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 homologues exist in other types of eukaryotes and pr

4 PHD inhibitors with different structural scaffolds behav

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

6 PHD was defined as diagnosis of myelodysplastic syndrome

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

8 erstand the path of allostery from the RAG-2 PHD finger to RAG-1, here we employed phylogenetic subst

9 o RAG-1 are separable functions of the RAG-2 PHD finger.

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

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

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

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

14 f VERNALIZATION INSENSITIVE 3 (VIN3)(5-7), a PHD protein that functions with Polycomb repressive comp

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

16 During cold, a PHD-PRC2 complex metastably and digitally nucleates H3K2

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

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

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

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

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

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

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

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

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

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

33 Both B3 and PHD-like domains are required for enrichment of HSI2 and

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

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

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

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

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

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

40 Combined knockdown of FIH and PHD-selective inhibition did not further increase perice

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

42 nker region connecting the different TTD and PHD histone modification-binding domains causes distinct

43 Multiple isoforms of HIFs and PHDs exist, and isoform-selective roles have been identi

44 e clinic, understanding the role of HIFs and PHDs in inflammation outcomes is an essential step in av

45 ll and context-specific activity of HIFs and PHDs.

46 lighting the multifunctional nature of ATXR5 PHD domain.

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

48 The BAH-PHD bivalent histone reader complex silences a substanti

49 We found that the BAH-PHD module associates with CPL2, a plant-specific Pol II

50 al domain (CTD) phosphatase, to form the BAH-PHD-CPL2 complex (BPC) for transcriptional repression.

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

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

53 subunit that contains the chromatin binding PHD finger domains attenuates enhancer functions, but un

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

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

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

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

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

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

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

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

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

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

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

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

66 to pollen-induced symptom loads reported by PHD users during birch and grass pollen season.

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

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

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

70 We here report a PRC2-associated cofactor, PHD finger protein 19 (PHF19; also known as polycomb-lik

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

72 rom PHF23, KDM5A and BPTF, suggests a common PHD finger-dependent mechanism that promotes leukemogene

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

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

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

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

77 Furthermore, CXXC-PHD recruits 94 nuclear factors involved in replication,

78 fy the mechanism of KDM2A played by its CXXC-PHD domain.

79 We propose that CXXC-PHD promotes permissiveness for nuclear factors to inter

80 ci, as substantiated by the result that CXXC-PHD recruits POLR1A to the rDNA promoter.

81 ether with the XRCC5/6 complex, and the CXXC-PHD domain regulates the CpG-rich IGFBPL1 promoter.

82 In vitro, CXXC-PHD enhances binding of nuclear extract ORC3 to the CpG-

83 results in the Premier Healthcare Database (PHD).

84 e during presynaptic homeostatic depression (PHD), implying that the reported reduction in Ca(2+) inf

85 th the aid of the patient's hay-fever diary (PHD).

86 sing capacity of the PHDs and that different PHD HIF-alpha substrate combinations might have differen

87 nsight into the factors underlying different PHD substrates and properties, we carried out biochemica

88 s deploy three closely related dioxygenases (PHD 1, 2 and 3) to signal oxygen levels by catalysing ox

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

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

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

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

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

94 on of HIF-alpha prolyl-4-hydroxylase domain (PHD) enzymes and HIF-alpha asparagine hydroxylase factor

95 he oxygen-sensing prolyl hydroxylase domain (PHD) enzymes are key to maintaining tissue homeostasis d

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

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

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

99 promoters of the proline hydroxylase domain (PHD) proteins to increase expression.

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

101 Prolyl hydroxylase domain (PHD)-2 protein, a major PHD in ECs, plays a critical rol

102 The prolyl hydroxylase domain (PHD)-hypoxia inducible factor (HIF) pathway is a key mam

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

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

105 e reported reduction in Ca(2+) influx during PHD is achieved through functional adaptions to pre-exis

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

107 urgical discharge estimates using the entire PHD and weights based on hospital characteristics.

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

109 The HIF prolyl hydroxylase domain enzymes (PHDs) are Fe(II)- and 2-oxoglutarate-dependent oxygenase

110 ases, the prolyl hydroxylase domain enzymes (PHDs).

