ライフサイエンスコーパス: heme

1 eptor to transiently engage Hb to remove its heme.

2 ethods for the quantitative determination of heme.

3 hat an EAG channel, hERG3 (Kv11.3), binds to heme.

4 TP synthesis to thermogenesis in response to heme.

5 including the acquisition and utilization of heme.

6 nd show that the transporter is specific for heme.

7 these cysteines are available to bind Fe(3+)-heme.

8 he toxic effects of cell-free hemoglobin and heme.

9 ed by the challenging chemical properties of heme.

10 We propose that O(2) binding to heme a(3) in Tt ba(3) causes CO to dissociate from Cu(B)

11 Here, we investigate how the presence of heme, a highly relevant iron source during infection, af

12 ings reveal a unique strategy of nutritional heme acquisition and provide the first example of an ECF

13 10-heme cytochrome, MtrC, which presents its hemes across a large surface area for electrical contact

14 In human macrophages in vitro, heme activates an AMPK (AMP-activated protein kinase)/AT

15 In this study, we demonstrate that heme activates at least three signaling pathways that co

16 Using heme-affinity pulldown assays and proteomics of lysates

17 sceptible to malaria and develop high plasma heme and acute kidney injury.

18 gand alters the ability of ribosomes to bind heme and disrupts cellular heme bioavailability as measu

19 protein Spbhp-37 was impaired for growth on heme and hemoglobin iron.

20 le, thus preventing these drugs from binding heme and inhibiting its detoxification.

21 e separation of labile and permanently bound heme and its high aggregation potential.

22 Our study highlights the importance of heme and its synthesis in these parasites.

23 re1 double mutant accumulated high levels of heme and mitochondrial iron, regulating the similar path

24 Transition metal complexes containing heme and non-heme ligands have been selected to discuss

25 and subsequent deployment of HsmA to capture heme and reduce redox damage caused by inflammatory medi

26 model in which T. cruzi senses intracellular heme and regulates heme transport activity by adjusting

27 02A1 linker region, connecting the catalytic heme and the diflavin reductase domains, further highlig

28 The reasons for this are the toxicity of the heme and the fact that it acts as a hemolytic and pro-in

29 se a model where GAPDH obtains mitochondrial heme and then forms a complex with apo-sGCbeta to accomp

30 ma2Delta cells synthesized WT levels of ISCs/hemes and had normal aconitase activity.

31 uced endogenously by oxidative catabolism of heme, and the understanding of its spatial and temporal

32 teraction of nitric oxide (NO) with the P450 heme are necessary for NO to trigger ubiquitination and

33 findings reveal an irreversible mechanism of heme-ART adduct inhibition of heme crystallization, uniq

34 The cytochrome P450 proteins contain heme as a cofactor and are involved in oxidoreduction.

35 The results identify heme as a regulator of hERG3 channel activity.

36 ssed in the context of the emerging role for heme as a regulator of ion channel activity in cells.

37 hemoglobin and sequesters the released toxic heme as innocuous hemozoin crystals.

38 ng only Fe-containing protoporphyrins, i.e., heme, as electron mediators, we use here porphyrins with

39 Taken together, these findings show that heme assimilation and metabolism in the anaerobe B. frag

40 genome encodes two heme uptake systems, the heme assimilation system (Has) and the Pseudomonas heme

41 he liberation of high concentrations of host heme at infection sites.

42 rypanosomatids relevant to human health, are heme auxotrophs, meaning they must import it from their

43 overed a reversible pH-induced switch of the heme axial ligation within this simplified scaffold.

44 Heme b concentrations in surface waters ranged from 0.10

45 observed and modelled heme b suggested that heme b could account for between 0.17-9.1% of biogenic i

46 OC as the cut-off between heme b replete and heme b deficient (anemic) phytoplankton.

47 Here we report particulate heme b distributions across the Atlantic Ocean (59.9 deg

48 Heme b is an iron-containing cofactor in hemoproteins th

49 We identified the ratio of 0.10 umol heme b mol(-1) POC as the cut-off between heme b replete

50 n (POC) exhibited a mean value of 0.44 mumol heme b mol(-1) POC.

51 We also demonstrate that the heme B prosthetic group present at the subunit dimer int

52 Our large scale observations of heme b relative to organic matter provide further eviden

53 ol heme b mol(-1) POC as the cut-off between heme b replete and heme b deficient (anemic) phytoplankt

54 Comparison of observed and modelled heme b suggested that heme b could account for between 0

55 The ratio of heme b to particulate organic carbon (POC) exhibited a m

56 The heme-based oxygen sensor protein AfGcHK is a globin-coup

57 nal changes were consistent with transfer of heme between binding sites.

