ライフサイエンスコーパス: hemopexin

1 s after exposure to hypoxia and heme or heme/hemopexin.

2 plasma retinol binding protein, albumin, and hemopexin.

3 nt importance in cellular protection by heme-hemopexin.

4 es of cellular events upon encountering heme-hemopexin.

5 n, is involved in use of hemoglobin and heme-hemopexin.

6 HO-1 remains responsive to induction by heme-hemopexin.

7 ermediate between those of serum albumin and hemopexin.

8 ted by pre-treatment with the heme scavenger hemopexin.

9 iron, the chaperone proteins haptoglobin and hemopexin.

10 osine residues and one tryptophan residue of hemopexin.

11 ated by treatment with either haptoglobin or hemopexin.

12 LDI-MS analysis for a low abundance protein, hemopexin.

13 ue, haptoglobin, or the heme-binding protein hemopexin.

14 ickle mice by treating them with recombinant hemopexin.

15 ich was similarly nitrated in rabbit and rat hemopexins.

16 Hemopexin, a heme scavenging protein, accumulates in the

17 me with lipopolysaccharide was suppressed by hemopexin, a plasma heme-binding protein.

18 Thus, our findings demonstrate that hemopexin accumulates in the kidneys and worsens kidney

19 creased in SCD mice, which were corrected by hemopexin administration.

20 Hemopexin also inhibited bacterial hemin binding.

21 an-Americans, sE-selectin, VCAM-1, BFL-1 and Hemopexin among Caucasians, and ALCAM, VCAM-1, TFPI and

22 umin), our observations further suggest that hemopexin, an abundant protein with a serum concentratio

23 Hemopexin and a putative hemopexin receptor on hepatocyt

24 ects were largely blocked by heme-scavenging hemopexin and by the PS antagonist annexin-a5, in vitro

25 a genetic dissection of the functions of the hemopexin and catalytic domains of a canonical MMP in Dr

26 tis strain rapidly induced the expression of hemopexin and haptoglobin in the lung and serum, both of

27 had pronounced hemolysis and depleted plasma hemopexin and haptoglobin.

28 the heme and hemoglobin scavenger proteins, hemopexin and haptoglobin.

29 Next, the interaction of hemopexin and hemoglobin in vitro was investigated using

30 Degradation of hemopexin and transferrin in human serum by Kgp was also

31 ns (gingipains R) were also found to degrade hemopexin and transferrin in serum; however, this was ob

32 proteins (serum amyloid A, haptoglobin, and hemopexin) and depleted of paraoxonase-1 after SFA-HFD i

33 ons of the endogenous chelators haptoglobin, hemopexin, and alpha1- microglobulin.

34 s, i.e., alpha-1-antitrypsin, ceruloplasmin, hemopexin, and complement protein C3.

35 APP genes, including thiostatin, fibrinogen, hemopexin, and haptoglobin.

36 organism to degrade hemoglobin, haptoglobin, hemopexin, and transferrin but also with an increase in

37 neutrophil gelatinase-associated lipocalin, hemopexin, and transferrin were increased in FtH(PT-/-)

38 tyrosines reside in the heme-binding site of hemopexin, and we found that one, Tyr-199, interacts dir

39 ibitor p21(WAF1/CIP1/SDI1) generated by heme-hemopexin appear to be of paramount importance in cellul

40 hemopexin knockout mice, further implicating hemopexin as a mediator of iron toxicity in AKI.

41 Utilization of heme-hemopexin as a source of heme by Haemophilus influenzae

42 n bound to haptoglobin and heme complexed to hemopexin as heme sources; however, the mechanism by whi

43 rum albumin (HSA) and myoglobin (Mb) but not hemopexin as iron sources.

44 e development of human plasma-derived Hp and hemopexin as therapeutics for patients with excessive in

45 moproteins hemoglobin and myoglobin, but not hemopexin, as iron sources for bacterial growth.

46 hemoglobin, hemoglobin-haptoglobin, or heme-hemopexin, as iron sources.

