ライフサイエンスコーパス: prolyl hydroxylase

1 members, Phd2 appears to be the primary HIF prolyl hydroxylase.

2 , but is not present in bacteria, which lack prolyl hydroxylase.

3 olog of Caenorhabditis elegans Egl9 as a HIF prolyl hydroxylase.

4 was shown to be operative in the absence of prolyl hydroxylase.

5 S)-2HG, but not (R)-2HG, to inhibit the EglN prolyl hydroxylases.

6 ted for degradation via hydroxylation by HIF-prolyl hydroxylases.

7 nteracts with both HIF-1alpha and HIF-1alpha prolyl hydroxylases.

8 otein to counteract any residual activity of prolyl hydroxylases.

9 which is related to hypoxia-inducible factor prolyl hydroxylases.

10 We demonstrate that a combination of prolyl hydroxylase 1 and factor inhibiting HIF hydroxyla

11 hydroxylation and form complexes with either prolyl hydroxylase 1 or factor inhibiting HIF.

12 The human hypoxia-inducible factor prolyl hydroxylases 1, 2, and 3 (HIF-PHD1, -2, and -3) a

13 and (3beta-adiol)-dependent transcription of prolyl hydroxylase 2 (PHD2) also known as Egl nine homol

14 be a mouse line with conditional loss of HIF prolyl hydroxylase 2 (PHD2) in very early hematopoietic

15 se mutation in the EGLN1 gene, which encodes prolyl hydroxylase 2 (PHD2), that contributes to this ad

16 R-199a and is responsible for downregulating prolyl hydroxylase 2, required for stabilization of Hif-

17 A cross with mice deficient in prolyl hydroxylase 2, which hydroxylates hypoxia-inducib

18 enic effects during acute colitis via a NTR1-prolyl hydroxylase 2/HIF-1alpha-miR-210 signaling pathwa

19 Overexpression of prolyl-hydroxylase 2 (PHD2) transgene, a predominant iso

20 Specific knockout of prolyl hydroxylase-2 (PHD2) increased HIF-2alpha/Notch3

21 ible factor-1 alpha is naturally degraded by prolyl hydroxylase-2 (PHD2) protein.

22 8 expression by either transfection with HIF-prolyl hydroxylase-2 small interfering RNA or overexpres

23 oxalylglycine or a small hairpin RNA against prolyl hydroxylase-2, increased both hypoxia-inducible f

24 in augmented S-nitrosation of caspase-3 and prolyl-hydroxylase-2, the enzyme responsible for targeti

25 Interaction of PKM2 with prolyl hydroxylase 3 (PHD3) enhances PKM2 binding to HIF

26 nction, we have shown that MUC1 up-regulates prolyl hydroxylase 3 (PHD3) expression and promotes HIF-

27 Here we report that prolyl hydroxylase 3 (PHD3) interacts with nonmuscle act

28 orter for hypoxia, expressing EGFP driven by prolyl hydroxylase 3 (phd3) promoter/regulatory elements

29 itin ligase Siah2 has been shown to regulate prolyl hydroxylase 3 (PHD3) stability with concomitant e

30 he ability of Siah2 to target its substrates prolyl hydroxylase 3 and Spry2 (Sprouty2) for ubiquitin-

31 dulate HIF-1alpha degradation by suppressing prolyl hydroxylase 3 expression.

32 , and 3 (PHD1, -2, and -3; also known as HIF prolyl hydroxylase 3, 2, and 1, respectively), have rece

33 ) is hydroxylated on proline 419 and 426 via prolyl hydroxylase 3.

34 , including MMP-3, ADAMTS-5, syndecan 4, and prolyl hydroxylase 3.

35 including specific roles for HIF-1alpha and prolyl hydroxylase-3.

36 ted-like ER kinase pathway by suppression of prolyl hydroxylase 4.

37 Inhibition of PHD3 prolyl hydroxylase activity by dimethyloxalylglycine als

38 of different HIF target genes to changes in prolyl hydroxylase activity differ, quantitatively and q

39 s a negative regulator of NF-kappaB, and its prolyl hydroxylase activity is required for this effect.

