ライフサイエンスコーパス: HIF1alpha

1 HIF1alpha and HIF2alpha are both necessary to initiate t

2 HIF1alpha expression decreased and HIF2alpha expression

3 HIF1alpha expression was not associated with survival.

4 HIF1alpha inhibition causes a reduction of weight gain i

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 limits intestinal barrier dysfunction, but the

10 HIF1alpha stabilized by LSD1 cooperates with CBP and MTA

11 HIF1alpha was induced due to energy stress shown by a de

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

13 HIF1alpha, SLC2A1, and VEGFA expression could be evaluat

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

15 cription factor hypoxia inducible factor 1a (HIF1alpha) is a key element in the cellular response to

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

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

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

19 poxia-inducible transcription factor 1alpha (HIF1alpha) and HIF2alpha protein.

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

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

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 Hypoxia-inducible factor 1alpha (HIF1alpha) regulates pathways in energy metabolism that

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

26 lization of hypoxia-inducible factor 1alpha (HIF1alpha), resulting in reduced HIF1alpha-induced expre

27 ancement of hypoxia-inducible factor 1alpha (HIF1alpha)-directed VEGF A, angiopoietin 4, and EGLN3 tr

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

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

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

31 2 (HK2) and hypoxia-inducible factor-1alpha (HIF1alpha) and associated negatively with PFK-2b express

32 tion of the hypoxia-inducible factor-1alpha (HIF1alpha) and autophagy.

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 ssion of the hypoxia-induced factors-1alpha (HIF1alpha) and HIF2alpha has been suggested as a pivotal

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

41 to activate HIF1 target gene promoters in a HIF1alpha HLH/PAS and N-TAD dependent manner while HIF2a

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

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

44 thelial growth factor antibodies, accumulate HIF1alpha/pY654-beta-catenin complexes and develop an in

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

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

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

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

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

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

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

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

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

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

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

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

57 carcinomas accumulate pY654-beta-catenin and HIF1alpha.

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

59 mainly by increasing expression of cJUN and HIF1alpha.

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

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

62 controlling the feedback between IGFBP2 and HIF1alpha.

63 influencing histone and DNA methylation, and HIF1alpha hydroxylation.

64 ccurred together with activation of NRF2 and HIF1alpha signaling in CXCL14-expressing CAF.

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

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

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

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

69 n of beta-catenin to HIF1alpha signaling and HIF1alpha-mediated tumor EMT.

70 d as a translational activator of TWIST1 and HIF1alpha.

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

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

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

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

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

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

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

78 ential of ALK-rearranged NSCLC required both HIF1alpha and HIF2alpha.

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

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

81 ouse did not diminish bone accrual caused by HIF1alpha stabilization.

82 1 is under direct transcriptional control by HIF1alpha.

83 aptive mechanisms like autophagy mediated by HIF1alpha and finally leads to apoptosis.

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

85 al of tumor cells in vitro is phenocopied by HIF1alpha knockdown in hypoxic cells, whereas STAT3 knoc

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

87 dependent aspects of the pY654-beta-catenin/ HIF1alpha pathway may attenuate untoward biological effe

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

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

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

91 to form enhanceosome complexes that contain HIF1alpha, STAT3, CBP, p300 and RNA Pol II on HIF1 targe

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

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

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

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

96 cible dominant negative HIF1alpha mutant (dn-HIF1alpha).

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

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

99 PDH availability in TEM resulted in elevated HIF1alpha expression.

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

101 dial growth plates, associated with elevated HIF1alpha levels, cell death, and intracellular retentio

102 al results, genetic inhibition of endogenous HIF1alpha activity prompts similar metabolic improvement

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

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

105 ion factor containing an inducibly expressed HIF1alpha subunit and a constitutively expressed HIF1bet

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

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

108 (EMT) and stabilize the transcription factor HIF1alpha, which mediates hypoxia through an elevation o

109 of the hypoxia-sensing transcription factor HIF1alpha.

110 s with EGFR, IGF1R, and transcription factor HIF1alpha.

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

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

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

114 etabolism, whereas a reduction in functional HIF1alpha expression consolidates the inhibition of glyc

115 Functionally, HIF1alpha interacts with STAT3 to activate HIF1 target g

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 However, HIF1alpha and HIF2alpha differentially regulated cell pr

122 However, HIF1alpha negatively regulates adult muscle regeneration

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

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

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

126 Increases in HIF1alpha and HIF2alpha protein levels due to silencing

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

128 pha and Src kinase as critically involved in HIF1alpha signaling and tumor invasion.

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

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

131 as genes important for osteolysis, including HIF1alpha, JAG1, IL6, and VEGF.

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

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

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

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

136 y suppresses the high-fat-diet (HFD)-induced HIF1alpha activation in adipose tissue.

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

138 onizing the crosstalk between PTMs involving HIF1alpha protein degradation.

