ライフサイエンスコーパス: protoporphyrin

1 the attachment mechanism is specific for Fe protoporphyrin.

2 iated by HO using the chemical inhibitor tin protoporphyrin.

3 -positive bacteria) are unable to synthesize protoporphyrin.

4 f core metabolic intermediates that includes protoporphyrin.

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

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

7 ciency does not result in an accumulation of protoporphyrins.

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

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

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

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

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

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 in and, more importantly, the effects of tin protoporphyrin, an inhibitor of HO activity, on the anti

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

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

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

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

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

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

24 ed apoptosis, whereas pretreatment with zinc protoporphyrin attenuated morphine-induced macrophage ap

25 e other hand, pretreatment of MRCs with zinc protoporphyrin attenuated the effect of morphine on both

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

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

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

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

30 ibition of HO activity by treatment with tin protoporphyrin blunted survival advantage in Tg mice and

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

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

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

34 as evidenced by an elevated erythrocyte zinc protoporphyrin concentration.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 an be monitored by following the decrease in protoporphyrin fluorescence intensity (with excitation a

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

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

52 al evidence of recurrent hepatotoxicity from protoporphyrin in the graft liver.

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

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

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

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

57 nd concomitant intracellular accumulation of protoporphyrin intermediates.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 Photosensitizer protoporphyrin IX (PpIX) fluorescence, intracellular loc

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

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

80 at the hemoglobin (Hb) metabolites hemin and protoporphyrin IX (PPIX) interact with the BZ site on th

81 Protoporphyrin IX (PPIX) is considered a conserved endog

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

108 rkness drastically increased the level of Mg-protoporphyrin IX and Mg-protoporphyrin IX monomethyl es

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

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

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

112 and identified the chlorophyll precursor Mg-protoporphyrin IX as a key signalling molecule.

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

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

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

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

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

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

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

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

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

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

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

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

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

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 These transfectants still require hemin or protoporphyrin IX for growth but produce porphyrin when

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

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

137 vo heme oxygenase enzyme inhibition with tin protoporphyrin IX in common bile duct ligation animals w

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

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

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

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

142 s-histidyl N delta 1/N epsilon 2-coordinated protoporphyrin IX iron.

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

144 ct of the ferrochelatase-catalyzed reaction, protoporphyrin IX is fluorescent, and therefore the prog

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 sed the level of Mg-protoporphyrin IX and Mg-protoporphyrin IX monomethyl ester in the PS I-less/ch/L

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

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

156 reduced amounts of Crd1/CHL27 accumulate Mg-protoporphyrin IX monomethyl ester, the substrate of the

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

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

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

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

161 As neither protoporphyrin IX nor coproporphyrin export improved wit

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

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

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

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

166 Protoporphyrin IX synthesis in TMEM14C-deficient erythro

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

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

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

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

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

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

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

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

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

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

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

178 he physiological substrates ferrous iron and protoporphyrin IX under strictly anaerobic conditions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Heme is a complex of iron with protoporphyrin IX, and the iron-containing structure of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

216 like red chlorophyll catabolite or exogenous protoporphyrin IX.

217 ndent conversion of protoporphyrinogen IX to protoporphyrin IX.

218 rotoporphyrinogen IX to the fully conjugated protoporphyrin IX.

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

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

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

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

223 due near the propionate carboxyl function of protoporphyrin IX.

224 osynthesis by insertion of ferrous iron into protoporphyrin IX.

225 rmediates from 5-aminolevulinic acid through protoporphyrin IX.

226 hetic pathway by inserting ferrous iron into protoporphyrin IX.

227 y ferrochelatase inserting ferrous iron into 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 -propionato coordination dimers of iron(III) protoporphyrin IX.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 e show that the tetrapyrrole intermediate Mg-protoporphyrin (Mg-ProtoIX) acts as a signalling molecul

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

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 eased in the presence of HO-1 inhibitor, tin protoporphyrin (SnPPIX).

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

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

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

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

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

283 udies have indicated that accumulation of Mg-protoporphyrin, the first committed precursor of chlorop

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

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

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

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

288 8.0) but not with levels of free erythrocyte protoporphyrin, transferrin saturation, or hemoglobin (p

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

290 Tin protoporphyrin treatment normalized carboxyhemoglobin an

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

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

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

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

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

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

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

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

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

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