducible nitric oxide synthase (iNOS) coo

155 SAD inhibited multiple HIF1alpha/VEGF-arbitrated angiogenesis dynamics as score

156 ated by HIF1alpha and TP53 and included nine HIF1alpha-regulated genes, which were highly expressed i

157 st that a better understanding of nonhypoxic HIF1alpha stabilization through NOX-induced ROS generati

158 Therein, high levels of HIF2alpha, but not HIF1alpha, significantly correlate with expression of ne

159 evelopment, such as BMP-TGFbeta, WNT, Notch, HIF1alpha, TWIST1 and HOX family genes, are regulated by

160 s disease and recently identified as a novel HIF1alpha target, was found to abrogate maintenance of c

161 n pathway leads to reduced levels of nuclear HIF1alpha, promoter occupancy, HIF-dependent gene expres

162 endent but glucose-dependent accumulation of HIF1alpha protein via both transcriptional activation of

163 get of rapamycin (mTOR)-Akt, accumulation of HIF1alpha, Notch3 intracellular domain and beta-catenin,

164 otein via both transcriptional activation of HIF1alpha mRNA and the phosphatidylinositol 3 kinase-AKT

165 D2), the enzyme which prevents activation of HIF1alpha, in macrophages.

166 mTORC1 induces activation of HIF1alpha, which reprograms ILC3 metabolism toward glyco

167 ted PRAS40 and mTORC1-mediated activation of HIF1alpha.

168 and inhibits the transcriptional activity of HIF1alpha by upregulating FIH1.

169 study, we investigated the contributions of HIF1alpha and HIF2alpha to ccRCC initiation in the conte

170 than preventing the lysosomal degradation of HIF1alpha, disrupting the V-ATPase results in intracellu

171 gase that induces the hypoxic degradation of HIF1alpha.

172 ition of glycolysis, or genetic depletion of HIF1alpha, attenuated IgG IC-induced activation of macro

173 mtDNA damage, resulting in downregulation of HIF1alpha and attenuated phosphorylation of Akt.

174 FGFR1 silencing also reduced expression of HIF1alpha, which in addition to its roles in hypoxic res

175 ted delivery of active and inactive forms of HIF1alpha results in reciprocal changes in the expressio

176 interacts with and promotes the function of HIF1alpha.

177 , and PHD3) that mediate the inactivation of HIF1alpha and HIF2alpha under normal oxygen conditions.

178 ugh a NAD/Sirtuin 1-mediated inactivation of HIF1alpha-driven CXCR4 gene transcription, leading to mo

179 ia induces Bhlhe40 expression independent of HIF1alpha but through a novel p53-dependent signaling pa

180 nd sufficient for the paracrine induction of HIF1alpha in such cells under normoxic conditions.

181 GDC0941, and TGX221 blocked the induction of HIF1alpha protein and its targets vascular endothelial g

182 le treatment with rapamycin or inhibition of HIF1alpha ablates UBE2O-dependent tumor biology.

183 ese results argue against the involvement of HIF1alpha in promoting renal cyst growth and suggest tha

184 Interestingly, double knockouts of HIF1alpha and HIF2alpha (HIF1alpha/2alpha dKO) generated

185 igated whether Spry2 regulates the levels of HIF1alpha and HIF2alpha proteins.

186 that LMP1 significantly increases levels of HIF1alpha in exosomes.

187 Increased levels of HIF1alpha were also associated with increased tissue fac

188 ethanol-induced damage by reducing levels of HIF1alpha.

189 for these effects by elevating the levels of HIF1alpha.

190 addition, ANKDD1A decreases the half-life of HIF1alpha by upregulating FIH1, decreases glucose uptake

191 Specific loss of HIF1alpha exacerbated MMP13 expression and cartilage des

192 Loss of HIF1alpha resulted in activation of ATF4 and p53, the la

193 cells and that pharmacologic manipulation of HIF1alpha is also capable of enhancing homing and engraf

194 ulator of Lys63-linked polyubiquitination of HIF1alpha.

195 re pVHL/associated E3 ligase in proximity of HIF1alpha and increase its ubiquitylation and degradatio

196 , where CHD4 in turn enhanced recruitment of HIF1alpha, leading to HIF target gene transcription.

197 est a new role for PTEN in the regulation of HIF1alpha and importantly that PI3K-AKT activation is re

198 Negative regulation of HIF1alpha by AMPK1 is bypassed in hypoxic cells, due to

199 e primarily post-translational regulation of HIF1alpha.

