ライフサイエンスコーパス: PHD

1 PHD catalysis regulates HIFalpha levels, and FIH catalys

2 PHD expression analysis in 124 colorectal cancer patient

3 PHD inhibition was found to be associated with increases

4 PHD inhibitors with different structural scaffolds behav

5 PHD proteins limit pulmonary type helper (Th)-1 response

6 PHD site specifically prolyl hydroxylates the transcript

7 PHD was defined as diagnosis of myelodysplastic syndrome

8 inducible factor prolylhydroxylase domain-1 (PHD-1) enzyme.

9 Binding of H3K4me3 to the RAG-2 PHD induces conformational changes in RAG-1 within a DNA

10 Thus, engagement of H3K4me3 by the RAG-2 PHD is associated with dynamic conformational changes in

11 information regarding occupancy of the RAG-2 PHD is transmitted to RAG-1.

12 Injection of either of these 2 PHD inhibitors stabilized HIF-1alpha protein expression

13 t homeodomain-Polycomb repressive complex 2 (PHD-PRC2) and indicates a role for the transcriptional r

14 y profiling identified the adaptor TAB1 as a PHD substrate, and TGF-beta- or EGF-stimulated Map3k1(m)

15 rm for hepatic Epo expression regulated by a PHD-HIF2alpha-EpoHE cascade in vivo.

16 tor MS1 (MALE STERILITY 1), which contains a PHD domain associated with chromatin re-organization.

17 MAP3Ks, MEKK1 (encoded by Map3k1) contains a PHD motif.

18 TRIM24 contains a PHD/bromodomain offering the opportunity to develop prot

19 VIN3 encodes a PHD-finger domain that binds to modified histones in vit

20 M2A consisting of a CXXC type zinc finger, a PHD domain and a newly identified Heterochromatin Protei

21 , rather than poly-ubiquitinates AURKA, in a PHD-independent reaction targeting AURKA for degradation

22 An AF10 region consisting of a PHD finger-Zn knuckle-PHD finger (PZP) folds into a sing

23 period at diagnosis (or first suspicion of a PHD) was 41 mo (range, 15-84 mo).

24 to ob/ob mice for 2 weeks increased adipose PHD levels and decreased anti-adipogenic protein levels

25 The interaction between CaM and Akt(PHD) is enthalpically driven, and the affinity is greatl

26 ctable binding has been observed between Akt(PHD) and PI(3,4,5)P3-free nanodiscs, demonstrating that

27 The CaM-binding interface in Akt(PHD) was mapped to two loops adjacent to the PI(3,4,5)P3

28 However, the molecular details of Akt(PHD) interaction with CaM are not known.

29 We also show that Akt(PHD) binds to both layers of the nanodisc, indicating pr

30 We show that PI(3,4,5)P3 binding to Akt(PHD) displaces the C-terminal lobe of CaM but not the we

31 I(3,4,5)P3-embedded membrane nanodisc to Akt(PHD) with a 10(3)-fold tighter affinity than PI(3,4,5)P3

32 echniques to characterize CaM binding to Akt(PHD).

33 and membrane mimetics (nanodisc) bind to Akt(PHD).

34 The loss of all PHD isoforms results in both polycythemia, which is caus

35 nnection between amino-acid availability and PHD activity.

36 ribe a dual inhibitor of the bromodomain and PHD finger (BRPF) family member BRPF2 and the TATA box b

37 ining protein 24) and BRPF1 (bromodomain and PHD finger containing protein 1) are involved in the epi

38 Bromodomain and PHD finger-containing protein 1 (BRPF1) is a multivalent

39 The BRPF (bromodomain and PHD finger-containing) family are scaffolding proteins i

40 Bromodomain- and PHD finger-containing protein 1 (BRPF1) is a multivalent

41 BRPF1 (bromodomain- and PHD finger-containing protein 1) is a unique chromatin r

42 minal RING (really interesting new gene) and PHD (plant homeo domain) fingers and a carboxyl-terminal

43 ated in structure and function to the animal PHDs.

44 o called ZMYND11) contains tandemly arranged PHD, BROMO, and PWWP domains, which are chromatin recogn

45 lighting the multifunctional nature of ATXR5 PHD domain.