47 mice, the administration of human exogenous hemopexin attenuates the inflammatory phenotype of macro

48 -binding proteins TbpA and TbpB, the 100-kDa hemopexin-binding protein HxuA, and the hemoglobin-bindi

49 h stimulation seen with 0.1-0.75 microM heme-hemopexin but HO-1 remains responsive to induction by he

50 Treatment with haptoglobin or hemopexin but not albumin improved the survival rate and

51 reatment with exogenous human haptoglobin or hemopexin can ameliorate adverse effects of resuscitatio

52 bound to haptoglobin and hemin complexed to hemopexin can be used as heme sources, indicating that P

53 ia were able to grow on Hb, heme, myoglobin, hemopexin, catalase, human and bovine serum albumin-heme

54 uA mutant was unable to utilize soluble heme-hemopexin complexes for growth in vitro unless soluble H

55 This protection is sustained by heme-hemopexin complexes in biological fluids that resist oxi

56 uenzae type b culture supernatant bound heme-hemopexin complexes in solution.

57 ults indicated that the heme present in heme-hemopexin complexes is rendered accessible to H. influen

58 e in alpha-1 microglobulin (A1M) relative to hemopexin concentration is associated with acute kidney

59 Significantly, heme binding by hemopexin declined as tyrosine nitration proceeded in vi

60 This study identifies acquired hemopexin deficiency as a risk factor of AKI in SCD and

61 We discovered that hemopexin deficiency in SCD is associated with a compens

62 However, AKI was blocked when hemopexin deficiency in sickle mice was corrected with i

63 one marrow chimeric tools, we confirmed that hemopexin deficiency promotes AKI in sickle mice under h

64 d, Ofori-Acquah et al investigate hemolysis, hemopexin deficiency, and kidney function in sickle cell

65 elevations in heme lead to kidney damage in hemopexin-deficient states, and (2) a compensatory rise

66 The biochemical responses to heme-hemopexin depend on its extracellular concentration and

67 is critical for proMMP-2 activation, whereas hemopexin-dependent dimerization is important for degrad

68 Final studies show that hemopexin directly interacts with FLVCR, which also help

69 The structure of MT1-MMP includes the hemopexin domain (PEX) that is distinct from and additio

70 includes a catalytic domain, a hinge, and a hemopexin domain (PEX), which are followed by a transmem

71 a non-proteolytic mechanism and the proMMP-9 hemopexin domain (PEX9).

72 domains, we confirmed the importance of the hemopexin domain also in primary organoids of the mammar

73 ctivity of MMP3 as the central player to its hemopexin domain and add a new dimension to HSP90beta's

74 t pro-Mmp proteins lacking the COOH-terminal hemopexin domain fail to bind to Mmp-8(-/-)x Mmp-9(-/-)

75 Thus, we find that this MMP hemopexin domain has an apparent specialization for tiss

76 Moreover, the hemopexin domain is also required for MT1-MMP-mediated i

77 ty to TIMP2-inhibited MMP-2, while the MMP-2 hemopexin domain is not required for reactivation.

78 Here we show that the conserved hemopexin domain is required for MT1-MMP-mediated invasi

79 atrix remodeling of the tracheal system, the hemopexin domain is required specifically for tissue inv

80 null alleles with alleles that have specific hemopexin domain lesions, and we also examine phenotypes

81 nding domain of alpha-2-macroglobulin or the hemopexin domain of matrix metalloproteinase 9) induces

82 P-3 with the hinge region and the C-terminal hemopexin domain of MMP-1 did not express any collagenol

83 is substrate by decreasing K(m), just as the hemopexin domain of MMP-1 enhances its triple helical pe

84 The pattern of binding of the free hemopexin domain of MMP-13 was similar to that of the fu

85 that there are two TIMP binding sites on the hemopexin domain of MMP-2: one with high affinity that i

86 racellular matrix component gelatin, and the hemopexin domain of MMP-9 (PEX9) inhibits this degradati

87 protein (MMP-9-PEX), which includes only the hemopexin domain of MMP-9, replicated the activities of

88 An antibody targeting the hemopexin domain of MMP-9, which mediates the interactio

89 xtracellularly, and its interaction with the hemopexin domain of MMP3 is critical for invasion.

90 The noncatalytic hemopexin domain of MMP9 binds to the low-density lipopr

91 , it is proposed that cross-talk between the hemopexin domain of MT1-MMP and adjacent cell surface mo

92 ny component of this pathway, including MMP9 hemopexin domain or claudin-1 siRNA, enables an opioid p

93 Thus, targeting the MMP-14 hemopexin domain represents a novel approach to inhibit

94 vasion and branching, we show that it is the hemopexin domain that directs these processes.