40 ts of Toxoplasma on HIF-1alpha abundance and prolyl hydroxylase activity require activin-like recepto

41 alpha downregulation was suppressed when HIF-prolyl hydroxylase activity was pharmacologically inhibi

42 ferrioxamine, and hypoxia, all inhibitors of prolyl hydroxylase activity, led to repression of C2C12

43 xygen availability, which is crucial for HIF-prolyl hydroxylase activity.

44 rbate reversed albumin-induced inhibition of prolyl-hydroxylase activity.

45 es were expressed coding for the subunits of prolyl hydroxylase, an enzyme that post-translationally

46 ING4 directly associates with the HIF prolyl hydroxylase, an Fe(II)-dependent oxygenase previo

47 ylase domain protein (PHD, also known as HIF prolyl hydroxylase and egg laying-defective nine protein

48 roles such as the regulation of activity of prolyl hydroxylases and adaptive responses to hypoxia.

49 result from fumarate-dependent inhibition of prolyl hydroxylases and subsequent evasion from von Hipp

50 e been previously found to be substrates for prolyl hydroxylases and subsequent O-glycosylation of th

51 ha1 collagen IV by upregulation of alpha(II) prolyl-hydroxylase and increased the release of Arresten

52 D34, fibroblast-specific protein 1,4-hydroxy-prolyl-hydroxylase, and factor XIIIa.

53 The collagen prolyl hydroxylases are enzymes that are required for pr

54 Hydroxylase Domain-Containing Protein (PHD) prolyl hydroxylases are oxygen-sensitive enzymes that tr

55 Here we show that responsible prolyl hydroxylases are targets for both nickel(II) and

56 onal progenitor cells and requires the EglN3 prolyl hydroxylase as a downstream effector.

57 ly identified EGLN3, a member of a family of prolyl hydroxylases, as a negative regulator of the NF-k

58 ind to the 2-oxoglutarate site of HIF-1alpha prolyl hydroxylases, but their effects on HIF-1 are not

59 in addition to regulating HIF stability, HIF prolyl hydroxylases can modulate HIF function through th

60 Either hypoxia or mutations in egl-9, a prolyl hydroxylase cellular oxygen sensor, result in the

61 g pathway through depletion of HIF-targeting prolyl hydroxylase-containing protein 2 (PHD-2) further

62 In mammals, prolyl hydroxylases control levels of the central transc

63 at this effect is a result of an increase in prolyl hydroxylase-dependent degradation of HIF1alpha.

64 TM causes HIF-1alpha downregulation in a HIF-prolyl hydroxylase-dependent manner.

65 The enzymatic activity of prolyl hydroxylases depends on iron as the activating me

66 n mice by injecting 2 structurally unrelated prolyl hydroxylase domain (PHD) enzyme inhibitors: dimet

67 to analyze the expression and regulation of prolyl hydroxylase domain (PHD) enzymes and factor-inhib

68 The HIF prolyl hydroxylase domain (PHD) enzymes are non-heme, ir

69 ducible factor (HIF)-regulating O2-dependent prolyl hydroxylase domain (PHD) enzymes, could represent

70 ns, such as iron chelators and inhibitors of prolyl hydroxylase domain (PHD) enzymes, have broad-spec

71 Prolyl hydroxylase domain (PHD) proteins are well recogn

72 Prolyl hydroxylase domain (PHD) proteins catalyze oxygen

73 Prolyl hydroxylase domain (PHD) proteins, including PHD1

74 EK2) stress pathway activation, and enhanced prolyl hydroxylase domain (PHD)-3 (EGLN3) mRNA expressio

75 oxygen concentrations are directly sensed by prolyl hydroxylase domain (PHD)-containing proteins, whi

76 In these domain-swapping experiments, prolyl hydroxylase domain 1 (PHD1) and PHD2 preferential

77 Treatment of these mice with Fg4497, a prolyl hydroxylase domain 2 (PHD2) inhibitor, activated

78 Prolyl hydroxylase domain 2 (PHD2) is deemed a primary o

79 Prolyl hydroxylase domain 2 (PHD2) plays an important ro

80 AM features, cancer cells were inoculated in prolyl hydroxylase domain 2 (PHD2)-haplodeficient mice,

81 protein, increased HIF-1alpha, and decreased prolyl hydroxylase domain 2 in nuclear fractions, which

82 that 2-hydroxyglutarate-enabled catalysis by prolyl hydroxylase domain 2 is not enantiomer-specific a