46 Third, we show that ATXR5 PHD domain employs a narrow binding pocket to selectivel

47 are essential for H3 binding and that BAZ2B PHD-BRD establishes a polyvalent interaction with H3K14a

48 we report that acidic residues in the BAZ2B PHD domain are essential for H3 binding and that BAZ2B P

49 Because PHD activity is sensitive to oxygen levels and certain b

50 NA-binding ARID domain and a histone-binding PHD domain into the Jumonji domain, which separates the

51 rget genes, it is important to consider both PHD and FIH activity, and in the case of some sets of ta

52 s decreased only under conditions where both PHD and chromodomains were lost, generally in the second

53 recruitment to the nucleosome, however both PHDs are required to alter the NCP dynamics.

54 The BRD, PHD, and HAT domains form an integral structural unit to

55 The BRD, PHD, and ZZ domains interact with small ubiquitin-like m

56 d the adjacent bromodomain/PHD finger (bromo/PHD) region of the transcriptional coactivator p300.

57 We found that the bromo/PHD region of p300 can bind to the acetylated catalytic

58 Bromodomain PHD finger transcription factor (BPTF) is the largest su

59 BRPF1 (bromodomain PHD finger 1) is a core subunit of the MOZ histone acety

60 URF was disabled by silencing of bromodomain PHD-finger containing transcription factor (BPTF), the l

61 igenome reader domain families (Bromodomain, PHD finger, Chromodomain, MBT, PWWP and Tudor).

62 as a quaternary complex with the bromodomain-PHD finger protein 1 (BRPF1), inhibitor of growth 5 (ING

63 nsferase domain and the adjacent bromodomain/PHD finger (bromo/PHD) region of the transcriptional coa

64 Tumor colonization is accompanied by PHD-protein-dependent induction of pulmonary Treg cells

65 ion downstream of HIF-alpha hydroxylation by PHD enzymes.

66 ich HIF target gene expression is induced by PHD or FIH inhibition.

67 e investigated the functional role played by PHD during RIAD.

68 HIF, which is negatively regulated by PHD, activates numerous genes, including ones involved i

69 The EGLN (also called PHD) prolyl hydroxylase enzymes and their canonical targ

70 ISWI subunit BAZ1B and for the non-canonical PHD and bromodomain modules of the paralog BAZ1A.

71 these effects did not involve the classical PHD/VHL pathway for HIF upregulation, but instead involv

72 HD structures with those of HIF and collagen PHDs reveals conservation in substrate recognition despi

73 Collectively, PHD proteins function in T cells to coordinate distinct

74 ssing the bromodomain (BRD), CH2 (comprising PHD and RING), HAT, and ZZ domains at 2.4-A resolution.

75 rase 1 (DNMT1) and ubiquitin-like containing PHD and RING finger domains 1 (UHRF1) proteins.

76 UHRF1 (ubiquitin-like, containing PHD and RING finger domains 1) has a well-established ro

77 The ubiquitin-like, containing PHD and RING finger domains protein 1 (UHRF1) is essenti

78 UHRF1 (ubiquitin-like, containing PHD and RING finger domains, 1) recruits DNMT1 to hemime

79 regulator ubiquitin-like protein containing PHD and RING finger domains 1 (uhrf1) in zebrafish leads

80 A specific module containing a conventional PHD finger followed by an extended PHD finger exists in

81 byproducts of the tricarboxylic acid cycle, PHDs act as sensors of the cell's metabolic state.

82 A plant homeo domain (PHD) in Bye1 binds histone H3 tails with trimethylated l

83 sphate using the pleckstrin-homology domain (PHD) and engage in rapid membrane fission during synapti

84 ions between its pleckstrin homology domain (PHD) and phosphatidylinositol 3,4,5-trisphosphate (PI(3,

85 ions between its pleckstrin homology domain (PHD) and phosphatidylinositol 3,4,5-trisphosphate (PI(3,

86 movements of the pleckstrin homology domain (PHD) from a 'closed' conformation docked near the stalk

87 is regulated by prolyl-4-hydroxylase domain (PHD) dioxygenases PHD1, PHD2, and PHD3, which function a

