ライフサイエンスコーパス: iron-binding

1 N(5)-hydroxylated l-ornithines essential for iron binding.

2 he interior of the active site, and the heme iron binding.

3 family of proteins and is likely involved in iron binding.

4 oxyornithine residues, which are involved in iron binding.

5 r understand the role of the third C site in iron binding.

6 ed conformation of Fe-Af that is enforced by iron binding.

7 ow for distinguishing between two models for iron binding.

8 he MBD binds to iron and that azide disrupts iron binding.

9 that this function of FHC was independent of iron binding.

10 Iron binding ability of MPC enhanced significantly (P<0.

11 ct of AA and EDTA on the catechol or galloyl iron binding ability of pure phenolics, coffee and tea.

12 is reversible but in combination with their iron binding ability to disrupt the active site competit

13 odel of AILI, which was not dependent on its iron-binding ability, inhibition of acetaminophen (APAP)

14 cherichia coli, IscA has a unique and strong iron binding activity and can provide iron for iron-sulp

15 d with the thioredoxin reductase system, the iron binding activity of IscA is fully restored.

16 s of iron-sulfur clusters, we reevaluate the iron binding activity of IscA under physiologically rele

17 in IscA with serine completely abolishes the iron binding activity of the protein.

18 peroxide, however, IscA completely loses its iron binding activity, whereas CyaY becomes a competent

19 rminal domains of CaM and about the relative iron binding affinities of the N- and C-terminal domains

20 The ferrous iron binding affinity ( K d approximately 6.0 microM) an

21 bpA(Y196I), resulted in a greatly diminished iron binding affinity Kd=5.2 x 10(-4) M(-1), approximate

22 The iron binding affinity of amychelin was determined using

23 Substitution mutations in the putative iron-binding amino acid residues E20A and E107A within t

24 cally demethylated H3K4me1/2/3 via conserved iron-binding amino acids in vitro and in vivo.

25 magnetic resonance spectroscopy and chemical iron-binding analyses to demonstrate that catecholamine

26 e active site glutamate is required for both iron binding and activity.

27 y conserved His-Glu motifs are essential for iron binding and catalysis.

28 s, revealing dynamic structural changes upon iron binding and core formation, as reflected by a quick

29 Here, we investigate the iron binding and oxidation chemistry of Escherichia coli

30 The chemistry of iron binding and oxidation in Listeria Dps (LiDps, forme

31 the iron primary coordination sphere through iron binding and redox potential modulation may have in

32 Iron binding and release kinetics of the AfFtn and AfFtn

33 he N- and C-lobes may influence the rates of iron binding and release.

34 respect to the delineation of the process of iron binding and release.

35 nters in iron-dependent enzymes as transient iron binding and shuttling sites to ensure full metal lo

36 dues involved in coordinating Fe(2+) inhibit iron binding and thymidine hydroxylation.

37 o deprotonate the amide moiety of Cys20 upon iron binding and transfer the resulting proton away, thu

38 2.1- to 6-fold while that of genes used for iron binding and transport increased 2.1- to 7.7-fold in

39 ertebrates, where they serve a major role in iron binding and transport.

40 Although only beta is capable of iron binding and Tyr(*) formation, cells lacking beta' a

41 ate the role of the synergistic anion in the iron-binding and iron-donating properties of human trans

42 toferrin variants exhibited nearly identical iron-binding and iron-releasing activities and equivalen

43 contrast agents or (phosphorus) metabolites, iron-binding and iron-storage proteins to accumulate iro

44 Human serum transferrin (hTF) is a bilobal iron-binding and transport protein that carries iron in

45 The data (O(2) uptake, iron binding, and conventional and stopped-flow kinetics

46 relates with monomeric configuration, labile iron binding, and dynamic contacts with components of th

47 lor and an absorbance spectrum indicative of iron binding, and it bound Fe(III) but not Fe(II).

48 ant correlation between disease severity and iron-binding antioxidant protection (R =.48; p =.00067)

49 Plasma iron-binding antioxidant protection was negatively corre

50 Iron-binding antioxidant protection was not significantl

51 and total protein, total antioxidant status, iron-binding antioxidant protection, iron-oxidizing anti

52 n addition to playing a facilitative role in iron binding, appears to have a "gatekeeper" role, there

53 Both rRNA and mRNA showed twice the iron binding as tRNA.

54 Iron binding assays using isothermal titration calorimet

55 In vitro iron binding assays, including both (59)Fe overlay assay

56 ic and ferrous iron, both involving specific iron binding at the cell surface.