83 tion of 2-oxoglutarate oxygenases, including prolyl hydroxylase domain 2, the most important human pr

84 ue, affecting HIF2alpha interaction with the prolyl hydroxylase domain 2-containing protein, decreasi

85 lization of HIF-2alpha using an inhibitor of prolyl hydroxylase domain 3 (an upstream inhibitor of HI

86 Treatment of macrophages with the prolyl hydroxylase domain 3 inhibitor AKB-6899 stabilize

87 Cofactors involved in prolyl hydroxylase domain activity were increased in PAH

88 through its interaction with the O2-sensing prolyl hydroxylase domain containing protein EGLN3 (or P

89 ble factor (HIF) by a set of closely related prolyl hydroxylase domain enzymes (PHD1, 2 and 3) regula

90 nchymal pluripotent stem cells revealed that prolyl hydroxylase domain protein (PHD) levels significa

91 In this pathway, prolyl hydroxylase domain protein (PHD) site-specificall

92 en-dependent control of red cell mass is the prolyl hydroxylase domain protein (PHD):hypoxia inducibl

93 Under normoxic conditions, prolyl hydroxylase domain protein (PHD, also known as HI

94 Prolyl hydroxylase domain protein 2 (PHD2) (also known a

95 Prolyl hydroxylase domain protein 2 (PHD2) belongs to an

96 Prolyl hydroxylase domain protein 2 (PHD2) is a cellular

97 Here we show that prolyl hydroxylase domain protein 2 (PHD2), an enzyme mo

98 Prolyl hydroxylase domain protein 2 (PHD2, also known as

99 gene, which encodes for HIF-2alpha, and the prolyl hydroxylase domain protein 2 (PHD2, also known as

100 Tibetans bear a genetic signature in the prolyl hydroxylase domain protein 2 (PHD2/EGLN1) gene, w

101 ed with lentiviral short hairpin RNA against prolyl hydroxylase domain protein 2 (shPHD2) to silence

102 K2), associated with and was hydroxylated by prolyl hydroxylase domain protein 3 (PHD3).

103 ay for controlling red cell mass is the PHD (prolyl hydroxylase domain protein):hypoxia-inducible fac

104 Prolyl hydroxylase domain proteins (PHD isozymes 1-3) re

105 demonstrate that silencing and expression of prolyl hydroxylase domain proteins (PHD1-3) increase and

106 al inhibition of a class of enzymes known as prolyl hydroxylase domain proteins (PHDs) has neuroprote

107 Deficiencies in prolyl hydroxylase domain proteins (PHDs) may lead to th

108 Hypoxia-inducible factor (HIF) prolyl hydroxylase domain proteins (PHDs) serve as oxyge

109 Prolyl hydroxylase domain proteins hydroxylate substrate

110 PHD1, PHD2, and PHD3 are prolyl hydroxylase domain proteins that regulate the sta

111 srupt the hydroxylation domain recognized by prolyl hydroxylase domain-2 containing protein, leading

112 l and biophysical studies on the reaction of prolyl hydroxylase domain-containing enzyme (PHD) isofor

113 been identified as a family of O2-dependent prolyl hydroxylase domain-containing enzymes (PHD).

114 While canonically regulated by prolyl hydroxylase domain-containing enzymes (PHDs), the

115 Pharmacological inhibitors of prolyl hydroxylase domain-containing enzymes (PHDs), whi

116 The Prolyl Hydroxylase Domain-Containing Protein (PHD) proly

117 We recently demonstrated that Prolyl Hydroxylase Domain-containing Protein 2 (Phd2) is

118 1alpha) and Hif-2alpha is regulated by three prolyl hydroxylase domain-containing protein isoforms (P

119 a and -2alpha, respectively) via blockade of prolyl hydroxylase domain-containing proteins (HIF-PHDs)

120 ia-inducible factors (HIFs) by inhibition of prolyl hydroxylase domain-containing proteins (PHDs) is

121 Three enzymes, prolyl hydroxylase domain-containing proteins 1, 2, and

122 6 that binds the human oxygen sensing enzyme prolyl-hydroxylase domain containing protein (PHD)2 and

123 ographic analyses revealing that Pseudomonas prolyl-hydroxylase domain containing protein (PPHD) cont

124 eudomonas aeruginosa lacking the Pseudomonas prolyl-hydroxylase domain-containing protein, which has

125 s lacking the hypoxia response component and prolyl hydroxylase egl-9, with impaired subcellular loca

126 Three HIF prolyl hydroxylases (EGLN1, EGLN2, and EGLN3) have been

127 The three EglN prolyl hydroxylases (EglN1, EglN2, and EglN3) regulate t

128 ulatory feedback loop involving the HIFalpha prolyl hydroxylase, Egln3.

