ライフサイエンスコーパス: protoporphyrin

1 R parameters in the presence of heme or zinc protoporphyrin.

2 the attachment mechanism is specific for Fe protoporphyrin.

3 rrin receptor (sTfR), as well as erythrocyte protoporphyrin.

4 -positive bacteria) are unable to synthesize protoporphyrin.

5 f core metabolic intermediates that includes protoporphyrin.

6 ciency does not result in an accumulation of protoporphyrins.

7 Pretreatment with cobalt protoporphyrin 24 h before LPS challenge normalized this

8 oneally administered the HO-1 inducer cobalt protoporphyrin (3 mg/kg CoPP) with and without the HO in

9 Inhibition of HO by tin protoporphyrin abrogated the impairment of resistance to

10 in precursors to zebrafish larvae results in protoporphyrin accumulation and a reproducible nongeneti

11 evulinic acid (ALA) (mimicking intracellular protoporphyrin accumulation in EPP).

12 on hematopoietic progenitors was mediated by protoporphyrin accumulation, driving heme production and

13 g that attenuates ALAS2 mRNA translation and protoporphyrin accumulation.

14 at iron regulatory protein-1 (IRP1) inhibits protoporphyrin accumulation.

15 The cobalt protoporphyrin-activated hBVR phosphorylated a threonine

16 Treating VSMCs with zinc protoporphyrin, an HO-1 inhibitor, or HO-1 small interfe

17 The hea mice also have elevated Zn protoporphyrin and serum iron.

18 nistration of the HO inducers heme or cobalt protoporphyrin and the effect of HO inhibition using sys

19 ncentrations of hemoglobin, free erythrocyte protoporphyrin, and ferritin.

20 ed levels of free protoporphyrin IX and zinc protoporphyrin are generated in IRP2-/- erythroid cells.

21 Surprisingly, Zn and Sn protoporphyrins are potent inhibitors of the pathways, a

22 e status of haem and its precursors iron and protoporphyrin at the site of haem synthesis.

23 Herein, we investigated the effect of exo- Protoporphyrin based SDT (PpIX-SDT) on SAS cells in vitr

24 IRP1 attenuates protoporphyrin biosynthesis by binding to the 5'-iron re

25 O-1 or inhibition of HO-1 activity with zinc protoporphyrin blocked these effects of gAcrp.

26 The HO-1 inhibitor, tin protoporphyrin, blocked MP4CO protection, consistent wit

27 with the insertion of Fe(2+) or Mg(2+) into protoporphyrin by ferrochelatase or magnesium chelatase,

28 (PDS), a 20S proteasome subunit (PB7) or Mg-protoporphyrin chelatase (Chl H) encoding genes in Nicot

29 in transferrin saturation, erythrocyte zinc protoporphyrin concentration, hemoglobin concentration,

30 as evidenced by an elevated erythrocyte zinc protoporphyrin concentration.

31 lmar keratoderma, relatively low erythrocyte protoporphyrin concentrations, and recessive inheritance

32 cytic anemia, with an elevated red cell zinc protoporphyrin, consistent with functional erythroid iro

33 ction of heme oxygenase-1 (HO-1) with cobalt protoporphyrin (CoPP) markedly attenuated the developmen

34 We used cobalt protoporphyrin (CoPP) treatment to evaluate the effect o

35 OV replication, we treated cells with cobalt protoporphyrin (CoPP), a selective HO-1 inducer, and ass

36 Cobalt protoporphyrin (CoPP), a well known heme oxygenase 1 ind

37 Cobalt protoporphyrin (CoPP)-induced HO-1 overexpression amelio

38 e in which NRF2/HO-1 was induced with cobalt protoporphyrin (CoPP).

39 ated overexpression or induction with cobalt protoporphyrin (CoPP, a potent HO-1 inducer), pre- and p

40 d with the pharmacologic HO-1 inducer cobalt protoporphyrin demonstrated amelioration of active colit

41 seline laboratory testing, total erythrocyte protoporphyrin (ePPIX) testing, and molecular genetic te

42 Heme oxygenase inhibition by tin protoporphyrin exacerbates stasis in sickle mice.

43 ch as vital staining with methylene blue and protoporphyrin fluorescence can increase the yield of me

44 itting is used to distinguish the faint zinc protoporphyrin fluorescence from the much greater tissue

45 eal injection of the FECH inhibitor N-methyl protoporphyrin had similar effects.