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

112 We cannot exclude PHD-catalysed prolyl hydroxylation occurring under condi

113 Here we show that an extended PHD domain (ePHD(6)) involving the sixth PHD domain and

114 regulates the HIF (hypoxia-inducible factor)/PHD-2 (prolyl hydroxylase 2)-constituted oxygen machiner

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

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

117 ability of an injectable hydrogel-formulated PHD inhibitor, 1,4-dihydrophenonthrolin-4-one-3-carboxyl

118 f these affect the formation of a functional PHD domain.

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

120 ia or conditions of pharmacologic or genetic PHD inactivation.

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

122 ide no support for the wide range of non-HIF PHD substrates that have been reported.

123 ic conditions by HIF-prolyl hydroxylase (HIF-PHD).

124 Inhibition of HIF-PHD by roxadustat leads to increased EPO production, bet

125 Genetic interventions on HIF/PHD pathways reveal multiple phenotypes that extend the

126 dly targeting the main components of the HIF/PHD pathway, permitting timed bi-directional interventio

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

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

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

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

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

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

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

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

135 The roles of Plant Homeodomain (PHD) fingers in catalysis of histone modifications are u

136 Binding of H3K4me3 by a plant homeodomain (PHD) in RAG-2 induces conformational changes in RAG-1, a

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

138 tion is recognized by the plant homeodomain (PHD) present at the C-terminus of the five ING proteins.

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

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

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

142 o-adjacent homology (BAH)-plant homeodomain (PHD)-containing protein, EPR-1 (effector of polycomb rep

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

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

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

146 HD2 is the most important of the three human PHDs.

147 a protein by activating proline hydroxylase (PHD) and the ubiquitin proteasome system (UPS) in primar

148 mily, including the HIF proline hydroxylase (PHD, alias EGLN), and an E3 ubiquitin ligase component f

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

150 ar hypoxia are sensed by prolyl hydroxylase (PHD) enzymes which regulate HIFs.

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

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

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

154 IF-1alpha degradation by prolyl hydroxylase (PHD) under normoxic conditions is emerging as a promisin

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

156 The discovery of the HIF prolyl-hydroxylase (PHD) enzymes as oxygen sensors raises a key question as

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

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

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

160 -inducible factor (HIF) prolyl hydroxylases (PHD) inhibitors on PC12 cells and primary rat neurons fo

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

162 hypoxia is mediated by prolyl hydroxylases (PHDs) that regulate the levels of hypoxia-inducible tran

163 ccinate, which inhibits prolyl hydroxylases (PHDs).

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

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

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

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

168 bind H3K4me3 in the same way as the isolated PHD.

169 nal region of the protein, distinct from its PHD and helicase domains.

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

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

172 how that the ubiquitin ligase ubiquitin-like PHD and RING finger domain-containing protein 1 (UHRF1)

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

174 hydroxylase domain (PHD)-2 protein, a major PHD in ECs, plays a critical role in intracellular oxyge

175 In ClkDelta19/Delta19 mice, PHD levels were low, and HIF1alpha protein levels were i

176 with the corresponding residues in the mouse PHD and testing for rescue of allostery, we demonstrate

177 a chimeric RAG-2 protein in which the mouse PHD finger is replaced by the corresponding domain from

178 t correlation between the abilities of NUP98-PHD finger fusion chimeras to associate with H3K4me3-enr

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

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

181 The new class of PHD inhibitors (FG4592, FG2216, GSK1278863, Bay85-3934)

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

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

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

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

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

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

188 tance of understanding the complex nature of PHD regulation.

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

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

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

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

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

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

195 2 (PHD2) transgene, a predominant isoform of PHDs in renal tubules, to reduce HIF-1alpha level signif

196 d out biochemical and biophysical studies on PHD homologues from the cellular slime mold, Dictyosteli

197 Depletion of other PHD family members had no effect on HIF-2alpha expressio

198 increase in pericellular pO(2) by pan- over PHD-selective HIs likely reflects HIF hydroxylase indepe

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

200 pecific deleterious effects of pharmacologic PHD inhibition.

