ライフサイエンスコーパス: HFE

1 HFE 187C>G and, possibly, mitochondrial haplogroup J gav

2 HFE 187C/G heterozygotes (n = 23) had less limb fat loss

3 HFE and Fe-Tf can bind simultaneously to TfR to form a t

4 HFE and Nramp2 (DMT1) genes are reciprocally regulated.

5 HFE and transferrin receptor 2 (TFR2) are each necessary

6 HFE and transferrin receptor 2 (TFR2) are membrane prote

7 HFE C282Y homozygosity had the most marked independent a

8 HFE expression did not affect the mRNA levels of most of

9 HFE gene testing can be used to diagnose hemochromatosis

10 HFE genetic variations did not correlate with outcomes,

11 HFE interacts with the BMP6-SMAD signaling pathway to re

12 HFE is expressed in retinal pigment epithelium (RPE), an

13 HFE is not involved in regulation of BMP6 by iron, but d

14 HFE is the principal regulator of iron homeostasis, and

15 HFE mutations are associated with impaired hepatic bone

16 HFE mutations have traditionally been associated with th

17 HFE(-/-) livers were overloaded with ferritin but had lo

18 HFE, a major regulator of iron (Fe) homeostasis, has bee

19 HFE-associated hemochromatosis (HH) defined as homozygos

20 HFE-associated hemochromatosis is characterized by abnor

21 of BMP/Smad-related genes was examined in 20 HFE-HH males with significant iron overload, and compare

22 HAMP and HJV in 96 patients with PCT and 88 HFE C282Y homozygotes with marked hepatic iron overload.

23 g highly fluorinated electrolytes based on a HFE solvent.

24 Identifying the adaptive HFE variants in Asians will not only elucidate the evolu

25 In addition, HFE potentially modulates cellular iron uptake by intera

26 n stores and serum hepcidin level across all HFE genotypes.

27 in levels than subjects without iron for all HFE genotypes (P < 0.0001).

28 ogical role for this competition in altering HFE trafficking patterns.

29 Although HFE mutations (especially the most frequent H63D mutatio

30 study was to examine the relationships among HFE genotype, serum hepcidin level, hepatic iron deposit

31 hemochromatosis, which is often caused by an HFE mutation, may have retinal iron overload predisposin

32 elded in subjects with at least 1 copy of an HFE variant compared with wild-type subjects.

33 American ethnicity (OR: 1.8; P = 0.001) and HFE C282Y heterozygosity (OR: 1.9; P = 0.003) were assoc

34 rican ethnicity (OR </=0.9; P </= 0.049) and HFE C282Y (OR </=0.84; P </= 0.060) were independently a

35 We used the AGS and MKN1 gastric cancer and HFE-145 immortalized non-neoplastic gastric mucosa cell

36 s) in the COMT, NTRK1, BDNF, ErbB4, CLU, and HFE genes, and investigated their individual and aggrega

37 candidate SNPs (COMT, NTRK1, ErbB4, CLU, and HFE) explained approximately 6% of the variance in the a

38 tive age and are influenced by ethnicity and HFE C282Y.

39 ered by LPS, indicating that ferroportin and HFE protein down-regulation alone are insufficient to ma

40 The difference between halothane and HFE on channel dynamics can be attributed to their disti

41 or age, sex, ethnicity, body mass index, and HFE genotype status.

42 m was to assess the relationship of iron and HFE genetic variations to progression and outcomes in th

43 and transferrin saturation measurements and HFE genotyping.

44 Ectopic CagA expression in AGS, MKN1 and HFE-145 cells showed a significant increase in HER-2 gen

45 We conclude that, through Nef and HFE, HIV-1 directly regulates cellular iron metabolism,

46 imethyl ether, ammonia, R-152a, propane, and HFE-152a all performed effectively in a 1 ton window uni

47 s a cross-sectional study of iron status and HFE mutations in primary care patients at 5 centers in t

48 ndex, blood donation, menopausal status, and HFE genotype.

49 s associated with transferrin levels, TF and HFE, and found that a commonly carried polymorphism (H63

50 on transport protein transferrin (Fe-Tf) and HFE, the protein mutated in patients with the iron overl

51 gments physically disparate from the TfR and HFE binding sites.

52 TfR2-TfR1 and HFE-HLA-B7 chimeras were generated to map the domains of

53 eir similar overall structures with TfR2 and HFE, respectively.