88 turally unrelated prolyl hydroxylase domain (PHD) enzyme inhibitors: dimethyloxalyl glycine and FG-44

89 The HIF prolyl hydroxylase domain (PHD) enzymes are non-heme, iron-containing dioxygenases

90 The prolyl-4-hydroxylase domain (PHD) enzymes are regarded as the molecular oxygen sensor

91 and inhibitors of prolyl hydroxylase domain (PHD) enzymes, have broad-spectrum activities and off-tar

92 Prolyl hydroxylase domain (PHD) proteins are well recognized as oxygen sensors and

93 Prolyl hydroxylase domain (PHD) proteins catalyze oxygen-dependent prolyl hydroxyla

94 availability by prolyl-4-hydroxylase domain (PHD) proteins, with PHD2 being the main oxygen sensor th

95 ion, and enhanced prolyl hydroxylase domain (PHD)-3 (EGLN3) mRNA expression.

96 n Hippel-Lindau/prolyl-4-hydroxylase domain (PHD)/HIF axis in cell-expressing neural glial antigen 2,

97 Prolyl-4-hydroxylase-domain (PHD) proteins regulate the hypoxia-inducible factors (HI

98 2D, which is half the size, lacks the double PHD and Tudor domains that are epigenome readers and pre

99 H3 tail structure in complex with the double PHD finger (DPF) of the lysine acetyltransferase MOZ/MYS

100 Here, we show that the dual PHD fingers of Rco1, a member of the Rpd3S histone deace

101 analyze persistent hematologic dysfunction (PHD) after PRRT with (177)Lu-DOTATATE in patients with g

102 rolyl hydroxylase domain-containing enzymes (PHDs), which result in stabilization of HIFs, have recen

103 Prolyl hydroxylase enzymes (PHDs) sense cellular oxygen upstream of hypoxia-inducibl

104 ventional PHD finger followed by an extended PHD finger exists in the mammalian AF10 protein, among a

105 s essential for viability and that the first PHD finger contributes to the preferred binding of PHD1-

106 No risk factors for PHD could be identified for the GEP NET patients, not ev

107 l repressors thus recruits the machinery for PHD-PRC2 nucleation and epigenetic silencing.

108 y, mutations in the prolyl hydroxylase gene (PHD) 1 and 2 and in the hypoxia-inducible factor 2 alpha

109 Mec-3), RING (really interesting new gene), PHD (plant homeodomain) and ZZ (ZZ-type zinc finger) dom

110 ia or conditions of pharmacologic or genetic PHD inactivation.

111 Eleven (4%) of the 274 patients had PHD after treatment with (177)Lu-DOTATATE: 8 patients (2

112 Eight days after hatching (PHD) CB staining clearly delineated Area X.

113 ketoglutarate cofactor and inhibitor for HIF PHD, on postnatal day (P)3, P5, and P7.

114 Despite the critical role of the histone-PHD interaction in normal and pathological processes, se

115 histone reader modules, a plant homeodomain (PHD) and a bromodomain (BRD), linked by a largely disord

116 The plant homeodomain (PHD) and Bromodomain cassette in ZMYND8 mediated the com

117 ncluding those containing plant homeodomain (PHD) and double Tudor reader domains.

118 The plant homeodomain (PHD) finger is found in many chromatin-associated protei

119 The plant homeodomain (PHD) finger of Set3 binds methylated lysine 4 of histone

120 Plant homeodomain (PHD) finger-containing proteins are implicated in fundam

121 one 3 (H3K4me3) through a plant homeodomain (PHD) finger.

122 Binding of H3K4me3 by a plant homeodomain (PHD) in RAG-2 stimulates substrate binding and catalysis

123 In this state the plant homeodomain (PHD) mediates interaction with the extreme N terminus of

124 -specific proteins with a plant homeodomain (PHD) motif, SHORT LIFE (SHL) and EARLY BOLTING IN SHORT

125 e linked tandem Tudor and plant homeodomain (PHD) of UHRF1 (ubiquitin-like PHD and RING finger domain

126 re employed to identify a plant homeodomain (PHD) protein, TaR1 in wheat that plays a critical role d