46 ke natural systems having only Fe-containing protoporphyrins, i.e., heme, as electron mediators, we u

47 g erythroid cells leads to overproduction of protoporphyrin in amounts sufficient to cause photosensi

48 d biochemically by a high proportion of zinc-protoporphyrin in erythrocytes, in which a mismatch betw

49 However, despite massive accumulation of protoporphyrin in the liver, expression of the main gene

50 e liver disease results from accumulation of protoporphyrin in the liver, LT without hematopoietic st

51 sis pathway resulting in the accumulation of protoporphyrins in the blood, erythrocytes, and other ti

52 ndicator of iron status, red blood cell zinc protoporphyrin, in the microcirculation of the lower lip

53 nd concomitant intracellular accumulation of protoporphyrin intermediates.

54 sted by incorporation of a redox-inactive Zn-protoporphyrin into the protein, and the resulting cryst

55 skin photosensitivity upon leaching of blood protoporphyrin into the skin.

56 capable of binding the metalloporphyrin zinc protoporphyrin IX ((PPIX)Zn) have been synthesized.

57 ition of heme oxygenase via injection of tin protoporphyrin IX (20 micromol/kg intraperitoneally) res

58 Here, we demonstrate that cobalt protoporphyrin IX (CoPP) and zinc protoporphyrin IX (ZnP

59 Cobaltic protoporphyrin IX (CoPP) is a synthetic heme analog whic

60 HO-1 expression by administration of cobalt protoporphyrin IX (CoPPIX) to the graft donor restored g

61 with induction of HO-1 expression by cobalt protoporphyrin IX (CoPPIX).

62 in, a detoxified, crystalline form of ferric protoporphyrin IX (Fe(3+)-PPIX) produced by the parasite

63 l genetic systems that allow the use of iron-protoporphyrin IX (heme) have been described for the pat

64 here that the endogenous small molecule iron protoporphyrin IX (hemin) and several related porphyrin

65 Accumulation of magnesium-protoporphyrin IX (Mg-Proto), an intermediate in chlorop

66 oroplast and the nucleus involving magnesium protoporphyrin IX (MgP(IX)), the first dedicated interme

67 liana) knockout ntrc reveals lower magnesium protoporphyrin IX (MgP) and MgPMME steady-state levels,

68 m S-adenosyl-L-methionine (SAM) to magnesium protoporphyrin IX (MgP) forming MgP monomethylester (MgP

69 ts; gallium (Ga) or zinc (Zn) complexed with protoporphyrin IX (PP) or mesoprotoporphyrin IX (MP) tha

70 lic disease that causes excess production of protoporphyrin IX (PP-IX), the final biosynthetic precur

71 pical photosensitizing agents and subsequent protoporphyrin IX (PPIX) accumulation in photodynamic th

72 nanodrug by conjugating the photosensitizer protoporphyrin IX (PpIX) and polyethylene glycol (PEG) w

73 drug simvastatin (SV) and a photosensitizer protoporphyrin IX (PpIX) due to the n-n stacking of the

74 Photosensitizer protoporphyrin IX (PpIX) fluorescence, intracellular loc

75 clinical use of a natural fluorophore called protoporphyrin IX (PpIX) for image-guided surgical resec

76 ayed metabolism of 5-ALA and accumulation of protoporphyrin IX (PpIX) in the high fluorescence area.

77 Protoporphyrin IX (PPIX) is considered a conserved endog

78 FGS) using aminolevulinic-acid (ALA) induced protoporphyrin IX (PpIX) provides intraoperative visual

79 We also describe BcTSPO-mediated protoporphyrin IX (PpIX) reactions, including catalytic

80 (PCD) triggered by Pseudomonas syringae and protoporphyrin IX (PPIX) treatment.

81 is based upon the intracellular synthesis of protoporphyrin IX (PpIX), which absorbs light and target

82 Photodynamic therapy (PDT) with protoporphyrin IX (PpIX), which is endogenously derived

83 ng effects of reovirus therapy combined with protoporphyrin IX (PpIX)-mediated photodynamic therapy o

84 and iron pathways, associated with elevated protoporphyrin IX (PPIX).

85 lation of the heme biosynthesis intermediate protoporphyrin IX (PPIX).

86 of the tissue in to a photosensitizer called protoporphyrin IX (PPIX).

87 nic acid (ALA) to induce the accumulation of protoporphyrin IX (PpIX).