54 coproteins transferrin receptor 2 (TfR2) and HFE are associated with hereditary hemochromatosis.

55 beta-Thalassemia and HFE-related hemochromatosis are 2 of the most frequently

56 ion by known iron metabolic proteins such as HFE, hemojuvelin, and transferrin receptor 2 are expandi

57 could result from direct competition between HFE and Fe-Tf for their overlapping binding sites on eac

58 Interactions between HFE and transferrin receptor 1 (TfR1) have been mapped t

59 ls were fit to evaluate interactions between HFE genotype and particulate matter < or = 2.5 microm in

60 mally or highly fortified test meals between HFE C282Y-heterozygous and wild-type control subjects.

61 tudy was to examine the relationship between HFE mutations and histological severity in a large North

62 s studies examining the relationship between HFE mutations and severity of nonalcoholic steatohepatit

63 Compound heterozygotes (those who had both HFE C282Y and H63D mutations) absorbed more nonheme (but

64 R2 lower hepcidin levels, implying that both HFE and TfR2 are necessary for regulation of hepcidin ex

65 eously to TfR to form a ternary complex, but HFE binding to TfR lowers the apparent affinity of the F

66 pathway to regulate hepcidin expression, but HFE is not necessary for hepcidin induction by BMP6.

67 in, but it is hindered little, if at all, by HFE.

68 In Caucasians, C282Y HFE homozygotes are numerous, but they are only predispo

69 Patients with C282Y HFE hemochromatosis also have inappropriately low hepcid

70 spite increased iron level in cells carrying HFE H63D, it appeared that ER stress was not responsive

71 ssible, and testing for the common causative HFE mutations is now widely available in clinical labora

72 As in HepG2 cells, HFE expression inhibited NTBI uptake by approximately 50

73 We characterized HFE polymorphisms 845G>A and 187C>G and European mitocho

74 carrying the mouse equivalent of the common HFE C282Y human disease-causing mutation (murine C294Y)

75 opean ancestry at the 6p22 region containing HFE and LRRC16A was associated with higher Hgb.

76 anemia (ferritin < 10 ng/mL), iron-depleted HFE hemochromatosis, and juvenile hemochromatosis.

77 ene most often mutated in the human disease, HFE, has been deleted (Hfe(/)).

78 Mutations in either HFE or TfR2 lower hepcidin levels, implying that both HF

79 omponent was observed in persons with either HFE variant.

80 hromatosis include defects in genes encoding HFE, transferrin receptor 2, ferroportin, hepcidin, and

81 the risk of recurring heart failure events (HFEs) was a pre-specified substudy of MADIT-CRT (Multice

82 fically during brief, high-frequency events (HFEs) in the local field potential that are similar to r

83 life of Zip14 is lower in cells that express HFE.

84 ed ER stress, the number of cells expressing HFE H63D in early apoptosis was increased moderately.

85 in another cell line, HeLa cells expressing HFE under the tetracycline-repressible promoter were tra

86 TfR2, HJV, BMP6, and, to a lesser extent, HFE are required for the hepcidin response to acute iron

87 significant reduction in the risk of a first HFE (hazard ratio [HR]: 0.54, 95% confidence interval [C

88 iduals homozygous for the variant coding for HFE p.Cys282Tyr and 397 compound heterozygotes with vari

89 vel of the majority of adult homozygotes for HFE mutations does not rise over long periods of time, e

90 plasmic domain of HFE might be necessary for HFE-mediated induction of hepcidin.

91 confirmed all seven cases were negative for HFE mutations C282Y and H63D.

92 These results point to a role for HFE in inhibition of iron efflux in HT29 cells.

93 tinction suggests a multifunctional role for HFE that is dependent upon expression levels of proteins

94 This review considered genetic screening for HFE-related hereditary hemochromatosis in C282Y homozygo

95 my constitutes the established treatment for HFE-related hemochromatosis.

96 y treatment for potential complications from HFE-related hereditary hemochromatosis (HH).

97 Hearts from HFE(-/-) mice with hemochromatosis contained slightly mo

98 282Y heterozygotes have been identified from HFE gene sequencing.

99 1, ATP2B1, SH2B3/ATXN2, CSK, CYP17A1, FURIN, HFE, LSP1, MTHFR, SOX6) at array-wide significance (P <

100 r that mimics a human haemochromatosis gene (HFE) mutation.