57 at the E185 residue not only plays a role in iron binding, but also provides the dominant ET pathway

58 and its loss weakens carbonate and therefore iron binding, but maintains the ability of nitrilotriace

59 present in the dissolved form as a result of iron binding by the organic exudate.

60 tructure by circular dichroism spectroscopy, iron-binding by atomic absorption spectrophotometry, oli

61 Finally, we found that the iron binding capability of lactoferrin intervened in DA

62 p) of Ehrlichia canis was identified and its iron-binding capability was investigated.

63 itin, transferrin saturation (SAT) and total iron binding capacity (TIBC) in 2347 AAs participating i

64 ith available serum iron, ferritin and total iron binding capacity (TIBC) values were ultimately incl

65 -wide association study of serum iron, total iron binding capacity (TIBC), transferrin saturation, an

66 Interestingly, the difference of iron binding capacity disappeared after denaturation of

67 in secondary structure, DNA binding ability, iron binding capacity, and the ability to form higher-or

68 Reflecting the difference of iron binding capacity, oxidation of rRNA by the Fenton r

69 stance index and increased serum iron, total iron binding capacity, transferrin saturation, and serum

70 g, serum ferritin level >15 ng/mL, and total iron-binding capacity <425 mug/dL at the 12-week visit),

71 nsferrin level (1.77 +/- 0.08 g/L) and total iron-binding capacity (46.2 +/- 2.0 microM) were signifi

72 arameters (serum iron, serum ferritin, total iron-binding capacity and transferrin saturation), serum

73 Mean total iron-binding capacity decreased from 501 to 389 mug/dL (

74 pendent transport system, which exploits the iron-binding capacity of citrate and its natural abundan

75 ence time did not affect the carbon specific iron-binding capacity of the humic substances which was

76 ), changes in serum ferritin level and total iron-binding capacity, adverse effects.

77 ng women with higher concentrations of total-iron-binding capacity.

78 hand, hydrogen peroxide has no effect on the iron binding carboxyl groups in CyaY, allowing the prote

79 wed that the inter-planar angles between the iron-binding catecholamide units in the 5-, 6- and 8-LIC

80 ich the length of the linker between the two iron-binding catecholamide units was increased from four

81 re, we are able to characterize two distinct iron binding channels that facilitate iron ion transport

82 ticle aims to establish the judicious use of iron-binding chemistry of microbial chelators in order t

83 2,5-DHBA), which is similar to 2,3-DHBA, the iron-binding component of enterobactin.

84 tic iron chelators (e.g., EDTA), and natural iron binding compounds (e.g., desferrioxamine B, ferrich

85 ministration of CO, biliverdin, bilirubin or iron-binding compounds is protective in rodent disease m

86 Siderophores are extracellular iron-binding compounds that mediate iron transport into

87 Under iron-binding conditions, the recombinant Fbp exhibited a

88 for membranes and the changes observed upon iron binding could provide unique biological advantages

89 A range of iron binding dendrimers terminated with hexadentate liga

90 ion between M6A, an intrinsically disordered iron-binding domain, and an iron oxide particle was visu

91 ed by the presence of Rieske and mononuclear iron-binding domains.

92 At equivalent iron binding doses in the bile duct cannulated rodent, o

93 tect them from degeneration, suggesting that iron-binding drugs may one day prove useful in reducing

94 required for completely overcoming negative iron binding effects of polyphenols and similar samples.

95 or de novo biosynthesis and/or regulation of iron-binding enzymes in the cellular system.

96 hat is between 7- and 70-fold lower than the iron binding equivalence concentrations at which DFP inh

97 after 24 h of incubation at 110 microm IBE (iron-binding equivalents) in comparison to simple dialky

98 y after 30 min incubation at 110 microM IBE (iron-binding equivalents), as compared with deferiprone

99 , desferrioxamine, or deferasirox at similar iron-binding equivalents.

100 tryptophan residue in close proximity to the iron-binding ferroxidase site (W52 in E. coli Dps).