88 accumulation of the phototoxic intermediate protoporphyrin IX (PPIX).

89 ing for NSCLC surgery using the well-studied protoporphyrin IX (PPIX)/5-aminiolevulinic acid (5-ALA)

90 wn laf6 seedlings also showed an increase in protoporphyrin IX (Proto IX), Mg-proto, Mg-proto MME and

91 (+) We observed that HO inhibition using tin protoporphyrin IX (SnPP) decreased heme-iron recycling i

92 hat cobalt protoporphyrin IX (CoPP) and zinc protoporphyrin IX (ZnPP) are ligands that bind directly

93 Zinc protoporphyrin IX (ZnPP) is known to accumulate in most

94 Zinc protoporphyrin IX (ZnPP), an endogenous heme analogue th

95 The zinc(II)-protoporphyrin IX (ZnPPIX) fluorophore binds to G-quadru

96 complex with a heme analog, zinc-substituted protoporphyrin IX (ZnPPIX).

97 lated when HO-1 activity was blocked by zinc protoporphyrin IX (ZnPPIX).

98 and absence of neurohumoral inhibitors (tin protoporphyrin IX [SnPP IX] for CO synthesis, N(omega)-n

99 the Ccm system, and the negative effects of protoporphyrin IX accumulation.

100 EM14C-deficient cells was ameliorated with a protoporphyrin IX analog, indicating that TMEM14C primar

101 ing of photosensitizers in milk (riboflavin, protoporphyrin IX and a chlorophyllic compound) by front

102 gle-channel activity only in the presence of protoporphyrin IX and blue light.

103 n identified in avian eggshells: rusty-brown protoporphyrin IX and blue-green biliverdin IXalpha.

104 It is suggested that protoporphyrin IX and chlorophyll are responsible for ox

105 port other cyclic planar porphyrins, such as protoporphyrin IX and coproporphyrin.

106 ochrome oxidase, suggesting a defect between protoporphyrin IX and heme a.

107 to be dose dependent and specific for heme; protoporphyrin IX and other heme structural analogs did

108 HO-1 inhibition with tin-protoporphyrin IX and silencing with RNA interference re

109 ssion, and markedly increased levels of free protoporphyrin IX and zinc protoporphyrin are generated

110 BchD, and BchI) that inserts magnesium into protoporphyrin IX as the first committed step of (bacter

111 1) catalyzes the insertion ferrous iron into protoporphyrin IX as the last step in heme biosynthesis,

112 Our previous study has shown that endo-Protoporphyrin IX based SDT (ALA-SDT) could induce apopt

113 titrations demonstrated that both hemin and protoporphyrin IX bind to NikA with similar affinity.

114 e of human ferrochelatase with the substrate protoporphyrin IX bound as well as a higher resolution s

115 s the ATP-dependent insertion of Mg(2+) into protoporphyrin IX catalyzed by the multisubunit enzyme m

116 onomethyl ester oxidative cyclase (bchE), Mg-protoporphyrin IX chelatase (bchD), and phytoene dehydro

117 en intraperitoneal injections of cobalt(III) protoporphyrin IX chloride (CoPP), which up-regulates HO

118 rats were treated with HO-1 activator cobalt protoporphyrin IX chloride (Copp; 25 mg/kg body weight)

119 For this catalyst and iron protoporphyrin IX chloride, Fe(PPIX)Cl, two distinct and

120 The suppressive effect of HO-1 induction by protoporphyrin IX cobalt chloride (CoPP; a classical ind

121 Administration of HO-1 inhibitor tin protoporphyrin IX dichloride in infected BALB/c mice led

122 Tin protoporphyrin IX did not affect heme oxygenase-1 expres

123 strates 4-fluorostyrene, vinylferrocene, and protoporphyrin IX dimethyl ester were then coupled (in d

124 ations were carried out on both deutero- and protoporphyrin IX dimethyl esters.

125 zation of the beta-positions of deutero- and protoporphyrin IX dimethyl esters.

126 The HO-1 inducer cobalt protoporphyrin IX diminished proinflammatory cytokine le

127 Furthermore, upregulation of HO-1 by cobalt protoporphyrin IX diminished the production of TNF-alpha

128 retreatment with aminolevulinic acid or with protoporphyrin IX dramatically increased the light sensi

129 A was found to comigrate with both hemin and protoporphyrin IX during gel filtration.

130 Treatment with the HO-1 inhibitor zinc protoporphyrin IX exacerbated the inflammatory response

131 iron into protoporphyrin IX, is catalyzed by protoporphyrin IX ferrochelatase (EC 4.99.1.1).