101 ndrial haplogroups and hemochromatosis gene (HFE) polymorphisms have been associated with ART-induced

102 tion in the hereditary hemochromatosis gene (HFE).

103 in the hereditary hemochromatosis (hh) gene (HFE) explain the siderosis in approximately 20% patients

104 ci, some including known iron-related genes (HFE, SLC40A1, TF, TFR2, TFRC, TMPRSS6) and others novel

105 de significance, and 6 (FIGN, ULK4, GUCY1A3, HFE, TBX3-TBX5, and TBX3) at a suggestive level of P = 1

106 he prevalence of heterozygous C282Y and H63D HFE mutations was 14.3% and 21.4%, respectively, in the

107 biopsy and genotyping for the C282Y and H63D HFE mutations were performed in all subjects.

108 regulatory protein activity than WT or H63D HFE.

109 Similar to halothane, HFE had no measurable effects on the gA channel structur

110 In contrast to halothane, HFE produced no significant changes in the gA channel dy

111 e TfR1 cofactor hereditary hematochromatosis HFE protein.

112 Genotyping for hemochromatosis (HFE) gene status was performed.

113 ed in two genetic models of hemochromatosis (HFE-null mouse and HJV-null mouse) and in two nongenetic

114 nteracts with its receptor, hemochromatosis (HFE) protein, to modulate iron responsive pathways in ca

115 ts at the transferrin (TF), hemochromatosis (HFE), fatty acid desaturase 2 (FADS2)/myelin regulatory

116 cipants that tested for the hemochromatosis (HFE) C282Y genotype and iron status.We sought to determi

117 The protein product of the hemochromatosis (HFE) gene modulates uptake of iron and divalent cations

118 pecific polymorphism in the hemochromatosis (HFE) gene, H63D, is over-represented in neurodegenerativ

119 m (H63D at rs1799945) in the hemochromatotic HFE gene was associated with white matter fiber integrit

120 osis-associated proteins: HJV (hemojuvelin), HFE (hemochromatosis protein), and TfR2 (transferrin rec

121 emochromatosis-related proteins hemojuvelin, HFE and transferrin receptor 2, also regulates hepcidin

122 he presence and absence of hexafluoroethane (HFE), which structurally resembles the potent anesthetic

123 ncentration (HIC), hepatic iron index (HII), HFE mutation status, and survival after liver transplant

124 Hemojuvelin (HJV), HFE, and transferrin receptor-2 (TfR2) facilitate this p

125 s the other BMPs in association with the HJV/HFE/TfR2 complex; they provide an explanation for the co

126 one regulator of systemic iron homeostasis, HFE, is expressed in the RPE.

127 naling has not been characterized in a human HFE-HH cohort to date.

128 echocystis sp. PCC 6803 rbcL gene, and human HFE.

129 In this work, we report a hydrofluoroether (HFE) solvent-based electrolyte for electrochemical proce

130 ent emissions for several hydrofluoroethers (HFEs) and other potential replacements were compared to

131 To determine if HFE had a similar effect on Zip14 in another cell line,

132 ure episodes after a first post-implantation HFE.

133 er of insulin resistance, and iron burden in HFE hemochromatosis.

134 ession of BMP6 was appropriately elevated in HFE-HH compared to controls (P = 0.02), likely related t

135 e associated with elevated serum ferritin in HFE C282Y homozygotes.

136 ent studies suggest that the risk for HCC in HFE -associated HH may be much lower and occurs predomin

137 mapped to the alpha1- and alpha2-helices in HFE and to the helical domain of TfR1.

138 t ARNTL, TF, and TFR2 affect iron markers in HFE C282Y homozygotes at risk for hemochromatosis.

139 ho were homozygous for the C282Y mutation in HFE and had undergone a liver biopsy with quantification

140 However, we found that the same mutation in HFE does not affect the TfR2/HFE interaction.

141 Mutations in HFE are responsible for approximately 90% of cases of th

142 Mutations in HFE are the most common cause of the iron-overload disor

143 Mutations in HFE cause the most common form of hereditary hemochromat

144 Mutations in HFE lead to hereditary hemochromatosis (HH) because of i

145 In hereditary hemochromatosis, mutations in HFE lead to iron overload through abnormally low levels

146 Mutations in HFE, HJV, and TfR2 cause autosomal-recessive forms of he

147 Mutations in HFE, transferrin receptor 2 (Tfr2), hemojuvelin (HJV), o

148 on overload arising mostly from mutations in HFE.