129 , we have identified a critical role for the prolyl hydroxylase enzyme Phd2 in maintaining the balanc

130 hypoxia-inducible transcription factor (HIF)-prolyl hydroxylase enzymes (PHD1, PHD2, and PHD3) is a s

131 hypoxia-inducible transcription factor (HIF)-prolyl hydroxylase enzymes (PHD1, PHD2, and PHD3) is a s

132 Prolyl hydroxylase enzymes (PHD1-3) are molecular oxygen

133 Prolyl hydroxylase enzymes (PHDs) sense cellular oxygen

134 the cytosol, where they inhibit a family of prolyl hydroxylase enzymes (PHDs).

135 The EGLN (also called PHD) prolyl hydroxylase enzymes and their canonical targets,

136 The HIF prolyl hydroxylase enzymes PHD1, PHD2 and PHD3 regulate

137 replicated by the use of an inhibitor of the prolyl hydroxylase enzymes responsible for the von Hippe

138 nts that activate HIF, via inhibition of the prolyl hydroxylase enzymes, might be developed to induce

139 indicating an inhibition of the activity of prolyl-hydroxylases, enzymes promoting the degradation o

140 nes, is stabilized via regulation by Ofd1, a prolyl hydroxylase family member inhibited by hypoxia, a

141 the pharmacological manipulation of the HIF prolyl hydroxylase for ischemic diseases.

142 574 disrupts the binding of PHD2/HPH2, a key prolyl hydroxylase for oxygen-dependent proteolysis of H

143 y decreases PHD2 abundance, which is the key prolyl hydroxylase for regulating HIF-1alpha.

144 Recently, mutations in the prolyl hydroxylase gene (PHD) 1 and 2 and in the hypoxia

145 EGLN3, a member of the EGLN family of prolyl hydroxylases, has been shown to catalyze hydroxyl

146 pha a plausible mechanism, inhibition of HIF prolyl hydroxylases, has previously been suggested by in

147 Several prolyl hydroxylases have been found to specifically hydr

148 The egg-laying abnormal-9 (EGLN) prolyl hydroxylases have been shown to regulate the stab

149 P564) by an enzyme we have termed HIF-alpha prolyl-hydroxylase (HIF-PH).

150 elease erythropoietin under hypoxia, via the prolyl hydroxylase-HIF-2alpha axis, in the human kidney.

151 Loss-of-function mutations in Hif-1 prolyl hydroxylase (Hph), an enzyme involved in the cell

152 Hif-1 prolyl hydroxylase (Hph), another effector of CycD/Cdk4,

153 coding transcription/translation regulators, prolyl hydroxylases, hybrid cluster proteins, proteases,

154 hat the expression of the EGLN3-encoded PHD3 prolyl hydroxylase identifies proinflammatory macrophage

155 called Egln1) appears to be the primary HIF prolyl hydroxylase in cell culture experiments.

156 corbate is essential for maintaining iron in prolyl hydroxylases in the active iron(II) state, we sug

157 ffects of 2-hydroxyglutarate on catalysis by prolyl hydroxylases in vitro and suggest that non-enzyma

158 The roles of 2-oxoglutarate (2OG)-dependent prolyl-hydroxylases in eukaryotes include collagen stabi

159 Prolyl hydroxylase inhibition also potently suppressed m

160 inducible factor (HIF) stabilization via HIF prolyl hydroxylase inhibition using the isoquinolone Rox

161 cologic or genetic activation of HIF via HIF prolyl-hydroxylase inhibition protected wild-type animal

162 Indeed, HIF1alpha activation by a prolyl hydroxylase inhibitor (PHI) synergizes with gluco

163 odels, augmenting HIF-1alpha levels with the prolyl hydroxylase inhibitor 2-(1-chloro-4-hydroxyisoqui

164 the addition of proteasome inhibitors or the prolyl hydroxylase inhibitor 2-hydroxyglutarate, and bea