132 at is capable of ultrasensitive detection of protoporphyrin IX fluorescence in vivo, together with in

133 In vivo animal studies reveal that protoporphyrin IX fluorescence is strongly correlated wi

134 ity levels of Hexaminolevulinic Acid-induced Protoporphyrin IX fluorescence.

135 he ability of B. fragilis to utilize heme or protoporphyrin IX for growth was greatly reduced in a De

136 articularly striking is the structure of the protoporphyrin IX group, which is distorted from planari

137 Experiments with protoporphyrin IX in a glioma rodent model demonstrate i

138 cy of ferrochelatase (FECH), accumulation of protoporphyrin IX in erythrocytes, skin, and liver, and

139 ragilis does not synthesize the tetrapyrrole protoporphyrin IX in order to form heme that is required

140 xidase (MP) and 2-methylimidazole ligated Fe protoporphyrin IX in the 10 ns to 10 ms time window.

141 s accumulation of the endogenous hepatotoxin protoporphyrin IX in the liver through PXR-mediated alte

142 es results in a decreased ability to convert protoporphyrin IX into heme, leading to protoporphyria,

143 Protoporphyrin IX iron complex (heme) is an important co

144 e and its biosynthetic intermediates such as protoporphyrin IX is a complex and highly coordinated pr

145 The ATP-dependent insertion of Mg(2+) into protoporphyrin IX is the first committed step in the chl

146 elevated serum ferritins, elevated red cell protoporphyrin IX levels, and adult-onset neurodegenerat

147 nt with this, we observed increased cellular protoporphyrin IX levels, reduced mitochondrial heme a a

148 ealed accumulation of very high levels of Mg-protoporphyrin IX methyl ester and only traces of protoc

149 th the next enzyme in the pathway, magnesium protoporphyrin IX methyltransferase (BchM).

150 Sll1214 and the Chl biosynthesis enzymes Mg-protoporphyrin IX methyltransferase and protochlorophyll

151 ability of a DeltabluB strain to convert Mg-protoporphyrin IX monomethyl ester (MPE) into protochlor

152 Surprisingly, Mg-protoporphyrin IX monomethyl ester (oxidative) cyclase,

153 d strain containing reporter plasmids for Mg-protoporphyrin IX monomethyl ester oxidative cyclase (bc

154 izes 3,8-divinyl protochlorophyllide from Mg-protoporphyrin IX monomethyl ester, Ho1 oxidatively clea

155 the chlorophyll biosynthesis intermediate Mg-protoporphyrin IX monomethylester (Mg-proto MME), consis

156 RC stimulates in vitro activity of magnesium protoporphyrin IX monomethylester (MgPMME) cyclase, most

157 nin), coproporphyrinogen III oxidase, and Mg-protoporphyrin IX monomethylester cyclase.

158 The HO-1 inducer cobalt protoporphyrin IX more efficiently attenuated PGE2 and I

159 As neither protoporphyrin IX nor coproporphyrin export improved wit

160 ted ion channels to human subjects, applying protoporphyrin IX or its precursor aminolevulinic acid.

161 In contrast, HO-1 agonists hemin and cobalt protoporphyrin IX significantly increased DAF protein ex

162 HO-1 induction with metalloporphyrin cobalt protoporphyrin IX significantly reduces the loss of body

163 with BchM in Escherichia coli overproducing protoporphyrin IX suggests that the chelatase is the rat

164 Protoporphyrin IX synthesis in TMEM14C-deficient erythro

165 vating Mg-chelatase, the enzyme that commits protoporphyrin IX to chlorophyll biosynthesis.

166 catalyzes the insertion of ferrous iron into protoporphyrin IX to form heme.

167 catalyzes the insertion of ferrous iron into protoporphyrin IX to form protoheme IX (heme).

168 catalyzes the insertion of ferrous iron into protoporphyrin IX to form protoheme IX (heme).

169 catalyzes the insertion of ferrous iron into protoporphyrin IX to form protoheme IX.

170 valent cobalt, zinc, nickel, and copper into protoporphyrin IX to form the corresponding metalloporph

171 Zea mays) are deficient in the conversion of protoporphyrin IX to magnesium protoporphyrin IX, the fi

172 lei Pharmacological administration of cobalt protoporphyrin IX to mice resulted in an enhanced bacter

173 lyze the insertion of the imported iron into protoporphyrin IX to produce heme.