127 ressor protein contains a plant homeodomain (PHD) that reads the epigenetic code via recognition of h

128 ules, an H3K4me3-specific plant homeodomain (PHD) within the Yng2 subunit and an H3K36me2/3-specific

129 se screens identified the plant homeodomain (PHD)-finger domain protein PHF5A as differentially requi

130 in the identification of plant homeodomain (PHD)-like finger 6 (PHF6) as a potential TMZ-sensitizing

131 Plant homeodomain (PHD)-type zinc fingers play an important role in recogni

132 Pf1, also known as Phf12 (plant homeodomain [PHD] zinc finger protein 12), is a member of the PHD zin

133 mino-terminal of its two plant homeodomains (PHDs), PHD1, helps Aire target poorly transcribed loci b

134 However, if and how PHD enzymes affect macrophage metabolism are enigmatic.

135 However, PHD activity also depends on factors other than oxygen,

136 PHD2, the most important human PHD isoform, is proposed to be biochemically/kinetically

137 HIF-specific hydroxylase PHD-2 may represent a relevant target for cartilage repa

138 critical oxygen-sensing prolyl hydroxylase (PHD) enzymes (PHD1-3) in osteoprogenitors.

139 xoglutarate and Iron(II) prolyl hydroxylase (PHD) enzymes, which hydroxylate the HIFalpha subunit, fa

140 Inhibition of prolyl hydroxylase (PHD) is known to activate the transcription factor hypox

141 that the well described prolyl hydroxylase (PHD) oxygen sensors and HIF negative feedback regulators

142 t of an oxygen-dependent prolyl hydroxylase (PHD) reaction, with hypoxia-inducible factor alpha (HIFa

143 The role of prolyl hydroxylase (PHD)-3 as a hypoxia inducible factor (HIF)-1alpha cofact

144 ndent degradation by the prolyl hydroxylase (PHD)/von Hippel-Lindau (VHL) system.

145 on of the oxygen-sensing prolyl-hydroxylase (PHD) proteins is required to maintain local tolerance ag

146 oforms, as catalysed by prolyl hydroxylases (PHD 1-3).

147 ah2, and suppressed the prolyl hydroxylases (PHD) 2 and PHD3.

148 -inducible factor (HIF) prolyl hydroxylases (PHD) is described.

149 ongs to the family of prolyl-4-hydroxylases (PHDs) that is responsible for posttranslational modifica

150 -inducible factor (HIF) prolyl hydroxylases (PHDs) are alpha-ketoglutarate (alphaKG)-dependent dioxyg

151 s that oxygen-sensitive prolyl hydroxylases (PHDs) are important regulators of this entire system.

152 ccinate, which inhibits prolyl hydroxylases (PHDs).

153 mply that 2OG-dependent prolyl-hydroxylases (PHDs) homologous to those acting as sensing components f

154 racellular iron depletion, thereby impairing PHD activity and leading to HIF activation.

155 se Map3k1 (Map3k1(m) (PHD)) with an inactive PHD motif.

156 results suggest that rosiglitazone increases PHD expression in a PPARgamma-dependent manner and that

157 al cells and examined the role of individual PHDs in REPC pool size regulation and renal EPO output.

158 -PCR, implying that rosiglitazone may induce PHD up-regulation directly by PPARgamma activation.

159 ranscripts, but does not need a cold-induced PHD protein required for the epigenetic silencing.

160 s to investigate the interaction of the ING3 PHD finger (ING3PHD) with the active transcription mark

161 at albumin-induced oxidative stress inhibits PHD activity to accumulate HIF-1alpha, which mediates al

162 eered the classical dynamin by replacing its PHD with a polyhistidine or polylysine linker.

163 cent studies have implicated PHD2 as the key PHD isoform regulating red cell mass.

164 region consisting of a PHD finger-Zn knuckle-PHD finger (PZP) folds into a single module that recogni

165 t homeodomain (PHD) of UHRF1 (ubiquitin-like PHD and RING finger domain-containing protein 1) operate

166 (bromodomain- and plant homeodomain-linked (PHD) zinc finger-containing protein 1) recognizes differ

167 Map3k1(m) (PHD) (/+) mice exhibit aberrant cardiac tissue, B-cell d

168 Map3k1(m) (PHD) ES cells demonstrate that the MEKK1 PHD controls p3

169 , and TGF-beta- or EGF-stimulated Map3k1(m) (PHD) ES cells exhibit defective non-canonical ubiquitina

170 a knockin mutant of mouse Map3k1 (Map3k1(m) (PHD)) with an inactive PHD motif.