165 al cancer cell lines, was insensitive to the prolyl hydroxylase inhibitor dimethyloxaloyl glycine, an

166 We used the prolyl hydroxylase inhibitor ethyl-3,4-dihydroxybenzoate

167 One such agent, the HIF prolyl hydroxylase inhibitor FG-4383, was active in the

168 zation of hypoxia inducible factors with the prolyl hydroxylase inhibitor FG-4497 did not influence I

169 een the dose of the hypoxia-inducible factor-prolyl hydroxylase inhibitor GSK1278863 and hemoglobin r

170 Systemic administration of a HIF-prolyl hydroxylase inhibitor replicated the Phd2-deficie

171 bioavailable hypoxia-inducible factor (HIF) prolyl hydroxylase inhibitor that promotes coordinated e

172 and show that ethyl 3,4-dihydroxybenzoate, a prolyl hydroxylase inhibitor, decreases tumor fibrosis a

173 d the effect of systemic administration of a prolyl hydroxylase inhibitor, dimethyloxalylglycine, in

174 ls lacking MIF are defective in hypoxia- and prolyl hydroxylase inhibitor-induced HIF-1alpha stabiliz

175 ent study, we report the discovery of an HIF prolyl-hydroxylase inhibitor, DMOG [N-(2-Methoxy-2-oxoac

176 this phase 1 study, we used an orally active prolyl-hydroxylase inhibitor, FG-2216, to stabilize HIF

177 protective effects were not observed in HIF prolyl-hydroxylase inhibitor-treated animals lacking end

178 Several HIF-prolyl hydroxylase inhibitors (PHIs) induced erythropoie

179 -2alpha in the neuroprotective mechanisms of prolyl hydroxylase inhibitors and in an endogenous cell

180 Presently used prolyl hydroxylase inhibitors are lipophilic 2-oxoglutar

181 ions for the development of paralog-specific prolyl hydroxylase inhibitors as therapeutic agents.

182 dition to exhibiting pro-angiogenic effects, prolyl hydroxylase inhibitors can modulate the plasminog

183 The prolyl hydroxylase inhibitors ethyl 3,4-dihydroxybenzoic

184 rovides rationale for the therapeutic use of prolyl hydroxylase inhibitors in the setting of acute or

185 To investigate whether prolyl hydroxylase inhibitors modulate the net plasminog

186 This study assesses the effect of prolyl hydroxylase inhibitors on plasminogen activation

187 IF-1alpha overexpression or HIF accumulating prolyl hydroxylase inhibitors reduced ErbB4 endocytosis,

188 Hypoxia-inducible factor prolyl hydroxylase inhibitors stabilize levels of hypoxi

189 The use of prolyl hydroxylase inhibitors such as l-mimosine (L-MIM)

190 abilization achieved by using small-molecule prolyl-hydroxylase inhibitors reduced M-MITF expression,

191 Collagen prolyl hydroxylase is a known target of hydralazine.

192 The EglN2/PHD1 prolyl hydroxylase is an important oxygen sensor contrib

193 lyl 4-hydroxylase related to animal HIFalpha prolyl hydroxylases is required for optimal parasite pro

194 droxylase domain 2, the most important human prolyl hydroxylase isoform.

195 lycerate kinase 1 and Glucokinase but not of prolyl hydroxylase isoforms.

196 ver-specific deletions of genes encoding HIF-prolyl-hydroxylase isoforms (PHD1, PHD2, and PHD3) that

197 particularly, hypoxia-inducible factor (HIF) prolyl hydroxylases, JmjC domain-containing histone deme

198 l nervous system, inhibition of collagen and prolyl hydroxylases lead to altered microenvironment and

199 Thus, prolyl hydroxylase mediated hydroxylation and subsequent

200 ion in ischemic tissues because of increased prolyl hydroxylase-mediated hydroxylation (P<0.05) and p

201 lish the prognostic significance of collagen prolyl hydroxylase mRNA expression in human breast cance

202 phages, increasing HIF-1alpha and decreasing prolyl hydroxylase mRNA production in a TLR4-dependent f

203 However, neither inhibition of prolyl hydroxylases nor mutation of HIF-1 alpha-hydroxyl

204 When oxygen is present, the prolyl hydroxylase Ofd1 down-regulates Sre1N activity in

205 ereas over-expression of hph (Drosophila HIF prolyl hydroxylase) only accelerated BCM.