95 N-terminal catalytic domain; 2) a C-terminal hemopexin domain that regulates substrate recognition as

96 an antibody preventing binding of the MMP-9 hemopexin domain to beta1-integrin.

97 The presence of an intact active site and hemopexin domain were required for full angiogenesis-ind

98 her MMP genes, with its C-terminal half (the hemopexin domain) encoded by 4 instead of 6 exons, as in

99 rodomain, (2) the hinge region preceding the hemopexin domain, and (3) the hemopexin domain.

100 s, mainly in the relative orientation of the hemopexin domain, between the pro form and active form o

101 that RWTNNFREY, together with the C-terminal hemopexin domain, is essential for collagenolytic activi

102 egrin alpha(v)beta3 binding to MMP2, via its hemopexin domain, result in significantly reduced cellul

103 PAR1 cleavage by MMP-2 by binding the MMP-2 hemopexin domain, thus favoring the interaction of the e

104 An exosite in the hemopexin domain, which binds the leucine 10 residues C-

105 ctivity of MMP14 but absolutely required the hemopexin domain.

106 MMP in addition to the previously identified hemopexin domain.

107 bition of either the catalytic domain or the hemopexin domain.

108 preceding the hemopexin domain, and (3) the hemopexin domain.

109 Deletion of the hemopexin domains in MT1-, MT2-, MT3-, MT5-, and MT6-MMP

110 hat communications between the catalytic and hemopexin domains of matrix metalloprotease-1 (MMP1) on

111 The hemopexin domains of MMP-12 and -9 each increased k(cat)

112 that the distance between the catalytic and hemopexin domains of MMP1 increases or decreases as the

113 tween two dyes attached to the catalytic and hemopexin domains of MMP1.

114 asiveness in vivo, our data suggest that the hemopexin domains of MT-MMPs should be targeted for the

115 ha(2) I domain interacts with the linker and hemopexin domains of pro-MMP-1, not with the pro-domain.

116 Thus, the COOH-terminal hemopexin domains of pro-Mmp-8 and pro-Mmp-9 are require

117 ecific participation of MT-MMP catalytic and hemopexin domains.

118 the cooperative action of its catalytic and hemopexin domains.

119 There was an increase in CSF hemopexin during this interval.

120 hat the Townes SCD mice had higher levels of hemopexin-free heme in the serum and increased cardiomyo

121 n K, Kgp) can efficiently cleave hemoglobin, hemopexin, haptoglobin, and transferrin.

122 Together, these data argue that hemopexin has a role in assuring systemic iron balance d

123 l Hb and the hemin-scavenger proteins Hp and hemopexin have a strong potential to neutralize the adve

124 to utilize hemoglobin and complexes of heme-hemopexin, heme-albumin, and hemoglobin-haptoglobin and

125 f apolipoprotein A-I (Apo A-I), haptoglobin, hemopexin, hemoglobin, and myeloperoxidase (MPO) were me

126 After 24 h exposure to 10 microM heme-hemopexin, Hepa cells become refractory to the growth st

127 An increase in the heme-binding protein hemopexin (Hpx) 3 months after anthracycline initiation

128 fucosylation and apply it to a comparison of hemopexin (HPX) and complement factor H (CFH), two liver

129 henotypic feature of GS) and iron, decreased hemopexin (Hpx) and Hpt and in up-regulated biliverdin r

130 that homodimerization of MT1-MMP through its hemopexin (Hpx) domain is essential for cleaving type I

131 risingly, in a nonproteolytic manner via its hemopexin (HPX) domain.