101 s the Mrs3p/Mrs4p mitochondrial carriers and iron-binding frataxin (Yfh1p).

102 acteriostatic activity of transferrin to its iron-binding function: neither iron-saturated transferri

103 y of interlobe interactions modulating these iron-binding functions has been described.

104 coordinate the active site metal, unlike the iron-binding glutamate it replaced.

105 ortem human brain tissue have shown that the iron-binding glycoprotein lactoferrin is upregulated in

106 Human lactoferrin is an iron-binding glycoprotein that is particularly prominent

107 of the lactotransferrin family of non-haem, iron-binding glycoproteins and is found at high concentr

108 rin is a member of the transferrin family of iron-binding glycoproteins present in milk, mucosal secr

109 ich Transpolar Drift (TPD), we found that HS iron binding groups were largely occupied by iron (49%).

110 e nonfluorescent ferribactin, containing two iron binding groups, into a fluorescent pyoverdine, form

111 ments with PSII(-Mn,+Fe) membranes show that iron binding has little effect on the maximum and minimu

112 usual R2 because three residues required for iron binding have been mutated.

113 In the Rnr2 homodimer, one of the iron-binding helices, helix alphaB, is not well-ordered.

114 ygen depletion in a process that required an iron-binding hemerythrin-like domain in its N terminus.

115 The iron binding hETHE1 enzyme is related to the 'classical'

116 FA2H also contains the iron-binding histidine motif conserved among membrane-bo

117 Induction of specific iron binding implies that (1) the structure of mICA rese

118 ctions, thus underlining the significance of iron binding in Dph4.

119 we generated mice with mutations to abrogate iron binding in either lobe (TfN-bl or TfC-bl).

120 cysteine residues that are essential for the iron binding in IscA abolishes the copper binding activi

121 The iron binding in IscA appears to prevent the formation of

122 edoxin reductase system, suggesting that the iron binding in IscA is specific.

123 ctase system are essential for mediating the iron binding in IscA, only catalytic amounts of thioredo

124 nds abolishes anion binding and consequently iron binding in the affected lobe.

125 expression results in increased capacity for iron binding in the chloroplast of iron-limited cells, w

126 ding thiol groups in IscA, thus blocking the iron binding in the protein.

127 histidine and aspartate residues involved in iron-binding in ETHE1, occupy similar positions to those

128 This demonstrates the role of iron-binding in the activity observed.

129 ent to maintain anion binding, and therefore iron binding, in the mutated lobe.

130 helical plane in a manner that includes its iron-binding interface.

131 does not affect aggregation, suggesting that iron binding is a non-conserved part of a more complex c

132 Identical iron binding kinetics for AfFtn and AfFtn-AA suggest tha

133 Because Gly65 is hydrogen-bonded to the iron-binding ligand Asp63, it comprises part of the seco

134 ic ligands composing a large fraction of the iron-binding ligand pool throughout the water column.

135 containing longer tether lengths between the iron binding ligands (C5) were more efficacious and led

136 entrations of redox-active compounds, strong iron binding ligands (i.e., log K(FeL) > 6), and compoun

137 s) environments and (ii) hotspots of natural iron binding ligands production up to 50 muM in the whea

138 Here, we reveal how the iron-binding ligands desferrioxamine (DFO), di-2-pyridyl

139 ure electroactive humics, dissolved iron and iron-binding ligands simultaneously from surface to dept

140 presumed "dissolved" iron (and probably also iron-binding ligands) are present in colloidal size rang

141 hETHE1 is a mono-iron binding member of the metallo-beta-lactamase (MBL)

142 glycine spacers, whereas in enterobactin the iron-binding moieties are directly attached to a tri-l-s

143 hore structures have been characterized, the iron-binding moieties often contain catecholate or hydro

144 Pathogens secrete small iron-binding moieties, siderophores, to acquire host iro

145 Here, we show that the iron-binding moiety of the 24p3-associated mammalian sid

146 Transferrin, the major plasma iron-binding molecule, interacts with cell-surface recep

147 gricultural inoculant, the structures of its iron-binding molecules remain unknown.