171 We identified PHD2 as the main PHD responsible for HIF peak duration.

172 functional redundancy between the three main PHD proteins.

173 Both the MEKK1 PHD and TAB1 are critical for ES-cell differentiation an

174 The MEKK1 PHD binds and mediates the transfer of Lys63-linked poly

175 m) (PHD) ES cells demonstrate that the MEKK1 PHD controls p38 and JNK activation during TGF-beta, EGF

176 Acute exposure to a small molecule PHD inhibitor (PHI) (2-(1-chloro-4-hydroxyisoquinoline-3

177 results demonstrate that the total amount of PHD activity is more important than the specific functio

178 crocyclic calixarenes can disrupt binding of PHD fingers to methylated lysine 4 of histone H3 in vitr

179 The incidence and course of PHD were analyzed in 274 GEP NET patients from a group o

180 sk factors were found for the development of PHD in GEP NET patients.

181 The effects of PHD inhibition on GI radioprotection will be described i

182 Consequently, pharmacological inhibition of PHD enzymes, leading to stabilization of HIF, may be of

183 the outcome of pharmaceutical inhibition of PHD in mice with MALA induced through the administration

184 ic deletion or pharmacological inhibition of PHD proteins limits tumor colonization of the lung and i

185 Although all three isoforms of PHD are expressed within vulnerable dopaminergic (DAergi

186 tance of understanding the complex nature of PHD regulation.

187 The prevalence of PHD after PRRT with (177)Lu-DOTATATE was 4% in our patie

188 one H3T3/T6 phosphorylation and retention of PHD finger proteins in chromatin during mitosis.

189 Here, we assessed the significance of PHD enzymes during the metastatic spread of colorectal c

190 fold that constitutes the catalytic site of PHD isoforms appeared responsible for the oxidative dime

191 differences between genetic inactivation of PHDs, responses to hypoxia and responses to a pharmacolo

192 Inhibition of PHDs increased the interaction between TR-alpha and nucl

193 more, pharmacologic or genetic inhibition of PHDs induced autophagy and prevented mammalian target of

194 Pharmacological inhibition of PHDs using EDHB might represent a novel and safe strateg

195 Pharmacological inhibition of PHDs using EDHB might represent a novel and safe strateg

196 2 (PHD2) transgene, a predominant isoform of PHDs in renal tubules, to reduce HIF-1alpha level signif

197 es were identified in the promoter region of PHDs by ChIP-PCR, implying that rosiglitazone may induce

198 662) blunted the effects of rosiglitazone on PHD regulation.

199 ntrol of HIF2alpha expression dominates over PHD/VHL-mediated regulation of HIF2alpha stability in ju

200 A point mutation in the p300 PHD finger that is related to the Rubinstein-Taybi syndr

201 assess the effect of the small molecule pan-PHD inhibitor ethyl-3,4-dihydroxybenzoate (EDHB) on live

202 assess the effect of the small molecule pan-PHD inhibitor ethyl-3,4-dihydroxybenzoate (EDHB) on live

203 pecific deleterious effects of pharmacologic PHD inhibition.

204 was submaximal, as hypoxia or pharmacologic PHD inhibition further increased the REPC fraction among

205 is known about the effect of pharmacological PHD inhibition on tumor expansion, and on liver regenera

206 is known about the effect of pharmacological PHD inhibition on tumor expansion, and on liver regenera

207 Further optimization led to potent PHD-1 inhibitors with good physicochemical and pharmacok

208 ated degradation of HIF-1alpha by preventing PHDs from interacting with HIF-1alpha.

209 rolyl-hydroxylase domain containing protein (PHD)2 and thereby inhibits PHD2-dependent hydroxylation

210 aled that prolyl hydroxylase domain protein (PHD) levels significantly increased during rosiglitazone

211 ss is the prolyl hydroxylase domain protein (PHD):hypoxia inducible factor (HIF) pathway.