206 radation of HIF-2alpha whereas inhibitors of prolyl hydroxylases or proteosome were ineffective.

207 ses succinate availability to regulate HIF-1 prolyl hydroxylases, or stimulates mitochondrial reactiv

208 nactivation or pharmacological inhibition of prolyl hydroxylase oxygen sensors, indicating the molecu

209 alpha is rapidly degraded by 2 hydroxylases: prolyl hydroxylase (PHD) and factor-inhibiting HIF-1 (FI

210 Therefore, HIF prolyl hydroxylase (PHD) enzymatic activity is critical

211 inactivation of the critical oxygen-sensing prolyl hydroxylase (PHD) enzymes (PHD1-3) in osteoprogen

212 The hypoxia-inducible factor (HIF) prolyl hydroxylase (PHD) enzymes represent novel targets

213 rest in the development of inhibitors of the prolyl hydroxylase (PHD) enzymes that regulate the hypox

214 regulated by the 2-oxoglutarate and Iron(II) prolyl hydroxylase (PHD) enzymes, which hydroxylate the

215 a structural class of pan-inhibitors of the prolyl hydroxylase (PHD) family of enzymes for the treat

216 ermore, eEF2 phosphorylation was mimicked by prolyl hydroxylase (PHD) inhibition with dimethyloxalylg

217 For these purposes, we used a novel prolyl hydroxylase (PHD) inhibitor (FG-4497) that readil

218 Inhibition of prolyl hydroxylase (PHD) is known to activate the transc

219 ecent studies suggest a differential role of prolyl hydroxylase (PHD) isoforms in controlling hypoxia

220 We postulated that the well described prolyl hydroxylase (PHD) oxygen sensors and HIF negative

221 ts substrates as part of an oxygen-dependent prolyl hydroxylase (PHD) reaction, with hypoxia-inducibl

222 ion of the HIF-1alpha subunit is mediated by prolyl hydroxylase (PHD), the von Hippel-Lindau (VHL)/El

223 The role of prolyl hydroxylase (PHD)-3 as a hypoxia inducible factor

224 of which, when in excess, inhibits HIFalpha prolyl hydroxylase (PHD).

225 ndergoes oxygen-dependent degradation by the prolyl hydroxylase (PHD)/von Hippel-Lindau (VHL) system.

226 CODD) of HIFalpha isoforms, as catalysed by prolyl hydroxylases (PHD 1-3).

227 athway, Siah1, and Siah2, and suppressed the prolyl hydroxylases (PHD) 2 and PHD3.

228 te-specific hydroxylation carried out by HIF prolyl hydroxylases (PHD) and subsequent proteasomal deg

229 inhibitors of hypoxia-inducible factor (HIF) prolyl hydroxylases (PHD) is described.

230 nhibitors of the iron-dependent enzyme class prolyl hydroxylases (PHD), which target alpha subunits o

231 poxia-inducible factor-1alpha (HIF-alpha) by prolyl hydroxylases (PHD).

232 tor (HIF-1alpha) is rapidly degraded via the prolyl hydroxylases (PHD)/VHL pathways.

233 l-intrinsic expression of the oxygen-sensing prolyl-hydroxylase (PHD) proteins is required to maintai

234 stimulated in normoxia by the oxygen-sensing prolyl hydroxylase PHD1 (also known as EGLN2).

235 le factor (HIF), which is inhibited by three prolyl hydroxylases (PHD1, PHD2, and PHD3).

236 In humans, they comprise three prolyl hydroxylases (PHD1-3 or EGLN1-3) and factor inhib

237 hydroxylases; in humans there are three HIF prolyl hydroxylases (PHD1-3) and an asparaginyl hydroxyl

238 tivity are regulated by the oxygen-sensitive prolyl hydroxylases (PHD1-3), but the role of PHDs in ne

239 Egln-9-type prolyl hydroxylases, PHD1 and PHD2, coimmunoprecipitated

240 Although three HIF prolyl hydroxylases, PHD1, PHD2, and PHD3, have been ide

241 ression of the three most well characterized prolyl-hydroxylases, PHD1, PHD2, and PHD3, and the expre