200 Thus, LSD1 is a key regulator of HIF1alpha/VEGF-mediated tumor angiogenesis by antagonizi

201 Here, we explored the role of HIF1alpha during murine skeletal muscle development and

202 In addressing the controversial role of HIF1alpha in cardiomyocytes (CMs) during heart developme

203 study sought to further examine the role of HIF1alpha in ccRCC using bioinformatic analyses of 530 c

204 tributes to the understanding of the role of HIF1alpha in OA and highlights the HIF1alpha-beta-cateni

205 We studied the role of HIF1alpha in regulating Wnt signaling in cartilage and O

206 ts highlight previously undescribed roles of HIF1alpha and interactions among major cell stress pathw

207 Silencing of HIF1alpha expression sensitized an intrinsically unrespo

208 is required for the hypoxic stabilization of HIF1alpha and that hypoxia alone is not sufficient to re

209 Brief stabilization of HIF1alpha in SP7-positive cells in postnatal mice dramat

210 metabolic adaptation is the stabilization of HIF1alpha, which leads to increased glycolysis and lacta

211 pha) expression, leading to stabilization of HIF1alpha.

212 By fusing an oxygen sensitive subdomain of HIF1alpha to a CAR scaffold, we generated CAR T-cells th

213 pha6beta1-dependent nuclear translocation of HIF1alpha.

214 Lys63-linked ubiquitination of HIF1alpha by XIAP is dependent on the activity of E2 ubi

215 stability and enhances the ubiquitylation of HIF1alpha by a von Hippel-Lindau protein (pVHL)-dependen

216 In ALCL, the upregulation of HIF1alpha and HIF2alpha in hypoxic conditions required A

217 The EML4-ALK-mediated upregulation of HIF1alpha, HK2 and glycolytic metabolism was also highly

218 Prognostic value of HIF1alpha, SLC2A1, and VEGFA was determined by immunohis

219 poxia-driven copy gains are not dependent on HIF1alpha or HIF2alpha; however, they are dependent on t

220 Moreover, the action of MDM2 on HIF1alpha under hypoxia occurs in the cytoplasm and is c

221 phages by completely inhibiting C/EBPbeta or HIF1alpha or by partially inhibiting STAT3 may hold ther

222 the inflammatory or glycolytic HIF2alpha or HIF1alpha target genes.

223 val difference based on either HIF1A mRNA or HIF1alpha protein expression.

224 In mouse models, mice that overexpressed HIF1alpha or HIF2alpha specifically in intestinal epithe

225 tein-protein interactions: p53-MDM2 and p300-HIF1alpha.

226 ggest that regulation of ATP13A2 by the PHD2-HIF1alpha signaling pathway affects cellular iron homeos

227 Knockdown of PKM2, HIF1alpha and glycolysis-related genes uniformly decreas

228 ent Lys63-linked polyubiquitination promotes HIF1alpha nuclear retention leading to an increase in th

229 HIF1alpha at lysine (K) 391, which protects HIF1alpha against ubiquitin-mediated protein degradation

230 ation with bevacizumab would not only reduce HIF1alpha to overcome hypoxia-induced resistance, but al

231 Furthermore, GAPDH overexpression reduced HIF1alpha expression and impaired proliferation and surv

232 in a manner that was associated with reduced HIF1alpha levels but not blood vessel alterations.

233 to uncover cellular processes that regulate HIF1alpha.

234 lammatory and hypoxic response by regulating HIF1alpha expression in macrophage.

235 at hypoxia alone is not sufficient to render HIF1alpha resistant to proteasomal cleavage and degradat

236 ssion of PRKD2 was able to partially restore HIF1alpha and secreted VEGF-A levels in hypoxic cancer c

237 f proteolytic degradation, and the resulting HIF1alpha-HIF1beta heterodimers undergo post-translation

238 ose Cd and hypoxia induce miR-210 via a same HIF1alpha modulated pathway.

239 oxia-associated decreases in PlGF secretion; HIF1alpha silencing had no significant effect on PlGF se

240 ecific HIF1alpha knockout (SftpcCreERT2(+/-);HIF1alpha(f/f)) mice.

241 endothelial (but not myeloid) cell-specific HIF1alpha doubled pulmonary fibrin deposition, and trebl

242 repair was attenuated in ATII cell-specific HIF1alpha knockout (SftpcCreERT2(+/-);HIF1alpha(f/f)) mi

243 est that tumor and endothelial cell-specific HIF1alpha may have opposing roles in cancer-associated c

244 mbly factors, TMEM199 and CCDC115, stabilise HIF1alpha in aerobic conditions.

245 e as it does in CD4 T cells, mROS stabilizes HIF1alpha and RORgammat in ILC3s and thereby promotes th

246 importantly, overexpression of oxygen stable HIF1alpha reversed attenuated proinflammatory and glycol

247 imal tubular cells and podocytes with stable HIF1alpha and/or HIF2alpha suppression displayed cell ty

248 The mechanism of LPS-stimulated HIF1alpha induction involves succinate, which inhibits p

249 E as well as the CUL2-RING ligase substrate HIF1alpha.

250 dimers of an oxygen-sensitive alpha subunit, HIF1alpha or HIF2alpha, and a constitutively expressed b

251 Differential expression of the HIF subunits HIF1alpha and HIF2alpha occurs in many human tumor types

252 CRLX101 durably suppressed HIF1alpha, thus potentially counteracting undesirable ef

253 sion through suppressing BRD4 and its target HIF1alpha.