149 esting that impaired BMP signaling occurs in HFE-HH.

150 es have confirmed that disease penetrance in HFE-related hereditary hemochromatosis is lower than pre

151 is associated with a high-iron phenotype in HFE C282Y homozygotes and may participate in hepcidin re

152 itors of BMP signaling, were up-regulated in HFE-HH compared to controls (P = 0.001 and P = 0.018, re

153 ith variability of iron overload severity in HFE-associated hemochromatosis, we performed exome seque

154 ntial for normal iron homeostasis, including HFE, transferrin receptor 2 (TfR2), and hemojuvelin, fun

155 lp hepcidin to monitor serum iron, including HFE and, in rarer instances, transferrin-receptor 2 and

156 The iron accumulation in HIV-1-infected HFE-expressing macrophages was paralleled by an increase

157 relation between food and nutrient intakes, HFE genotype, and iron status.

158 ellular iron content [anti-import: TFRC(Low)/HFE(High); or pro-export: SLC40A1 (ferroportin)(High)/HA

159 s in the heart, despite the absence of major HFE gene mutations.

160 rformed exome sequencing of DNA from 35 male HFE C282Y homozygotes with either markedly increased iro

161 nt iron overload, and compared to seven male HFE wild-type controls using quantitative real-time reve

162 ygous mutant or compound heterozygous mutant HFE genotypes.

163 that express either wild-type (WT) or mutant HFE to determine the cellular consequences of the mutant

164 hemochromatosis patients expressing mutated HFE.

165 sly associated with these traits (HBS1L-MYB, HFE, TMPRSS6, TFR2, SPTA1) as well as new associations (

166 opathological papers on several forms of non-HFE hemochromatosis were published and Wilson's disease

167 required to identify patients with rare, non-HFE forms of the disease.

168 < 8.56 x 10(-7) at four further loci (NPR3, HFE, NOS3, and SOX6).

169 s and cardiac failure despite the absence of HFE mutations.

170 Our results indicate parallel adaptation of HFE gene in Europeans and Asians with different genetic

171 further interrogate the structural basis of HFE function in the pathophysiology of HH.

172 It is shown that the characteristics of HFE hemochromatosis can be reproduced by increasing the

173 gnaling underlies the hepcidin deficiency of HFE-HH.

174 d mice homozygous for targeted disruption of HFE, beta(2)-microglobulin, and for a truncating mutatio

175 esized that the small, cytoplasmic domain of HFE might be necessary for HFE-mediated induction of hep

176 dues 104 and 250 and to the alpha3 domain of HFE, both of which differ from the TfR1/HFE interacting

177 We examined the effect of HFE mutations on posttransplantation survival in patient

178 of Zip14 with siRNA abolished the effect of HFE on NTBI uptake.

179 The effect of HFE was independent of its interaction with TF receptor

180 uggesting that some or all of the effects of HFE on iron homeostasis result from competition with Fe-

181 In the present study, the expression of HFE and the HFE-interacting proteins TfR1, TfR2, and bet

182 Expression of HFE decreased both TBI and NTBI uptake.

183 Expression of HFE has not been investigated in the retina.

184 Expression of HFE in intact retina was investigated by in situ hybridi

185 his is the first report on the expression of HFE in the retina.

186 RT-PCR was used to detect the expression of HFE mRNA in neural retina and the RPE-eyecup.

187 RT-PCR showed predominant expression of HFE mRNA in the RPE-eyecup.

188 Expression of HFE-interacting proteins was also analyzed using similar

189 ndations on returning incidental findings of HFE variants in individuals undergoing genome-scale sequ

190 both TfR1 and TfR2 binding, a mutant form of HFE (W81AHFE) that has an approximately 5,000-fold lower

191 cellular consequences of the mutant forms of HFE.

192 of this work was to assess the influence of HFE mutations and serum and hepatic measures of iron sta

193 The specific localization of HFE and its interacting proteins, TfR1 and TfR2, at the

194 abrogated by disease-associated mutations of HFE and TFR2, and that TFR2 competes with TFR1 for bindi

195 Mutations of HFE are best known as being associated with cellular iro

196 regulation is central to the pathogenesis of HFE hemochromatosis.