242 oxylation of HIF-1alpha or HIF-2alpha by the prolyl hydroxylase PHD2 is required for binding of the v

243 in vitro did not inhibit the activity of the prolyl-hydroxylase PHD2, experiments with mouse liver sh

244 that are heterozygous for the principal HIF prolyl hydroxylase, PHD2, show enhanced ventilatory sens

245 Here we show that the prolyl hydroxylase PHD3 restrains tumour growth in respo

246 We report in this study that the prolyl hydroxylase PHD3-encoding EGLN3 gene is specifica

247 Hypoxia-inducible factor (HIF) prolyl hydroxylases (PHDs) are alpha-ketoglutarate (alph

248 ting evidence suggests that oxygen-sensitive prolyl hydroxylases (PHDs) are important regulators of t

249 Prolyl hydroxylases (PHDs) are oxygen sensors that stabi

250 Prolyl hydroxylases (PHDs) perceive intracellular oxygen

251 uitin ligase as well as the oxygen-sensitive prolyl hydroxylases (PHDs) represent essential regulator

252 tion factor HIF-1alpha relies on a family of prolyl hydroxylases (PHDs) that hydroxylate hypoxia-indu

253 er normoxia but stabilized when O2-dependent prolyl hydroxylases (PHDs) that target its O2-dependent

254 ine residues are hydroxylated by a family of prolyl hydroxylases (PHDs).

255 mselves controlled by the oxygen-sensing HIF prolyl hydroxylases (PHDs).

256 induction involves succinate, which inhibits prolyl hydroxylases (PHDs).

257 ich are modified by the oxygen-dependent HIF prolyl hydroxylases (PHDs/HPHs).

258 ver, bioinformatics imply that 2OG-dependent prolyl-hydroxylases (PHDs) homologous to those acting as

259 The PHD family of oxygen-dependent prolyl hydroxylases plays a pivotal role in regulating H

260 We show that expression of collagen prolyl hydroxylases promotes cancer cell alignment along

261 e conclude that the oxygen dependence of the prolyl hydroxylase reaction is sufficient to mediate HIF

262 Prolyl hydroxylases require oxygen as a substrate, and t

263 by mutations in its negative regulator egl-9/prolyl hydroxylase shifts behavioral oxygen preferences

264 ver, under hypoxic conditions, inhibition of prolyl hydroxylase significantly increased erythropoieti

265 respiratory oxygen-dependent targets such as prolyl hydroxylases so that they do not register hypoxia

266 emically delivered siRNAs targeting the EglN prolyl hydroxylases specifically in the liver, leading t

267 Here we show that OGFOD1 is a prolyl hydroxylase that catalyzes the posttranslational

268 lin D/Cdk4-stimulated growth requires Hph, a prolyl hydroxylase that is a key component of a cell's a

269 -independent manner, expression of the EGLN1 prolyl hydroxylase that regulates HIF-1alpha degradation

270 PCBP2 are required for iron delivery to the prolyl hydroxylase that regulates HIF1.

271 the transcription of genes encoding collagen prolyl hydroxylases that are critical for collagen depos

272 the family of hypoxia-inducible factor (HIF) prolyl hydroxylases that regulate HIF stability in respo

273 Inhibition of prolyl hydroxylases that regulate the degradation of hyp

274 expression, could be mimicked by inhibiting prolyl-hydroxylases that activate HIF1, suggesting that

275 Using a strain that does not contain prolyl hydroxylase, the same folding mechanism was shown

276 EglN1, the main HIFalpha prolyl-hydroxylase, undergoes oxidative self-inactivatio

277 Inhibition of prolyl hydroxylases, using either dimethyloxalylglycine

278 o-substrate for the hypoxia-inducible factor prolyl hydroxylases via enzyme-catalysed oxidation to 2-

279 ion of the HIF-1alpha subunit is mediated by prolyl hydroxylase, von Hippel-Lindau protein (VHL)/Elon

280 he degradation of HIF-1alpha is regulated by prolyl hydroxylases, we examined the effect of systemic

281 r (HIF) and 2-HG is a known inhibitor of HIF prolyl hydroxylases, we hypothesized that 2-HG may be re

282 are responsible for the interaction with HIF-prolyl hydroxylase, were deleted.

283 The work identifies a human prolyl hydroxylase with a role in translational regulati