174 Concomitantly, upon cobalt protoporphyrin IX treatment, there is a significant upre

175 The crystal structure of Co3+-protoporphyrin IX V349A/W387F oPGHS-1 in a complex with

176 ible drug-induced precipitation of iron(III) protoporphyrin IX was postulated to account for this.

177 of PGHS-1 reconstituted with heme or mangano protoporphyrin IX with a lipid hydroperoxide, 15-hydrope

178 Although PfHO bound heme and protoporphyrin IX with modest affinity, it did not catal

179 akly electron-polarizing 2,4-vinyl groups of protoporphyrin IX with strongly electron-polarizing acet

180 We observed that BchM uses protoporphyrin IX without bound metal as a substrate.

181 tion of heme oxygenase1 (HO-1) activity with protoporphyrin IX zinc(II) blocked MLP nuclear accumulat

182 ators of heme synthesis (succinylacetone and protoporphyrin IX) and cellular iron content (holotransf

183 Proteins containing heme, iron(protoporphyrin IX) and its variants, continue to be one

184 nit of Mg-chelatase, as well as a substrate (protoporphyrin IX) and product (Mg-protoporphyrin IX) of

185 ctron-transfer reorganization energies of Zn(protoporphyrin IX) and Zn(octaethylporphyrin) are determ

186 r human methemoglobin, linking hemin (ferric protoporphyrin IX) disassociation and apoprotein unfoldi

187 n of transcription by hemoglobin and (cobalt protoporphyrin IX) globin but not by apoglobin or other

188 Hemin (iron protoporphyrin IX) is a crucial component of many physio

189 Heme (iron protoporphyrin IX) is a well-known prosthetic group for

190 ubstrate (protoporphyrin IX) and product (Mg-protoporphyrin IX) of Mg-chelatase.

191 xidizes to the hexacoordinate hemin (Fe(III)-protoporphyrin IX) or hemichrome form (hemiHtsA) with an

192 The hexacoordinate heme (Fe(II)-protoporphyrin IX) or hemochrome form of holoShp (hemoSh

193 pi-acceptor compounds (e.g., 1,4-dipyridine, protoporphyrin IX), aromatic compounds (e.g., 1,4-dihydr

194 or heme oxygenase-1 inhibitors (1400W or tin protoporphyrin IX).

195 the bound, light-activated chromophore, zinc protoporphyrin IX, (PPIX)Zn.

196 ficial protein specifically accumulated zinc protoporphyrin IX, a rare cofactor that is not used by n

197 hexylester, EMT6 cells accumulated abundant protoporphyrin IX, an endogenous photosensitizer formed

198 Interestingly, cobalt protoporphyrin IX, an HO-1 inductor, increased the paras

199 MGd used in combination with tin protoporphyrin IX, an inhibitor of HO1, resulted in syne

200 plicated DeltaPsim changes in PCD: ceramide, protoporphyrin IX, and the hypersensitive response elici

201 ed photosensitizers verteporfin, temoporfin, protoporphyrin IX, and trisulfonated hydroxyaluminum pht

202 biosynthesis, insertion of ferrous iron into protoporphyrin IX, is catalyzed by protoporphyrin IX fer

203 was induced in vivo by treatment with cobalt protoporphyrin IX, starting at week 5 or 12 of mice life

204 ee chelatase complexes insert magnesium into protoporphyrin IX, the activities range by a factor of 1

205 conversion of protoporphyrin IX to magnesium protoporphyrin IX, the first committed step of chlorophy

206 ose, weighted to the absorption spectrum for protoporphyrin IX, was calculated.

207 ion of the fluorescent tetrapyrrole product, protoporphyrin IX, was detected using a fluorescence pla

208 alpha or the beta subunits replaced by zinc protoporphyrin IX, which is unable to bind a ligand and

209 er bonds between the vinyl groups of heme b (protoporphyrin IX-Fe) and the thiol groups of cysteines

210 ocytochromes and the vinyl groups of heme b (protoporphyrin IX-Fe).

211 e only proton donating/accepting site, using protoporphyrin IX-monomethyl esters (PPIX(MME)) and N-me

212 Structural determinations of Co(3+)-protoporphyrin IX-reconstituted muCOX-2 with alpha-linol

213 d docosahexaenoic acid (DHA) bound to Co(3+)-protoporphyrin IX-reconstituted murine COX-2 to 2.1, 2.4

214 Irradiation of aminolevulinic acid/protoporphyrin IX-sensitized cells with 10 J cm(-2) of 5

215 -propionato coordination dimers of iron(III) protoporphyrin IX.