58 om the core to the HRMs and equilibration of heme between the core and HRMs.

59 HO2 has three heme binding sites: one at its catalytic site and the ot

60 d degradation rate of HO2 are independent of heme binding to the HRMs.

61 Upon heme binding to the N-terminal domain, MFSD7C dissociate

62 nositol-exchange activity is resuscitated in heme binding-deficient Sfh5 mutants.

63 dentified the PAS domain as the location for heme binding.

64 igh spin Fe(III) hemoprotein with an unusual heme-binding arrangement that involves a co-axial tyrosi

65 All of these proteins contain the typical heme-binding motif CXXCH and require the Ccm proteins fo

66 uracy of 85.6% for nucleotide- and 91.3% for heme-binding pockets.

67 A mutant in the hemoglobin/heme-binding protein Spbhp-37 was impaired for growth on

68 n-1 (NRAMP-1), transferrin, lactoferrin, and heme-binding proteins.

69 cytochrome reductases also possess atypical heme-binding sites, the NrfA nitrite reductase (CXXCK) a

70 rising two major domains: a cytochrome P450 (heme-binding) catalytic domain and a NADPH-cytochrome P4

71 ribosomes to bind heme and disrupts cellular heme bioavailability as measured by a genetically encode

72 dicate that the apicoplast has a key role in heme biology in T. gondii and is important for both mito

73 ber in hemozoin formation and underscore the heme biomineralization pathway as an attractive target f

74 Heme biosynthesis and iron-sulfur cluster (ISC) biogenes

75 We found SpxA1-activated genes encoding heme biosynthesis enzymes and catalase (kat) were requir

76 f its Fe-S cluster, which results in reduced heme biosynthesis in human cells.

77 sence of several genes necessary for de novo heme biosynthesis is a common characteristic of many ana

78 such as Toxoplasma gondii possess an unusual heme biosynthesis pathway whose enzymes localize to the

79 (mtClpX) activates the initiating enzyme for heme biosynthesis, 5-aminolevulinic acid synthase (ALAS)

80 e (ALAD), which catalyzes the second step of heme biosynthesis, is an Fe-S protein.

81 phyrinogen III synthase for an early step of heme biosynthesis, is conserved among the heme-requiring

82 ential for iron-sulfur cluster formation and heme biosynthesis.

83 or similar genetic deficiencies in porphyrin/heme biosynthesis.

84 tochondria for iron-sulfur cluster (ISC) and heme biosynthesis.

85 ron to enter mitochondria and be used in ISC/heme biosynthesis; thus, there appears to be no direct o

86 ), the first and rate-limiting enzyme in the heme biosynthetic pathway.

87 In these cells, heme can act as a prototypical damage-associated molecul

88 1 in its N-terminal plug domain required for heme capture to heme transport and signaling, respective

89 ds light on possible proton movements during heme-catalyzed oxygen activation, as well as on ascorbat

90 2/2 or 3/3 alpha-helical folding around the heme cavity.

91 he activation of O(2) is best exemplified by heme centers in biological systems.

92 Given that GAPDH displays properties of a heme chaperone for inducible NO synthase, here we invest

93 m as a novel therapeutic strategy to improve heme clearance in patients with hemolytic disorders.

94 Macrophages play a key protective role in heme clearance; however, the mechanisms that regulate me

95 firmed the formation of an inhibitory type I heme-clobetasol complex in CYP3A5 but not in CYP3A4, thu

96 ontrol the iron coordination geometry when a heme cofactor is allowed to bind to either histidine or

97 definition to support the rapid binding of a heme cofactor.

98 port protein, with each subunit containing a heme cofactor.

99 e nascent peroxidase activity of the protein-heme complex.

100 splits homolytically to form an iron(IV)-oxo heme (Compound II) and a free NO(2) radical via a small

101 levels decrease in response to increments in heme concentration, confirming it as a member of the hem

102 mainly derived from the studies on thiolate-heme containing epoxidases, such as cytochrome P450 epox

103 ing of the signal transduction mechanisms in heme-containing sensor proteins remains elusive.

104 inuclear complex by rearrangement of the CcP heme-coordinating helix.

105 into three phylogenetic classes differing in heme coordination and O(2) affinity.