212 utative human homologs of Bye1, the proteins PHD finger protein 3 and death-inducer obliterator, whic

213 known as prolyl hydroxylase domain proteins (PHDs) has neuroprotective effects in various in vitro an

214 ncies in prolyl hydroxylase domain proteins (PHDs) may lead to the accumulation of hypoxia-inducible

215 or (HIF) prolyl hydroxylase domain proteins (PHDs) serve as oxygen sensors and may therefore regulate

216 , promoter-focused and dependent on the RAG2 PHD, and the second is defined by H3K27Ac, enhancer-focu

217 Iron supplementation directly restores PHD catalytic activity following V-ATPase inhibition, re

218 is the prototypical member of the RPC (RING, PHD, CBD) family of ubiquitin-ligases, characterized by

219 ssive epigenetic mechanism in which ZMYND8's PHD-Bromo cassette couples H3K4me1-H3K14ac with downregu

220 ough mutations in either the first or second PHD finger allow for Rpd3S complex formation, the assemb

221 We show that the second PHD finger of CHD4 initiates recruitment to the nucleoso

222 A selective PHD inhibitor suppressed lipolysis in murine and human a

223 d and will be of use in developing selective PHD inhibitors.

224 Indeed, combined application of selective PHD and FIH inhibitors resulted in the transcriptional i

225 ional response to hypoxia than the selective PHD inhibitors, consistent with an important role for FI

226 ectroscopic approaches to show that the Set3 PHD finger binds di- and trimethylated states of H3K4 wi

227 investigate whether a keratinocyte-specific PHD deficiency may promote vascular survival and growth

228 show that coordinated activation of specific PHD isoforms fine-tunes the osteoblastic response to hyp

229 oes not depend on the more carboxyl-terminal PHD-2.

230 hieved by the binding of the PCL1 N-terminal PHD domain to the C-terminal domain of p53 through two u

231 0 fusion protein, which lacks the N-terminal PHD fingers of AF10.

232 The findings demonstrate that PHD enzymes modulate ventilatory sensitivity to hypoxia

233 Here we show that PHD finger protein 20-like 1 (PHF20L1) regulates DNMT1 t

234 king or deletion mutagenesis and showed that PHD movements function as a conformational switch to reg

235 heir reduced ubiquitination, suggesting that PHDs evoke the ubiquitination/proteasomal degradation of

236 The PHD finger functions as an epigenetic reader that binds

237 chromodomain-containing Eaf3 subunit and the PHD domain-containing Rco1 subunit to recognize nucleoso

238 concentration of O2 present, mediated by the PHD enzymes, forms the basis for one of the most signifi

239 erminants of methyllysine recognition by the PHD fingers of Set3 and its orthologs.

240 Furthermore, the PHD inhibitor also improved the rate of survival of MALA

241 Hence, the PHD finger appears to negatively regulate self-acetylati

242 ted screen for PI interactors identified the PHD finger of TAF3, a TATA box binding protein-associate

243 one-binding activity is not conserved in the PHD finger of Set4 suggests different functions for the

244 pathway for controlling red cell mass is the PHD (prolyl hydroxylase domain protein):hypoxia-inducibl

245 ous studies have reported specificity of the PHD domain for the unmodified N terminus of histone H3 a

246 demonstrate that deletion or mutation of the PHD domain reduces the catalytic efficiency (kcat/Km of

247 nalysis to scrutinize which parameter of the PHD feedback could control HIF timing and we probed for

248 stone H3, reduce the binding affinity of the PHD finger toward the histone substrate.

249 Deletion of the PHD finger, but not the bromodomain, impaired the abilit

250 n of the aromatic H3K4me-binding site of the PHD fingers appears to have no effect.

251 on differences in binding affinities of the PHD fingers for H3K4me and the methylation state of the

252 l role in determining the selectivity of the PHD fingers.

253 zinc finger protein 12), is a member of the PHD zinc finger family of proteins.