148 Siderophores are small iron-binding molecules secreted by bacteria to scavenge

149 Siderophores are small iron-binding molecules that are synthesized and secreted

150 y to capture and deplete siderophores, small iron-binding molecules that are synthesized by certain b

151 nate the processing and use of iron by these iron-binding molecules.

152 hese organisms use mycobactin, high-affinity iron-binding molecules.

153 boxylate model and may define an alternative iron binding motif, which we propose as His-3.

154 Conversion of the atypical iron-binding motif into a canonical one through genetic

155 KdoO contains the putative iron-binding motif, HXDX(n>40)H.

156 of another proposed antioxidant protein, an iron-binding, neutrophil-activating protein (NapA).

157 interaction with Isu while altering neither iron binding nor oligomerization.

158 rder structure may contribute to the greater iron binding of rRNA.

159 ones and inotropes could directly affect the iron binding of serum-transferrin so that the normally h

160 nism(s) by which the stress hormones perturb iron binding of these key innate immune defense proteins

161 iron to DOHH stoichiometry and dependence of iron binding on each of the four conserved His-Glu motif

162 l transferrins is the absolute dependence of iron binding on the concomitant binding of a synergistic

163 The soluble iron and iron-binding organic ligands are depleted at the surface

164 t concentrations of soluble iron and soluble iron-binding organic ligands are much lower than previou

165 strate Hs holofrataxin to be a high affinity iron binding partner for Hs ferrochelatase that is capab

166 t of interactions between Yfh1 and its major iron-binding partners, Isu1/Nfs1 or aconitase.

167 The effect of removing phytate (IP6), iron-binding polyphenols, and dietary fibers on iron bio

168 bove-mentioned tyrosine at the corresponding iron-binding position, with that of Schizosaccharomyces

169 The use of the synergistic anion and this iron binding process results in an extremely high affini

170 have characterized the overall stability and iron binding properties of the Drosophila frataxin homol

171 f the citric acid stereocenter perturbed the iron-binding properties and siderophore function of SB a

172 tes (one in each lobe), they differ in their iron-binding properties and their responsiveness to comp

173 wed that the ATCC 19606(T) NfuA ortholog has iron-binding properties compatible with the formation of

174 Whether the iron-binding properties of ferritin contributed to the p

175 Selective (lobe-specific) modulation of the iron-binding properties of hTF using recombinant forms o

176 The iron-binding properties of TTP-2D and the effect of iron

177 e fold but different thermal stabilities and iron-binding properties.

178 Here we have compared the iron binding property of IscA and the frataxin ortholog

179 ortholog of human Dph4 also shows a similar iron-binding property, indicating the conserved nature o

180 osynthesis- and metabolism-associated genes (iron binding protein and rhizopine catabolism).

181 tion via either transgenic expression of the iron binding protein ferritin or oral administration of

182 Aconitase was found to associate with the iron binding protein frataxin exclusively during reperfu

183 solved in complex with human transferrin, an iron binding protein normally responsible for delivering

184 iron transporter gene (CBU1766), a putative iron binding protein-encoding gene (CBU0970), and a cati

185 he levels of frataxin (FXN), a mitochondrial iron binding protein.

186 ), IgG-binding protein A (Spa), and the heme-iron-binding protein (IsdA) were most abundant in the ag

187 -3-phosphate dehydrogenase (SAG0823), and an iron-binding protein (SAG1007).

188 ut the dual effects of NGAL as a siderophore:iron-binding protein and as a growth factor and examines

189 g activity, whereas CyaY becomes a competent iron-binding protein and attenuates the iron-mediated pr

190 Lactoferrin (LTF) is an iron-binding protein canonically known for its innate an

191 Lactoferrin (LF) is an iron-binding protein found in milk, mucosal secretions,

192 This gene normally encodes the iron-binding protein frataxin (FXN), which is critical f

193 Deficiency in the mitochondrial iron-binding protein frataxin results in diminished acti

194 Lactoferrin (Lf), a major iron-binding protein in human milk, has been suggested t

195 Finally, LF was identified as the major iron-binding protein in parotid saliva by 59Fe autoradio

196 Frataxin is a mitochondrial iron-binding protein involved in iron storage, detoxific

197 Prior reports have suggested that the iron-binding protein lactoferrin (LF) may either kill Ac

198 The iron-binding protein lactoferrin is a ubiquitous and abu

199 The iron-binding protein lactoferrin is present at mucosal s

200 not macrophages, within the CSF express the iron-binding protein lipocalin-2 (LCN2) and its receptor

201 Lactoferrin (Lf), the main iron-binding protein of milk, has biological activities.

202 by reduced activity of frataxin, a conserved iron-binding protein of the mitochondrial matrix, though

203 Lactoferrin is an 80-kDa iron-binding protein present at high concentrations in m

204 xpression of frataxin (FXN), a mitochondrial iron-binding protein required for Fe-S cluster assembly.