106 Characterization of the specific heme coordination modes was done by using UV/Vis and Ele

107 models of the bimetallic active sites in the heme-copper oxidases are reviewed.

108 Heme-copper oxidases are transmembrane enzymes involved

109 sites, in addition to sites corresponding to heme-CPR domain interactions at the dimeric interface.

110 e mechanism of heme-ART adduct inhibition of heme crystallization, unique among antimalarials and com

111 insulated biomolecular wire possessing a 10-heme cytochrome, MtrA, insulated from the membrane lipid

112 intimate connection with an extracellular 10-heme cytochrome, MtrC, which presents its hemes across a

113 Bilirubin is a yellow-colored metabolite of heme degradation (a bile pigment), once believed to be t

114 adaptations that are required for effective heme degradation remain unclear.

115 le NO synthase, here we investigated whether heme delivery to apo-sGCbeta involves GAPDH.

116 rms a complex with apo-sGCbeta to accomplish heme delivery to sGCbeta.

117 e and tyrosine hydroxylase, thiolate-ligated heme-dependent cytochrome P450, and four nonheme oxygena

118 These enzymes include histidine-ligated heme-dependent dehaloperoxidase and tyrosine hydroxylase

119 The cytochromes P450 are heme-dependent enzymes that catalyze many vital reaction

120 quires a shift to the PPP that is induced by heme-derived CO, suggesting pharmacologic targeting of m

121 ngs demonstrate that metabolic adaptation to heme detoxification in macrophages requires a shift to t

122 rmation of hemozoin and in this way suppress heme detoxification.

123 ray scattering measurements demonstrate that heme disassociation leads to the loss of tetrameric stru

124 acilitate rapid intraflavin and trans FMN-to-heme electron transfers (ETs).

125 tryptophan with dioxygen is mediated by two heme enzymes, tryptophan 2,3-dioxygenase (TDO) and indol

126 tions that are unknown for histidine-ligated hemes enzymes.

127 atalytic site variant that is unable to bind heme exhibits a constant low protein level and an enhanc

128 in-5, which were significantly reduced after heme exposure.

129 ound that Hp strongly inhibits IsdH-mediated heme extraction and that Hp binding prevents local unfol

130 -mediated iron acquisition, here we measured heme extraction from the Hp-Hb complex by UV-visible spe

131 inhibition and the dynamics of IsdH-mediated heme extraction.

132 on activity induced by oxygen binding to the heme-Fe(II) complex located in the oxygen-sensing N-term

133 n important regulatory molecule (as "labile" heme) for diverse processes such as translation, kinase

134 unusual inhibition mode by binding the IDO1 heme-free (apo) form.

135 ant substrate-specific subunit LhaS accepted heme from diverse host-derived hemoproteins.

136 eme pocket, leaving IsdH unable to wrest the heme from Hb.

137 hylococcus aureus obtains iron by extracting heme from hemoglobin (Hb) using the closely related IsdB

138 e Isd components enable S. aureus to extract heme from hemoglobin (Hb), transport it into the bacteri

139 Consequently, B. fragilis acquires essential heme from host tissues during extraintestinal infection.

140 Moreover, we observed transfer of heme from the core to the HRMs and equilibration of heme

141 ires the acquisition of nutritional iron and heme from the host as Leishmania lacks the capacity for

142 he chemical mimicry existing between VER and heme group suggest that redox active residue C227 of Gra

143 e A), and two proteins that contain multiple heme groups (diheme cytochrome c from Rhodobacter sphaer

144 However, heme has also been shown to be an important regulatory m

145 procedures for quantitative determination of heme have been used for many years in different settings

146 of HO1 and HO2 is important for maintaining heme homeostasis.

147 est that ribosomes play a role in regulating heme homeostasis.

148 so equilibrate between the sites to maintain heme homeostasis.

149 ally derived thermodynamics lead to a ferric heme hydroperoxide OO-H BDFE determination, that Fe(III)

150 studies demonstrate that hemolysis and free heme in circulation cause endothelial barrier dysfunctio

151 ss involving A1M causing AKI, whereas excess heme in controls is transported to the liver as expected

152 ggest a close proximity of clobetasol to the heme in CYP3A5 but not in CYP3A4.

153 g for a possibility to identify and quantify heme in different physiological and pathological setting

154 els, here we investigated the role of labile heme in the regulation of mitochondrial biogenesis.