132 MP-3) nor the individual catalytic (Cat) and hemopexin (Hpx) domains of MMP-3 interact with the pepti

133 Hemopexin (hpx) facilitates the degradation of extracell

134 Hemopexin (HPX) is overexpressed in the retina of patien

135 Hemopexin (HPX) is the best-characterized permeability f

136 its scavenger proteins, haptoglobin (Hp) and hemopexin (Hx) are significantly increased in apoA-1-con

137 Hemopexin (Hx) is a plasma heme scavenger able to preven

138 Hemopexin (Hx) is an acute-phase protein synthesized by

139 The synergy was strongly suppressed by hemopexin (Hx), an endogenous heme-binding plasma protei

140 roteomic analysis, alpha1-antitrypsin (AAT), hemopexin (HX), and gelsolin (GSN), and tested against c

141 ed this deleterious effect of hemoglobin and hemopexin in proximal tubular cells, implicating iron to

142 However, the function of this accumulated hemopexin in the kidney is unclear.

143 AKI, we found accumulation of hemoglobin and hemopexin in the kidneys localized to the proximal tubul

144 t low (0.01-1 microM) concentrations of heme-hemopexin increase, albeit transiently, the protein carb

145 y state that was inhibited by haptoglobin or hemopexin infusion.

146 Soluble hemopexin inhibits the binding of pro-Mmp-8 and pro-Mmp-

147 a suggest that therapeutic administration of hemopexin is beneficial to counteract heme-driven macrop

148 We propose that during inflammation, apo-hemopexin is nitrated and oxidated in niches of the body

149 However, apo-hemopexin is vulnerable to inactivation by reactive nitr

150 old more efficient when the medium contained hemopexin (K(d) < 1 pm) compared with albumin (K(d) = 5

151 apparent in hemopexin wild type, but not in hemopexin knockout mice, further implicating hemopexin a

152 On the other hand, hemopexin-less MT1-MMP fails to promote cell invasion in

153 In fact, hemopexin-less MT5- and MT6-MMP activate proMMP2 better

154 triple-helix is bound initially by the MMP-1 hemopexin-like (HPX) domain via a four amino acid stretc

155 flexibility between the catalytic (CAT) and hemopexin-like (HPX) domains.

156 ially at an external site, at the top of the hemopexin-like (HX) domain, with a group of four Asp car

157 tivation were not affected by removal of the hemopexin-like C-terminal domain.

158 ant DNA approaches, we demonstrated that the hemopexin-like domain and a nonenzymatic component of th

159 the cloned MMP does not contain a consensus hemopexin-like domain because it lacks a critical trypto

160 epitope in the protein's carboxyl-terminal, hemopexin-like domain identified a post-translational cl

161 roles of specific residues within the MMP-1 hemopexin-like domain in substrate binding and turnover.

162 included the catalytic domain but lacked the hemopexin-like domain lost the proteolytic capacity; how

163 termined that both the linker domain and the hemopexin-like domain of MMP-1 were required for optimal

164 doxycycline disrupts the conformation of the hemopexin-like domain of MMP-13 and the catalytic domain

165 The C-terminal hemopexin-like domain of MMP-2, which interferes with th

166 The hemopexin-like domain of MMP2, which interferes with MMP

167 tin is greatly facilitated by the C-terminal hemopexin-like domain of the enzyme whereas the specific

168 cysteine residue, was not cleaved within the hemopexin-like domain when expressed in COS-7 cells.

169 nt of the short form (lacking the C-terminal hemopexin-like domain) of HS (sHS) has been prepared and

170 (iv) a zinc-binding catalytic domain, (v) a hemopexin-like domain, (vi) a 24-residue hydrophobic dom

171 ncated forms of MMP-8 and MMP-13 lacking the hemopexin-like domain, and a mutant form of truncated MM

172 ent of MMP-2, which comprises the C-terminal hemopexin-like domain, termed PEX, prevents this enzyme

173 istinct residues in blades III and IV of its hemopexin-like domain, while binding of collagen-like tr

174 te, a catalytic domain, a hinge-region and a hemopexin-like domain.

175 c domain with an HEIGHTLGLTH sequence, and a hemopexin-like domain.

176 eats, a catalytic zinc binding region, and a hemopexin-like domain.

177 at room temperature is achieved without the hemopexin-like domain.

178 in protein containing both a catalytic and a hemopexin-like domain.

179 ed MMP genes, whereas the exons encoding the hemopexin-like domains are similar to those of most othe

180 udies indicates that the MMP-1 catalytic and hemopexin-like domains collaborate in collagen catabolis

181 nces, and subsequently the catalytic and the hemopexin-like domains, have been performed.

182 anking the catalytic center and the carboxyl hemopexin-like region.