197 Because the penetrance of HFE hemochromatosis is low, traditional population scree

198 involved as a modulator of the penetrance of HFE hemochromatosis since fat mass is associated with ov

199 RSS6 might modify the clinical penetrance of HFE-associated hereditary hemochromatosis, raising the p

200 Presence of HFE mutations, in particular the H63D variation, was ass

201 ncommon disorder, although the prevalence of HFE (High Iron) 282 Cys --> Tyr (C282Y) homozygosity is

202 significant differences in the prevalence of HFE gene mutations among subjects with fibrosis (35.5%)

203 PCT was significantly reduced, regardless of HFE genotype, when compared with patients with hh but wi

204 hepcidin regulation in NAFLD, regardless of HFE genotype.

205 atments resulted in rapid down-regulation of HFE protein [encoded by the hemochromatosis gene (Hfe)]

206 In this study, we investigated the role of HFE in the regulation of both transferrin-bound iron (TB

207 However, the role of HFE in this process was never explored.

208 sm, hemojuvelin, and new data on the role of HFE mutations in the development of iron overload.

209 rivation of hepatic stem cells, the roles of HFE protein and other hepatic and intestinal transport p

210 dominantly in hepatocytes, the major site of HFE expression in the liver.

211 osine-based motif in the cytoplasmic tail of HFE.

212 The occurrence of HFEs greatly increased the risk of death.

213 of place-specific neural activity outside of HFEs.

214 imilar magnitude of reduction in the risk of HFEs subsequent to a first post-enrollment event (HR: 0.

215 chemically orthogonal electrolytes based on HFE solvents do not dissolve organic perovskite films an

216 rmed the signatures of positive selection on HFE in Asian populations and identified a candidate adap

217 Moreover, natural selection on HFE may have contributed to elevated Fe absorption in As

218 Thirty-five percent carried at least one HFE gene mutation.

219 mutations such that one TfR chain binds only HFE and the other binds only Fe-Tf.

220 Inhibition of either beta2-M or HFE results in reversion of EMT.

221 ecessive disorder associated with pathogenic HFE variants, most commonly those resulting in p.Cys282T

222 ates the macrophage-expressed MHC 1b protein HFE, which regulates iron homeostasis and is mutated in

223 The hereditary hemochromatosis protein HFE promotes the expression of hepcidin, a circulating h

224 press the hereditary hemochromatosis protein HFE these cells have increased ferritin levels.

225 Finally, the protein HFE associates with the transferrin receptor and is part

226 Defects in human hemochromatosis protein (HFE) cause iron overload due to reduced hepatic hepcidin

227 Mutations in hemochromatosis protein (HFE) or transferrin receptor 2 (TFR2) cause hereditary h

228 s in the hereditary hemochromatosis protein (HFE), transferrin-receptor 2 (TfR2), hemojuvelin, hepcid

229 nctional hereditary hemochromatosis protein, HFE, causes iron overload predominantly in hepatocytes,

230 s of the hereditary hemochromatosis proteins HFE and transferrin receptor 2 may intersect with the BM

231 ation therapy for the reduction in recurring HFEs was maintained after the occurrence of a first post

232 Data with regard to recurring HFEs were prospectively collected for all 1,820 MADIT-CR

233 A significantly reduced HFE expression was observed in individuals carrying T/T

234 In model cell lines, Nef reroutes HFE to a perinuclear structure that overlaps the trans-G

235 g for C282Y (rs1800562) and H63D (rs1799945) HFE mutations was performed in 786 adult subjects in the

236 The occurrences of first and second HFEs were associated with 7- and nearly 19-fold respecti

237 To test whether similar HFE residues are important for both TfR1 and TfR2 bindin

238 ion was performed in the fluorinated solvent HFE-7100.

239 D for the prevention of first and subsequent HFEs was pronounced among patients with left bundle bran

240 only risk for nonfatal first- and subsequent-HFEs was assessed by Cox proportional hazards and Anders

241 y down-regulates naturally expressed surface HFE in a Nef-dependent manner.

242 network, causing a 90% reduction of surface HFE.

243 finding indicates that the TfR2/HFE and TfR1/HFE interactions are distinct.

244 n of HFE, both of which differ from the TfR1/HFE interacting domains.

245 We further observed that, unlike TfR1/HFE, Tf does not compete with HFE for binding to TfR2 an

246 This finding indicates that the TfR2/HFE and TfR1/HFE interactions are distinct.

247 ame mutation in HFE does not affect the TfR2/HFE interaction.

248 ere generated to map the domains of the TfR2/HFE interaction.

249 tely 5,000-fold lower affinity for TfR1 than HFE was employed.