155 he interprotein ET across 6 angstrom between hemes in adjacent proteins was about 10(5) s(-1), about

156 ), a vitamin (pyridoxal-5P), and a cofactor (heme) in both the acute and latent stages of infection.

157 Heme, in a dose-dependent manner, induced a rapid drop i

158 In mouse bone marrow-derived macrophages, heme induced HO-1, lipid regulatory genes including LXR

159 ular mechanisms involved in the pathology of heme-induced barrier disruption remain to be elucidated.

160 tor Xa and thrombin significantly attenuates heme-induced microvascular stasis in mouse models of VOC

161 e and a Syk inhibitor differentially blocked heme-induced ROS, MAPK phosphorylation, and cytokine pro

162 Heme induces the expression of SPIC transcription factor

163 ontacts primarily function to destabilize Hb-heme interactions, thereby lowering DeltaH(*), while con

164 or porphyria disorders that accumulate toxic heme intermediates.

165 ay be a key factor in the selectivity of non-heme iron "rebound" processes.

166 Trp complex, where CO is photolyzed from the heme iron by X-rays at cryogenic temperatures (100 K).

167 center in AbCntA-WT to the mono-nuclear, non-heme iron center through the bridging glutamate E205 and

168 Non-heme iron complexes with cis-Fe(III)(OH)(SAr/OAr) coordi

169 ternary ammonium substrate, carnitine by non-heme iron containing Acinetobacter baumannii (Ab) oxygen

170 -Fe(III)(OH)(halide) intermediate in the non-heme iron halogenases were synthesized and examined for

171 enzymes (P450s whose Cys axial ligand to the heme iron has been replaced with Ser) generated variants

172 scription factors and direct sensing via non-heme iron(Fe(2+))-dependent-dioxygenases.

173 Herein, we report a mononuclear non-heme iron(II)-cyclam complex, 1-trans, that activates O(

174 or threonine residue, the inclusion of a non-heme iron, alpha-ketoglutarate-dependent oxygenase for h

175 ed oxygenic ligand at 1.88 angstrom from the heme iron.

176 Heme is an essential cofactor for many biological proces

177 show for the first time that cellular labile heme is critical for the post-translational regulation o

178 1 subunit (sGCbeta) for sGC to function, how heme is delivered to sGCbeta remains unknown.

179 Studies in mice showed that excess heme is directed to the kidneys in SCD in a process invo

180 t a PITP is supported by demonstrations that heme is not a readily exchangeable ligand, and that phos

181 e(3+)-heme transfer model in which HRM-bound heme is readily transferred to the catalytic site for de

182 Extracellular heme is sensed via the Has system, which encodes an extr

183 SCD) and report that (1) acute elevations in heme lead to kidney damage in hemopexin-deficient states

184 HsmR senses vertebrate heme, leading to increased expression of the hsmRA opero

185 e in P. falciparum, PfDegP, similarly lowers heme levels and DHA susceptibility.

186 utively active in neurons because endogenous heme levels are so low; HRI activity results in eIF2alph

187 wever, how these species import and regulate heme levels is not fully defined yet.

188 ntrolled modulation and monitoring of labile heme levels, here we investigated the role of labile hem

189 tion metal complexes containing heme and non-heme ligands have been selected to discuss the recent ad

190 tron transfer (IET) rate from the FAD to the heme, limited the sensor signals.

191 Here we demonstrate that heme loading drives a unique bioenergetic switch in macr

192 We validated the effects of heme loss on mitochondrial cytochromes by knocking down

193 ochromes by knocking down cytochrome c/c (1) heme lyase 1 (TgCCHL1), a mitochondrial enzyme that cata

194 Expression of a soluble heme lyase from an organism with cytochrome c maturation

195 These results expose the vulnerability of heme metabolism to genetic perturbations that can lead t

196 In contrast, HO-1-mediated heme metabolism was inhibited at subsaturating POR.

197 g role, but also form a bridge through which heme moves from Hb to the receptor.

198 Although heme must bind in the sGC beta1 subunit (sGCbeta) for sG

199 h sequential hopping in a biologically based heme network.

200 f CYP2B6, which may act synergistically with heme nitrosylation to target the enzyme for degradation.