254 In summary, HIF2alpha, rather than HIF1alpha, is most affected by reduced oxygen level duri

255 We conclude that HIF1alpha and HIF2alpha are dispensable for muscle stem

256 We conclude that HIF1alpha is activated in ATII cells after lung injury a

257 te cell dynamics on myofibers confirmed that HIF1alpha/2alpha dKO myoblasts exhibit reduced self-rene

258 Our findings demonstrate that HIF1alpha activation in cDCs is necessary to control ves

259 Our results demonstrate that HIF1alpha is dispensable during embryonic and fetal myog

260 In tumor MDSC, we determined that HIF1alpha was bound directly to a transcriptionally acti

261 Herein, we describe the first evidence that HIF1alpha can be degraded under hypoxic conditions via t

262 In addition, we provide evidence that HIF1alpha itself participates in exosome-mediated pro-me

263 Our data provide the first evidence that HIF1alpha regulates skeletal myogenesis in vivo and esta

264 We found that HIF1alpha formed a complex with the Notch effector hes f

265 l-specific HIF expression, we show here that HIF1alpha and HIF2alpha are preferentially expressed in

266 Taken together, the data indicate that HIF1alpha is not a target of 14q deletion in ccRCC and t

267 Furthermore, we show that HIF1alpha stimulates glycolysis in the absence of Pink1,

268 ignaling in hypoxic chondrocytes showed that HIF1alpha lowered transcription factor 4 (TCF4)-beta-cat

269 eted muscle progenitors further suggest that HIF1alpha represses myogenesis through inhibition of can

270 Under hypoxic conditions, the HIF1alpha subunit accumulates because of a decrease in t

271 e role of HIF1alpha in OA and highlights the HIF1alpha-beta-catenin interaction, thus providing new i

272 Mechanistically, the HIF1alpha/2alpha dKO blunted hypoxia-induced activation

273 Moreover, the HIF1alpha acetylation that occurs in a HIF1alpha methyla

274 apped in the pro-survival first phase of the HIF1alpha injury repair response with metabolism and the

275 e, we identify a new methylation site of the HIF1alpha protein antagonized by LSD1 and the interplay

276 revealed that pathologic upregulation of the HIF1alpha response, often observed in cancer and linked

277 ed by post-translational modification of the HIF1alpha subunit, which can alter its stability and/or

278 uc (HIF reporter) mice and expression of the HIF1alpha target gene GLUT1.

279 ting phosphorylation and inactivation of the HIF1alpha transcriptional coactivator p300.

280 Notably, of the HIF1alpha-activated glycolytic enzymes we evaluated by g

281 ute the second pro-regenerative phase of the HIF1alpha/PFKFB3 injury pathway.

282 In this study, we show that the HIF1alpha E3 ligase hypoxia-associated factor (HAF) comp

283 ISL1+ CPCs blocked Isl1 suppression via the HIF1alpha/HES1/SIRT1 complex and prevented CHDs induced

284 osterically blocks its dimerization with the HIF1alpha/2alpha transcriptional dimerization partner AR

285 Therefore, HIF1alpha-beta-catenin interaction is a negative regulat

286 rt1 and Sirt1/Cdk2 complex formation through HIF1alpha activation.

287 le in regulating metabolic phenotype through HIF1alpha.

288 a novel observation: feedback from IGFBP2 to HIF1alpha is integral to the sustained growth of gliobla

289 gests that downstream signaling from IGFI to HIF1alpha, which has been the target of many insulin sig

290 hat DDIT4 exert these effects down-stream to HIF1alpha.

291 lity of estrogenic GPER signaling to trigger HIF1alpha-dependent VEGF expression that supports angiog

292 Using HIF1alpha as a prototype, we show that Spry2 decreases H

293 elations between mTORC1 activation and VEGF, HIF1alpha, and c-Myc expression in human angiosarcoma sa

294 ding, HIF stabilization accelerated, whereas HIF1alpha shRNA delayed wound closure.

295 However, whether HIF1alpha regulates skeletal myogenesis in vivo is not k

296 yses revealed unexpected mechanisms by which HIF1alpha intersects with ATF4 and p53 pathways.

297 EGF-A blockade in tumors was associated with HIF1alpha expression and an increase in CD144(+) vasculo

298 Spry2 also exists in a complex with HIF1alpha.

299 on signature that was highly correlated with HIF1alpha and hypoxia-driven signatures and that strongl

300 with KDM1B while correlating positively with HIF1alpha and GBM progression in patients.