254 lt shows that the binding specificity of the PHD-finger domain of VIN3 plays a role in mediating a pr

255 alteration in the binding specificity of the PHD-finger domain of VIN3 results in a hypervernalizatio

256 re poorly characterized, and the role of the PHD/HIF-2 axis in renal EPO-producing cell (REPC) plasti

257 blished concurrent with the emergence of the PHD:HIF pathway in evolution.

258 ify a link between two ancient pathways, the PHD:HIF and the HSP90 pathways, and suggest that this li

259 A pair of readers, the PHD fingers of the protein CHD4, has been shown to bival

260 Here we targeted the PHD/HIF-2/EPO axis in FOXD1 stroma-derived renal interst

261 Our results indicate that the PHD acts as a catalyst in dynamin-induced membrane fissi

262 Furthermore, our data suggest that the PHD finger has a role in the recruitment of p300 to chro

263 We found that the PHD inhibitors significantly increased the expression le

264 one-binding affinity by interacting with the PHD domain.

265 show that CaM forms a tight complex with the PHD of Akt (dissociation constant = 100 nm).

266 Like the PHDs, FIH is proposed to have a hypoxia-sensing role in

267 target genes, simultaneous inhibition of the PHDs and FIH catalysis may be preferable.

268 This Perspective reviews the PHDs and small molecule drug discovery efforts.

269 s active at lower O2 concentrations than the PHDs and suggest that competition between HIF-alpha and

270 Therefore, PHDs sense not only oxygen but also respond to amino aci

271 These PHD proteins maintain an inactive chromatin conformation

272 In vivo stabilization of HIF-1a with these PHD inhibitors increased the proportion of phenotypic HS

273 This PHD conformational switch is impaired by a centronuclear

274 Three PHD isoforms (PHD1, 2, and 3) were found to be up-regula

275 GhCHR contains two DC1 and three PHD Cys/His-rich domains, suggesting that GhCHR encodes

276 lytic jumonji C domain, KDM5A contains three PHD reader domains, commonly recognized as chromatin rec

277 Thus, PHD represents a new therapeutic target for MALA, which

278 starvation leads to alphaKG depletion and to PHD inactivation but not to HIF stabilization.

279 ession of which was increased in response to PHD inhibitors.

280 of a subset of genes not fully responsive to PHD inhibition alone.

281 We found that the apo TTD-PHD module in solution comprises a dynamic ensemble of c

282 reveals a mechanism by which the dynamic TTD-PHD module can be allosterically targeted with small mol

283 e tandem tudor domain-plant homeodomain (TTD-PHD) histone reader module, including its 20-residue int

284 s with linker binding, and promotes open TTD-PHD conformations that are less efficient at H3K9me3 bin

285 could be modulated therapeutically by tuning PHD enzymatic activity.

286 e found that deleting any combination of two PHD isoforms induces polycythemia without steatosis comp

287 a unique chromatin regulator possessing two PHD fingers, one bromodomain and a PWWP domain for recog

288 Thus, Aire's two PHDs seem to play distinct roles in the scenario by whic

289 ar analyses reveal how wild-type and variant PHDs achieve ODD selectivity via different dynamic inter

290 ated in C3H10T1/2 cells during RIAD, whereas PHD knockdown and treatment with PHD inhibitors (dimethy

291 The median time at which PHD developed was 41 mo after the first PRRT cycle.

292 Ubiquitin-like with PHD and RING finger domains 1 (UHRF1) is an essential re

293 used by mutations in the ubiquitin-like with PHD and ring finger domains 1 (uhrf1) or DNA methyltrans

294 e, we report that UHRF1 (ubiquitin-like with PHD and RING finger domains 1) interacts with TIP60 both

295 d by an E3 ligase UHRF1 (ubiquitin-like with PHD and RING finger domains 1), which is commonly upregu

296 We identified the ubiquitin-like with PHD and ring finger domains 2 (UHRF2) gene as an importa

297 ubiquitin ligase UHRF1 (Ubiquitin-like, with PHD and RING finger domains 1) directly participates in

298 Seven patients with PHD developed anemia in combination with a rise in mean

299 AD, whereas PHD knockdown and treatment with PHD inhibitors (dimethyloxalyl glycine or ethyl-3,4-dihy

300 ncing experiments demonstrated that the Yng2 PHD specifically directs H4 acetylation near the transcr