201 w that the ability of B. fragilis to utilize heme or protoporphyrin IX for growth was greatly reduced

202 ave established that inactivation of nNOS by heme or tetrahydrobiopterin (BH(4)) alteration and loss

203 emolysis causes an increase of intravascular heme, oxidative damage, and inflammation in which macrop

204 talase, glutathione peroxidase 1 (GPX1), and heme oxygenase 1 (Hmox1) and transcription factor nuclea

205 We hypothesized that heme oxygenase 1 (HMOX1; HO-1), an enzyme responsible fo

206 Heme oxygenase 1 (HO-1) and the cytochromes P450 (P450s)

207 Importantly, mRNA expression of heme oxygenase 1 (HO-1), a potential modulator of immune

208 catalase, NF-E2-related factor 2 (Nrf2), and heme oxygenase 1 (HO-1).

209 ), intercellular adhesion molecule 1, IL-10, heme oxygenase 1 hypoxia-inducible factor 1 (HIF-1), mon

210 t upregulation of superoxide dismutase 2 and heme oxygenase 1 protein following hypoxia-reoxygenation

211 mmatory, and antioxidant (enzymes, including heme oxygenase isoforms [HO-1, HO-2]) markers.

212 Our data support roles for heme oxygenase isoforms in modulating recovery from syna

213 of the antioxidant/anti-inflammatory enzyme heme oxygenase-1 (HO-1) and increased neuroinflammation

214 d CXCL8 secretion and required activation of heme oxygenase-1 (HO-1) and phosphorylated adenosine mon

215 Although Heme Oxygenase-1 (HO-1) induction in various forms of ki

216 ctor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1).

217 mL; CO-E-CPR, 89 +/- 26 pg/mL; p < 0.05) and heme oxygenase-1 (sham, 1 +/- 0.1; cardiopulmonary resus

218 nd molecular markers (caspase-3 activity and heme oxygenase-1 expression) were analyzed.

219 lial NOS (eNOS), Nrf2, and Phase II enzymes (heme oxygenase-1, catalase, superoxide dismutase-1) in a

220 em macrophages through coregulation of HO-1 (heme oxygenase-1; HMOX1) and lipid homeostasis genes.

221 The C-terminal tail region of human heme oxygenase-2 (HO2) contains two HRMs whose cysteine

222 reverses vitamin C-induced up-regulation of heme-oxygenase-1 and ferritin in KRAS-mutant cancer cell

223 p-regulation of the stress-inducible protein heme-oxygenase-1.

224 The enzyme's central heme-oxygenase-like (HO-like) domain sequentially hydrox

225 The heme-peptide fragment then oxidized 2,2'-azino-bis(3-eth

226 ilized trypsin enzymes on NAA-NH(2) into the heme-peptide fragment.

227 sperm viability, and a spermathecal-derived heme peroxidase is required for long-term Anopheles gamb

228 Peroxidasin is a heme peroxidase that oxidizes bromide to hypobromous aci

229 p binding prevents local unfolding of the Hb heme pocket, leaving IsdH unable to wrest the heme from

230 tigation into barrier proteins revealed that heme primarily affected the tight junction proteins zona

231 ng advantage of a yeast strain deficient for heme production that enabled controlled modulation and m

232 Furthermore, we show that heme protects P. aeruginosa from CP-mediated inhibition

233 Similarly to P. aeruginosa, we show that heme protects S. aureus from CP-mediated inhibition of i

234 At basic pHs, the thiolate mini-heme protein can catalyze O(2) reduction when adsorbed o

235 kinetics of photoreduction of six different heme protein crystal species by X-ray radiation.

236 lograys already yields 50% ferrous iron in a heme protein crystal.

237 ng cytochrome c (M) (CytM), a cryptic c-type heme protein widespread in cyanobacteria.

238 which we assign to the presence of covalent heme-protein bonds.

239 and pods, which clearly suggests that these heme proteins play additional roles unrelated to nitroge

240 ptophan dioxygenase (hTDO) are two important heme proteins that degrade the essential amino acid, l-t

241 For ferrous heme proteins, doming is associated with the respiratory

242 tern is common to a wide diversity of ferric heme proteins, raising the question of the biological re

243 ons in the visible range, such as retinal or heme proteins.

244 alytic potential of simple, de novo-designed heme proteins.

245 promising approaches for future solutions to heme quantification are highlighted.

246 ires the erythroid-specific eIF2alpha kinase heme-regulated inhibitor (HRI), suggesting that HRI migh

247 Recently, we found that the eIF2alpha kinase heme-regulated inhibitory (HRI) induced a cytosolic unfo

248 prisingly mediated by eIF2alpha kinase 1, or heme-regulated kinase inhibitor (HRI).

249 Consequently, we found that labile heme regulates mitochondrial biogenesis and cell growth.

250 its catalytic site and the others at its two heme regulatory motifs (HRMs).