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

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

141 ually dependent interplay with Set9-mediated HIF1alpha methylation.

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

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

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

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

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

147 fic, doxycycline-inducible dominant negative HIF1alpha mutant (dn-HIF1alpha).

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

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

150 Finally, HIF2alpha, but not HIF1alpha, was required for ALCL growth in vivo whereas

151 Socs3 was identified as a novel HIF1alpha target gene based on chromatin immunoprecipita

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

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

154 Genetic ablation of HIF1alpha in adipose tissue decreased insulin resistance

155 N specifically inhibited the accumulation of HIF1alpha in response to hypoxia.

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

157 tractility and attenuate the accumulation of HIF1alpha, depletion of intramuscular glycogen, and oxid

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

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

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

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

162 gase that induces the hypoxic degradation of HIF1alpha.

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

164 h HIF1alpha that regulates the expression of HIF1alpha targets via the recruitment of RNA polymerase

165 o enhance tumor growth and the expression of HIF1alpha, VEGF, and the endothelial marker CD34 in a mo

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

167 he effect of expressing a stabilized form of HIF1alpha in osteoblast precursors.

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

169 interacts with and promotes the function of HIF1alpha.

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

171 lanoma, we demonstrated that inactivation of HIF1alpha or HIF2alpha abrogates metastasis without affe

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

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

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

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

176 STAT3-adiponectin pathway, and inhibition of HIF1alpha in adipose tissue was essential for ACF to imp

177 Here, acriflavine (ACF), an inhibitor of HIF1alpha, induced the expression of adiponectin and red

178 2), selectively disrupts the interaction of HIF1alpha with p300/CBP coactivators and downregulates t

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

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

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

182 that LMP1 significantly increases levels of HIF1alpha in exosomes.

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

184 for these effects by elevating the levels of HIF1alpha.

185 ethanol-induced damage by reducing levels of HIF1alpha.

186 Specific loss of HIF1alpha exacerbated MMP13 expression and cartilage des

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

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

189 ulator of Lys63-linked polyubiquitination of HIF1alpha.

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

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

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

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

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

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

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

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

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

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

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

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

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

203 hypoxia-inducible gene and direct target of HIF1alpha and HIF2alpha.

204 C surgical specimens correlated with that of HIF1alpha and VEGFa (P < 1 x 10(-4)).

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

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

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

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

209 leads to increased VEGF via upregulation of HIF1alpha.

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

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

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

213 an enhanced self-renewal capacity reliant on HIF1alpha.

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

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

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

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

218 Physically, HIF1alpha HLH and PAS domains are required for its inter

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

220 interact with HIF1alpha and Src, to promote HIF1alpha transcriptional activity, and for hypoxia-indu

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

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

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

224 tor 1alpha (HIF1alpha), resulting in reduced HIF1alpha-induced expression of IL-1beta.

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

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

227 to uncover cellular processes that regulate HIF1alpha.

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

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

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

231 gical inhibition of PDK1 completely reversed HIF1alpha-driven bone formation in vivo.

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

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

234 We used the selective HIF1alpha inhibitor PX-478, whose effectiveness has prev

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

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

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

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

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

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

241 ges in which paracrine IL-6-activated STAT3, HIF1alpha, and C/EBPbeta signaling are critical for macr

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

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

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

245 CRLX101 durably suppressed HIF1alpha, thus potentially counteracting undesirable ef

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

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

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

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

250 in melanoma progression and demonstrate that HIF1alpha and HIF2alpha activate independent transcripti

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

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

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

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

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

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

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

258 Earlier studies revealed that HIF1alpha in adipose tissue is markedly elevated in high

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

277 Pink1 reprograms glucose metabolism through HIF1alpha, sustaining increased cell proliferation.

278 Thus, HIF1alpha stimulates osteoblast formation through direct

279 Thus, HIF1alpha-driven bone formation is independent of VEGFA

280 tyrosine phosphorylation of beta-catenin to HIF1alpha signaling and HIF1alpha-mediated tumor EMT.

281 pY654-beta-catenin specifically complexed to HIF1alpha and Src kinase as critically involved in HIF1a

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

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

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

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

286 In turn, HIF1alpha was not required for Mincle expression, kinase

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

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

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

290 ion and inflammatory gene induction, whereas HIF1alpha controls Nos2 expression.

291 However, the exact mechanism whereby HIF1alpha regulates adiponectin remains unclear.

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

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

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

295 by assembling a transcriptional complex with HIF1alpha that regulates the expression of HIF1alpha tar

296 Spry2 also exists in a complex with HIF1alpha.

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

298 s required for beta-catenin to interact with HIF1alpha and Src, to promote HIF1alpha transcriptional

299 HIF1 target gene promoters, interacting with HIF1alpha protein and recruiting coactivators CREB bindi

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