183 curring human plasma proteins haptoglobin or hemopexin may have beneficial effects in conditions of s

184 ion coexists with blood degradation and that hemopexin may play a role in controlling inflammation in

185 ain K to cleave hemoglobin, haptoglobin, and hemopexin may provide P. gingivalis with a usable source

186 mplicating iron toxicity in the mechanism of hemopexin mediated injury.

187 plasma of patients with SCD and improved by hemopexin-mediated heme scavenging, PPARgamma agonists,

188 red blood cells, treatment with haptoglobin, hemopexin, or albumin did not cause harmful effects.

189 RBCs were given a coinfusion of haptoglobin, hemopexin, or albumin.

190 d CSF ferritin (p = 0.015) and decreased CSF hemopexin (p = 0.007).

191 and MMP-9 with catalytic domain mutation or hemopexin (PEX) domain deletion in wild-type parent cell

192 The hemopexin (PEX) domain of MMP-14 has been proposed as th

193 We previously demonstrated that the hemopexin (PEX) domain of MMP-9 is a prerequisite for en

194 In this work, compounds that target the hemopexin (PEX) domain of MMP-9 were identified using an

195 iations with erythrocyte count, haptoglobin, hemopexin, plasma heme, expression of receptors for heme

196 ice was corrected with infusions of purified hemopexin prior to the induction of hemolytic stress.

197 Hemopexin protects against heme toxicity in hemolytic di

198 Hemopexin protects cells lacking hemopexin receptors by

199 further demonstrate that the heme scavenger hemopexin protects reticulo-endothelial macrophages from

200 resulting in an up to 10-fold higher A1M-to-hemopexin ratio in SCD compared with healthy controls.

201 The A1M-to-hemopexin ratio is associated with markers of hemolysis

202 Hemopexin and a putative hemopexin receptor on hepatocyte membranes may mediate t

203 Hemopexin protects cells lacking hemopexin receptors by tightly binding heme abrogating i

204 However, whether there are sufficient hemopexin receptors on rat hepatocytes to account for th

205 nonspecific heme uptake, whereas cells with hemopexin receptors undergo a series of cellular events

206 eficiency as a risk factor of AKI in SCD and hemopexin replacement as a potential therapy.

207 Pharmacologic inhibition of TLR4 and hemopexin replacement therapy prior to hemin infusion pr

208 and endothelial cells, potentially impairing hemopexin's protective extracellular antioxidant functio

209 mplementary to this process, haptoglobin and hemopexin scavenge and shuttle the red blood cell toxins

210 eased cardiomyopathy, which was corrected by hemopexin supplementation.

211 c sites and the fibronectin type II-like and hemopexin/TIMP2 binding domains.

212 Hemopexin, transferrin, mammaglobin B, and secretoglobin

213 e cell surface in the absence of the MT1-MMP hemopexin, transmembrane, and cytosolic tail domains.

214 y is not confined strictly to the catalytic, hemopexin, transmembrane, or cytosolic domain sequences

215 Hemopexin treatment is a promising novel therapy to prot

216 porphyrin export improved with extracellular hemopexin (versus albumin), our observations further sug

217 the catalytic domain and carboxyl-terminal "hemopexin/vitronectin-like" domain.

218 rosine nitration of in vivo samples and when hemopexin was incubated in vitro with nitrating nitrite/

219 s, levels of serum albumin, transferrin, and hemopexin were found up to 100 times higher than control

220 esize the scavenger proteins haptoglobin and hemopexin, which bind extracellular hemoglobin and heme,

221 eme transport since cobalt-protoporphyrin IX-hemopexin, which binds to the receptor and activates sig

222 YCFQGNQFLR in the heme-binding site of human hemopexin, which was similarly nitrated in rabbit and ra

223 Plasma levels of hemopexin, which were decreased in women with preeclamps

224 nase-1 (an indicator of oxidative stress) in hemopexin wild type compared with knockout mice in both

225 ut mice were compared in both AKI models and hemopexin wild type mice had significantly worse kidney

226 ine in cisplatin-induced AKI was apparent in hemopexin wild type, but not in hemopexin knockout mice,

227 Next, hemopexin wild-type and knockout mice were compared in b

228 Co-incubation of hemopexin with hemoglobin resulted in hemoglobin deposit

229 NK) is rapidly activated by 2-10 microM heme-hemopexin, yet the increased intracellular heme levels a