251 Heme-regulatory motifs (HRMs) are present in many protei

252 bsites positioned ~20 angstrom apart trigger heme release by contacting Hb's F-helix.

253 Thus, IsdH triggers heme release from Hb via a flexible, low-affinity interf

254 Our results provide critical insight into heme release, signaling, and transport in P. aeruginosa

255 th the detoxification of enormous amounts of heme released during the proteolytic catabolism of eryth

256 of heme biosynthesis, is conserved among the heme-requiring Bacteroidales that inhabit the mammalian

257 centration, confirming it as a member of the heme response gene family.

258 Here, we identify the C. difficile heme-sensing membrane protein system (HsmRA) and show th

259 easured by a genetically encoded fluorescent heme sensor.

260 modalities, which we accomplish by using the heme signals from MALDI-MSI and iron signals from LA-ICP

261 provides unique insight into how the distal heme site of DyPs can be tuned to select aspartate or ar

262 These structures reveal a water-free distal heme site that, together with the presence of an asparag

263 ic mechanism, O(2) migrates to the catalytic heme site via a long hydrophobic tunnel and displaces Le

264 med via HAT reactivity of the partner ferric heme superoxide complex.

265 ng the cruciality of electrophilicity of the heme superoxide moiety in facilitating the initial indol

266 an electronically divergent series of ferric heme superoxo oxidants mediates the facile conversion of

267 gocytes, and Nfe2l2/Nrf2 deficiency restored heme-suppressed inflammation.

268 as Leishmania lacks the capacity for de novo heme synthesis and does not contain cytosolic iron-stora

269 on the growth, development, hemoglobin, and heme synthesis gene expression in the larvae of a model

270 oietic porphyria (CEP) is an inborn error of heme synthesis resulting from uroporphyrinogen III synth

271 dynamic modulation of tumor hypoxia with the heme-targeting drug treatments create important opportun

272 n-regulated DEGs enriched in photosynthesis, heme, tetrapyrrole binding, and antioxidant activity.

273 rapyrrole protoporphyrin IX in order to form heme that is required for growth stimulation and surviva

274 Cytochrome P450 monooxygenases (CYPs/P450s), heme thiolate proteins, are well known for their role in

275 me that catalyzes the covalent attachment of heme to c-type cytochromes.

276 1), an enzyme responsible for degradation of heme to carbon monoxide, bilirubin, and iron, is an impo

277 nduces a protective response that repurposes heme to counteract antimicrobial oxidative stress respon

278 ted with erythrocytes and co-cooperated with heme to promote the generation of mature RPMs through ac

279 ally faster energy flow from the dissociated heme to the protein moiety in cytochrome c, which we ass

280 n states of the iron ion, causing the ferric heme to undergo doming, which we identify.

281 We therefore propose an Fe(3+)-heme transfer model in which HRM-bound heme is readily t

282 ls and their complex formation and potential heme transfer using purified proteins.

283 sampling conformations that are suitable for heme transfer.

284 ears to trap IsdH in an initial state before heme transfer.

285 ruzi senses intracellular heme and regulates heme transport activity by adjusting the expression of T

286 arasite to gain insight into its function in heme transport and homeostasis.

287 Proteins involved in Leishmania iron and heme transport and metabolism have been identified and s

288 nal plug domain required for heme capture to heme transport and signaling, respectively.

289 ecombinant proteins from a surface-localized heme transport system containing near-iron transporter (

290 deling, was also significantly altered after heme treatment, both in HLMVECs and mice.

291 ferric iron uptake, ferrous iron uptake, or heme uptake at different points during infection.

292 tive PCR analyses, immunoblotting, and (13)C-heme uptake experiments, we delineated the differential

293 that P. aeruginosa upregulates expression of heme uptake machinery in response to CP.

294 al link between the ECF sigma factor and Phu heme uptake system.

295 The P. aeruginosa genome encodes two heme uptake systems, the heme assimilation system (Has)

296 ssimilation system (Has) and the Pseudomonas heme utilization (Phu) system.

297 tyrosine kinase (Syk) activation induced by heme were critical for most proinflammatory signaling pa

298 rugs are activated in vivo by newly released heme, which creates a carbon-centered radical that marke

299 exploited by C. difficile to repurpose toxic heme within the inflamed gut as a shield against antimic

300 , the incorporation of a second chromophore, heme, yields an electron transfer pathway in both micell