205 r, recent evidence indicated that IscA is an iron-binding protein that can provide iron for the iron-

206 er, recent studies indicated that IscA is an iron-binding protein that can provide iron for the iron-

207 reover, increased apical release of the host iron-binding protein transferrin during RSV infection pr

208 The related iron-binding protein transferrin lacked this capacity.

209 obtain this essential element from the host iron-binding protein transferrin.

210 l gelatinase-associated lipocalin (NGAL), an iron-binding protein up-regulated in response to kidney

211 which leads to the induction of ferritin, an iron-binding protein).

212 this recessive disorder, is a mitochondrial iron-binding protein, but how its deficiency leads to ne

213 ike proteins are oxygen-carrying non-heme di-iron binding proteins and their functions have effect on

214 However, host high-affinity iron binding proteins limit levels of free iron in fluid

215 ailable, being present only in high-affinity iron binding proteins such as transferrin.

216 In the present study, we tested whether iron binding proteins; apotransferrin, lactoferrin and o

217 To identify the iron-binding proteins acting either as an iron transport

218 , exomycobactins, compete for iron with host iron-binding proteins and, together with the iron-regula

219 anism against invading pathogens mediated by iron-binding proteins called transferrins.

220 f frataxins, a family of small mitochondrial iron-binding proteins found in organisms ranging from ba

221 tic transferrins comprise a class of bilobal iron-binding proteins in which each lobe carries a singl

222 This is achieved through a variety of iron-binding proteins including transferrin and ferritin

223 boratory cultures that ferritin and the main iron-binding proteins involved in photosynthesis and nit

224 ia also express outer membrane receptors for iron-binding proteins of the host and extract iron direc

225 Transferrins are a family of bilobal iron-binding proteins that play the crucial role of bind

226 olamines binding to the high-affinity ferric-iron-binding proteins transferrin (Tf) and lactoferrin,

227 were found, as well as other mRNAs encoding iron-binding proteins, bringing the total number of regu

228 wn siderophores but can employ host-derived, iron-binding proteins, including transferrin and lactofe

229 ke other members of the transferrin class of iron-binding proteins, is a bilobal structure, the produ

230 iron load is, perhaps, by the expression of iron-binding proteins, specifically the iron storage pro

231 sion of receptors that are specific for host iron-binding proteins, such as transferrin and lactoferr

232 ria gonorrhoeae is capable of utilizing host iron-binding proteins, such as transferrin, lactoferrin,

233 ity receptors for iron acquisition from host iron-binding proteins.

234 imiting conditions, presumably for essential iron-binding proteins.

235 sparing resulting from reduced synthesis of iron-binding proteins.

236 r findings have for the role of frataxins as iron-binding proteins.

237 cles (OMVs) by directly interacting with the iron-binding Pseudomonas quinolone signal (PQS), a cell-

238 native iron sequestration behavior; however, iron binding rates are altered, enabling assignment of s

239 , whereas mutations of the non-conserved/non-iron binding residues resulted in 20-30% reduction of SH

240 double stranded beta-helix fold and ferrous iron binding residues that are present in 2-oxoglutarate

241 site anion appears to arrange the C-terminal iron-binding residues conducive to complementary binding

242 Rnr4 is unique in that it lacks three iron-binding residues conserved in all other R2s.

243 We identified candidate iron-binding residues in the MCO1 sequence and found tha

244 Mutations of the putative iron-binding residues within the EXXH motifs of TAO abol

245 Putative iron-binding residues within the MavN protein were ident

246 om other organisms, Y4 lacks three conserved iron-binding residues, and its exact function is unclear

247 e of the beta-sheet, adjacent to the acidic, iron binding ridge, is important for interaction of Yfh1

248 Lactoferrin (LF) is an iron-binding salivary protein that has been shown to kil

249 The iron binding siderophore pyoverdine constitutes a major

250 The iron-binding siderophore pyoverdin is a key virulence me

251 ear whether ferric iron uptake or the ferric iron binding siderophores enterobactin and salmochelin a

252 o known as siderocalin, forms a complex with iron-binding siderophores (Ngal:siderophore:Fe).