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

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

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

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

205 omplex and identified an PhD-finger protein (PHD 1, PF3D7_1008100) that could mediate a cross-talk be

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

207 iated by prolyl hydroxylase domain proteins (PHDs), which use O(2) as a substrate to hydroxylate spec

208 By substituting residues in the C. punctatum PHD with the corresponding residues in the mouse PHD and

209 Purified PHD finger or full-length UBR7 monoubiquitinated H2BK120

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

211 aracterise their reactivity with recombinant PHD enzymes.

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

213 und that the B55alpha/PP2A complex restrains PHD-2 activity, promoting EC survival in a HIF-dependent

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

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

216 SPs possess functional domains (SAND, PHD, bromodomain) that dock to DNA or post-translational

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

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

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

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

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

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

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

224 that mono-methylates histone H3K4 and seven PHD fingers of unclear function.

225 ded PHD domain (ePHD(6)) involving the sixth PHD domain and its preceding zinc finger in MLL3 and MLL

226 Here we report a cortex-specific PHD finger protein, Phf21b, which is highly expressed in

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

228 ls, forced expression of the testis-specific PHD finger protein 7 (PHF7) disrupts oogenesis, leading

229 pan-HIF-alpha hydroxylase (broad spectrum), PHD-selective, and FIH-selective inhibitors, and investi

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

231 e combined results support the proposal that PHD homologues have evolved kinetic and structural featu

232 logical processes and diseases revealed that PHD finger protein 8 (PHF8, KDM7B) was significantly ass

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

234 The PHD finger functions as an epigenetic reader that binds

235 The PHD inhibitors at 100 uM significantly increased the LC3

236 lpha was stabilised in PC12 cells by all the PHD inhibitors at 100 uM except for DMOG, which stabilis

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

238 ed that the BAH domain protein AIPP3 and the PHD proteins AIPP2 and PAIPP2 cooperate to read H3K27me3

239 tified the co-chaperone SGT1b (EDM1) and the PHD-finger protein EDM2 as critical regulators of RPP7.

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

241 In conclusion, the PHD inhibitors stabilise HIF-1alpha in normoxia, induce

242 Our data support a critical role for the PHD fingers of NUP98-PHF23, and related NUP98-KDM5A and

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

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

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

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

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

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

249 analysis of the H3K4me3-binding sites of the PHD fingers from PHF23, KDM5A and BPTF, suggests a commo

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

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

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

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

254 The discovery of the PHD-HIF-pVHL system revolutionized our fundamental under

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

256 long-term silencing (perpetuated) phase, the PHD proteins are lost from the nucleation region and sil

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

258 Recently, the PHD domains of MLL3/4 have been reported to recruit the

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

260 cluding disulfiram that directly targets the PHD finger of PHF23 (PHF23PHD).

261 nger increase in pericellular pO(2) than the PHD/FIH-selective HIs.

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

263 We demonstrated that the PHD finger of Ubiquitin Protein Ligase E3 Component N-Re

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

265 At 100 uM, the PHD inhibitors did not cause cytotoxicity and apoptosis.

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

267 Pretreatment with the PHD inhibitors 24 hours followed by 24 hour reoxygenatio

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

269 Additionally, BdFTL2 could bind with the PHD-containing protein BdES43, an H3K4me3 reader.

270 mobile loops that enclose substrates in the PHDs are conserved, but the C-terminal helix of the PHDs

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

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

273 ntral to the hypoxia-sensing capacity of the PHDs and that different PHD HIF-alpha substrate combinat

274 red to, and binds at, the active site of the PHDs is important for the development of a chemical unde

275 e conserved, but the C-terminal helix of the PHDs is strikingly absent.

276 The unusual kinetic properties of the PHDs, in particular a high K(m) for dioxygen and slow re

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

278 This PHD conformational switch is impaired by a centronuclear

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

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

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

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

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

284 main, resulting in creation of a coupled TTD-PHD module.

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

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

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

288 could be modulated therapeutically by tuning PHD enzymatic activity.

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

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

291 the full-length protein reveals that the two PHD fingers of the dimer are chemically equivalent and i

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

293 eates H3K27me3 within FLC On return to warm, PHD-PRC2 spreads across the locus delivering H3K27me3 to

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

295 A domain is required for ubiquitin-like with PHD and RING finger domains 1 (UHRF1) E3 ubiquitin ligas

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

297 their molecular adaptor ubiquitin-like with PHD and RING finger domains-1 (UHRF1), was measured in h

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

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

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