216 like red chlorophyll catabolite or exogenous protoporphyrin IX.

217 ndent conversion of protoporphyrinogen IX to protoporphyrin IX.

218 chondria, with ferrochelatase adding iron to protoporphyrin IX.

219 rotoporphyrinogen IX to the fully conjugated protoporphyrin IX.

220 the carbon bearing the peroxyl group and the protoporphyrin IX.

221 re blocked by the HO-1 inhibitors Zn- and Sn-protoporphyrin IX.

222 osynthesis by insertion of ferrous iron into protoporphyrin IX.

223 rmediates from 5-aminolevulinic acid through protoporphyrin IX.

224 hetic pathway by inserting ferrous iron into protoporphyrin IX.

225 hares a biosynthetic pathway with haem up to protoporphyrin IX.

226 tizers verteporfin, temoporfin, S3AlOHPc, or protoporphyrin IX.

227 due near the propionate carboxyl function of protoporphyrin IX.

228 catalyzes the insertion of a Mg(2+) ion into protoporphyrin IX.

229 atalyzes the insertion of an Mg(2+) ion into protoporphyrin IX.

230 we determined the binding site for magnesium protoporphyrin IX.

231 Hepatic accumulation of protoporphyrin-IX (PP-IX) in erythropoietic protoporphyr

232 ccumulation of the PDT-activated ALA product protoporphyrin-IX (PpIX) up to 10-fold, mainly by alteri

233 changes, but had increased ductular reaction protoporphyrin-IX accumulation, and MDB-preventive K18 i

234 lirubin and abolished by incubation with tin protoporphyrin-IX and knock down of nuclear factor-E2-re

235 HCR24 and HO-1 small interfering RNA and tin-protoporphyrin-IX treatment abolished these effects.

236 ells with HO-1 small interfering RNA and tin-protoporphyrin-IX treatment did not inhibit the (A-I)rHD

237 ologic induction of HMOX-1 in vivo by cobalt protoporphyrin-IX treatment eradicated intestinal inflam

238 measurement of oxidative stress markers and protoporphyrin-IX were performed.

239 Treatment of the animals with tin protoporphyrin-IX, a global HO inhibitor, or HO-1 small

240 and HO-1 and systemic administration of tin-protoporphyrin-IX, an HO inhibitor, abolished these anti

241 nd the Roussin's red salt ester (mu-S,mu-S')-protoporphyrin-IX-bis(2-thioethyl ester)tetranitrosyldii

242 ng/mL, serum TS level <15%, and erythrocyte protoporphyrin level >1.24 micromol/L.

243 also revealed reduction in serum erythrocyte protoporphyrin levels and improved liver function.

244 ctive evaluation including serum erythrocyte protoporphyrin levels and liver function tests following

245 hanism could allow Gun4 to mediate magnesium protoporphyrin levels both for chlorophyll biosynthesis

246 ted erythropoiesis, including increased zinc protoporphyrin levels, decreased hemoglobin levels, and

247 resulted in elevated erythrocyte and plasma protoporphyrin levels.

248 roid cells exhibit a significant increase in protoporphyrin levels.

249 chlorophyll biosynthetic pathway, magnesium protoporphyrin methyltransferase.

250 than oxidative forms of Mb that retain their protoporphyrin moiety.

251 We choose here the biologically relevant protoporphyrin molecule as the electron mediator.

252 me-containing cytochrome f, diiron magnesium protoporphyrin monomethyl ester cyclase, and Fe2S2-conta

253 A antisense plants accumulate magnesium (Mg) protoporphyrin monomethylester and contain reduced proto

254 LCAA encodes an additional subunit of the Mg protoporphyrin monomethylester cyclase, is required for

255 educed content of CHL27, a subunit of the Mg protoporphyrin monomethylester cyclase.

256 ng RNA or by treatment with 5 mumol/L cobalt protoporphyrin or heme (known inducers of HO-1) decrease

257 g the Bach1 gene or by treatment with cobalt protoporphyrin or heme, decreases HCV replication.

258 Inhibition of HO by Sn(IV)-protoporphyrin or HO-1 small interfering RNA reversed OA

259 ogical inhibition of HO-1 activity using tin protoporphyrin or knockdown of HO-1 prevents the inducti

260 the hypothesis that the main source of toxic protoporphyrin originates from the erythrocytes.