253 ear whether frataxin is directly involved in iron binding, since the yeast orthologue, but not the hu

254 that in fact the Zn2 site is the regulatory iron binding site and the Zn1 site plays an auxiliary ro

255 human transferrin, a bilobal protein with an iron binding site in each lobe, we have selectively muta

256 ult of self-assembly of 24 subunits, to a di-iron binding site, the ferroxidase center, buried in the

257 The structures reveal a novel trinuclear iron binding site, which is implicated in catalysis and

258 ion of amino acids in close proximity to the iron binding site.

259 ins are highly conserved, EcFtnA has a third iron-binding site (C site) in close proximity to the din

260 MJD1A in intact cells, and disruption of the iron-binding site decreases binding of nickel ions to AB

261 ive activation only occurred when a putative iron-binding site in FirS and the key phosphorylation as

262 he presence of Fe(II), indicating a possible iron-binding site on frataxin.

263 homologous N- and C-lobes contains a single iron-binding site situated in a deep cleft.

264 The domain forms an iron-binding site with three cysteine residues located i

265 bal protein, with each lobe bearing a single iron-binding site, functions to transport iron into cell

266 nto the interdomain cleft region housing the iron-binding site.

267 iron release is likely the histidine in the iron-binding site.

268 generate a reactive oxidizing species at the iron-binding site.

269 considered to provide the greatest number of iron binding sites among cytoplasmic RNA species.

270 The iron binding sites in Fet3p and hCp appear to be very si

271 reement with previously reported results for iron binding sites in mammalian ferritin.

272 It is found that these iron binding sites play a major role in tuning the reduc

273 Three distinct iron binding sites were identified as determined from an

274 Each monomer contains two iron binding sites.

275 ity and identical ligand structures of their iron-binding sites (one in each lobe), they differ in th

276 These experiments showed that the six iron-binding sites do not tolerate change, even conserva

277 Iron-binding speciation plots are consistent with ELT do

278 d) locus encompasses isdC, specifying a heme-iron binding surface protein.

279 Consistent with the pH dependence of iron binding, the main trigger for iron release is likel

280 Because the mutant proteins are impaired in iron binding, these residues are concluded to coordinate

281 Hydrogen peroxide appears to oxidize the iron binding thiol groups in IscA, thus blocking the iro

282 As shown by others, Cp markedly increased iron binding to apotransferrin at acidic pH; however, th

283 r regulation and were all shown to influence iron binding to different extents.

284 Iron binding to frataxin has been quantitated by iron-de

285 Because iron binding to Fur has never been confirmed in vivo, th

286 Furthermore, we could show that iron binding to HMP-P synthase is essential for the reac

287 The regulation by metabolic iron binding to IRE-RNA to decrease inhibitor protein (I

288 minant negative Isu1p predicted to stabilize iron binding to Isu1p.

289 defect in heterocomplex stability supported iron binding to Nbp35 but impaired iron release.

290 A unique feature of the mechanism of iron binding to the transferrin (TF) family is the syner

291 Fur is an iron-binding transcriptional repressor that recognizes a

292 The major yolk protein of sea urchins is an iron-binding, transferrin-like molecule that is made in

293 R, making it available for the next cycle of iron binding, transport and delivery to tissues.

294 r iron revealed an uncommon mode of non-heme iron binding trapped by the non-catalytic Co(2+), which,

295 Iron binding was determined in parotid saliva by additio

296 s including acetylation, myristoylation, and iron binding were identified using only less than 800 ce

297 c binding parameters for protein partner and iron binding were measured for the yeast orthologs using

298 In this work, we explore proton and iron binding with microcystin-LR (MC-LR).

299 epcidin binding to ferroportin is coupled to iron binding, with an 80-fold increase in hepcidin affin

300 didacidal ability of Hst 5 was observed upon iron binding, with increasing iron concentrations being