250 Here we demonstrate that HFE and TFR2 interact in cells, that this interaction is

251 Furthermore, we found that HFE increases TfR2 levels in hepatic cells independent o

252 We hypothesize that HFE modulates erythropoiesis by affecting dietary iron a

253 patients with HFE mutations, indicating that HFE regulates hepcidin.

254 hybridization in intact retina revealed that HFE mRNA is expressed almost exclusively in RPE Immunofl

255 d immunogold electron microscopy showed that HFE protein was specifically associated with the basolat

256 These results suggest that HFE decreases the stability of Zip14 and therefore reduc

257 The HFE C282Y heterozygous mutation is associated with advan

258 present study, the expression of HFE and the HFE-interacting proteins TfR1, TfR2, and beta2M were ana

259 Patients with HH carrying the HFE gene who were homozygous for the Cys282Tyr mutation,

260 Studies on heterozygotes for the HFE mutation were excluded.

261 pathological forms based on mutations in the HFE gene and other iron-homeostatic genes such as transf

262 onstrate that the different mutations in the HFE gene have unique effects on the cells and provide in

263 Mutations in the HFE gene may influence development or progression of chr

264 verload disorder results from defects in the HFE gene product, a major histocompatibility complex cla

265 mozygous for the p.Cys282Tyr mutation in the HFE gene underwent LT between 1999 and 2008.

266 ar that the two most common mutations in the HFE gene, H63D and C282Y, may be genetic modifiers for r

267 ide polymorphism (SNP) discrimination in the HFE gene, responsible for hereditary hemochromatosis.

268 he disease and results from mutations in the HFE gene.

269 The C282Y mutation in the HFE hemochromatosis gene occurs more commonly in autoimm

270 n, has been associated with mutations in the HFE, transferrin receptor-2 (TfR2), and hemojuvelin (HJV

271 onvention, because it is not a member of the HFE family.

272 the variable penetrance of mutations of the HFE gene and the absence of any definitive trials addres

273 The discovery of the HFE gene in 1996 heralded a decade of major advances in

274 carry the missense Cys282Tyr mutation of the HFE gene.

275 osis is that caused by C282Y mutation of the HFE gene.

276 H-SY5Y, we reported that the presence of the HFE H63D protein activated the unfolded protein response

277 thway may be defective in the absence of the HFE protein.

278 s for future study about the function of the HFE protein.

279 Expression of the HFE-interacting proteins TfR1, TfR2, and beta2M was also

280 Overall, our studies indicate that the HFE H63D mutant protein is associated with prolonged ER

281 ansferrin concentrations transmitted through HFE, TfR2, and HJV augment BMP receptor sensitivity to B

282 total of 1051 out of 1145 subjects agreed to HFE mutational testing (C282Y, H63D, S65C).

283 that TFR2 competes with TFR1 for binding to HFE.

284 should not pose an additional health risk to HFE C282Y heterozygotes.

285 Two HFE polymorphisms (C282Y and H63D) associated with incre

286 by similar results using both the wild type HFE and the W81A mutant that binds TF receptor 1 with gr

287 ted ex vivo macrophages expressing wild-type HFE, but this effect was lost with Nef-deleted HIV-1 or

288 Uncommon HFE mutations resulting in phenotypic hemochromatosis am

289 rly diagnosis of hepatic iron overload using HFE gene testing and iron depletion prior to liver trans

290 a and human embryonic kidney 293 cells where HFE has been shown to inhibit TF-mediated iron uptake re

291 To more definitively determine whether HFE regulates hepcidin expression through an interaction

292 We investigated whether HFE is involved in BMP6-SMAD regulation of hepcidin expr

293 ar iron overload, but the mechanism by which HFE H63D might increase the risk of neuron degeneration

294 and sustained virologic responses (20% with HFE mutation vs 14% sustained virologic response without

295 t, unlike TfR1/HFE, Tf does not compete with HFE for binding to TfR2 and that binding is independent

296 nd for roles in host homeostasis (e.g., with HFE and ZAG).

297 tly, TfR2 was also reported to interact with HFE in transfected mammalian cells.

298 mochromatosis mouse models and patients with HFE mutations, indicating that HFE regulates hepcidin.

299 are significantly lower among patients with HFE-associated HH.

300 y component between persons with and without HFE variants was significant (P for interaction=0.02).

301 vs 14% sustained virologic response without HFE mutation; P = .009).