261 eggs with reddish brown speckles produced by protoporphyrin pigment.

262 e interactions of a-SWCNTs with heme (FePP), protoporphyrin (PP), coproporphyrin (CP), and uroporphyr

263 ed P-CNDs were developed via introduction of protoporphyrin (PPD, a photosensitizer) which has great

264 rrochelatase, leading to the accumulation of protoporphyrin predominantly in erythrocytes and hepatoc

265 -/-) mice by weekly administration of cobalt protoporphyrin prevented the increase in plasma creatini

266 n that sequesters the enzyme-bound magnesium protoporphyrin product prior to its delivery to the next

267 e protoporphyrin substrate and the magnesium protoporphyrin product.

268 in erythrocytes, in which a mismatch between protoporphyrin production and the heme requirement of di

269 the form of heme, enclosed within an organic protoporphyrin ring and functioning primarily as a prost

270 induction of HO-1 and was attenuated by tin protoporphyrin (SnPP) IX, an inhibitor of HO-1 activity,

271 Inhibition of HO-1 by tin protoporphyrin (SnPP) or siRNA downregulated Pax3/7-FoxO

272 hibitors (zinc protoporphyrin (ZnPP) and tin protoporphyrin (SnPP)) suppressed the channel in a manne

273 iferation was inhibited by ZnPP, whereas tin protoporphyrin (SnPP), another equally potent HO-1 inhib

274 a competitive inhibitor of HO activity, tin protoporphyrin (SnPP), in protocols affording a composit

275 The effects of the HO inhibitor, tin protoporphyrin (SnPP), on brain electrical activity and

276 abetic and diabetic animals treated with tin protoporphyrin (SnPP, a heme oxygenase-1 enzyme inhibito

277 tro with the heme oxygenase-1 inhibitor, tin protoporphyrin, substantially decreased survival and sig

278 ubunit, and an H subunit that binds both the protoporphyrin substrate and the magnesium protoporphyri

279 man ferrochelatase both with and without the protoporphyrin substrate bound have been determined prev

280 CO and cobalt protoporphyrin suppressed colonic IL-1beta, TNF, and IL-

281 itin, transferrin saturation, or erythrocyte protoporphyrin (the ferritin model).

282 ynthesis, the insertion of ferrous iron into protoporphyrin to form protoheme IX.

283 ociated with a decreased red blood cell zinc protoporphyrin to heme ratio, indicative of porphyrin in

284 ve contributions of hepatic and erythrocytic protoporphyrin to the pathophysiology of EPP remain uncl

285 eding, with or without treatment with cobalt protoporphyrin, to induce HO-1.

286 ytosis, and an increased red blood cell zinc-protoporphyrin-to-heme ratio.

287 8.0) but not with levels of free erythrocyte protoporphyrin, transferrin saturation, or hemoglobin (p

288 Moreover, despite massive elevation of serum protoporphyrin, transplanted mice showed minimal evidenc

289 gas-phase unfolding signatures for lipid and protoporphyrin TSPO binders, molecular classes that like

290 ve effect cannot be emulated by iron or free protoporphyrin, two major chemical components of the hem

291 Cobalt(III) protoporphyrin was used as an internal standard and the

292 ochrome c oxidase by treatment with n-methyl protoporphyrin (which selectively diminishes synthesis o

293 saturation, serum ferritin, and erythrocyte protoporphyrin, with the addition of abnormal hemoglobin

294 IsdC partially buries protoporphyrin within a large hydrophobic pocket that is

295 Rapid application of HO inhibitors (zinc protoporphyrin (ZnPP) and tin protoporphyrin (SnPP)) sup

296 BCs, combined with exogenous prooxidant zinc protoporphyrin (ZnPP) induce a potent tumoricidal respon

297 nzymatic activity, by administration of zinc protoporphyrin (ZnPPIX) at the time of transplantation,

298 nsferrin receptor (TfR; > 8.3 mg/L), or zinc protoporphyrin (ZP; > 80 mumol/mol) concentrations (ie,

299 ildren with iron deficiency, defined as zinc protoporphyrin (ZPP) >= 80 umol/mol heme, were randomly

300 n with CM or SMA, as well as 35 CC, had zinc protoporphyrin (ZPP) concentrations >/=80 mumol/mol heme