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1

Conrad, Marcel E., Jay N. Umbreit, Elizabeth G. Moore, et al. "Separate pathways for cellular uptake of ferric and ferrous iron." American Journal of Physiology-Gastrointestinal and Liver Physiology 279, no. 4 (2000): G767—G774. http://dx.doi.org/10.1152/ajpgi.2000.279.4.g767.

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Separate pathways for transport of nontransferrin ferric and ferrous iron into tissue cultured cells were demonstrated. Neither the ferric nor ferrous pathway was shared with either zinc or copper. Manganese shared the ferrous pathway but had no effect on cellular uptake of ferric iron. We postulate that ferric iron was transported into cells via β3-integrin and mobilferrin (IMP), whereas ferrous iron uptake was facilitated by divalent metal transporter-1 (DMT-1; Nramp-2). These conclusions were documented by competitive inhibition studies, utilization of a β3-integrin antibody that blocked up
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2

Conrad, Marcel E., and Jay N. Umbreit. "Pathways of Iron Absorption." Blood Cells, Molecules, and Diseases 29, no. 3 (2002): 336–55. http://dx.doi.org/10.1006/bcmd.2002.0564.

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3

Miethke, Marcus, and Mohamed A. Marahiel. "Siderophore-Based Iron Acquisition and Pathogen Control." Microbiology and Molecular Biology Reviews 71, no. 3 (2007): 413–51. http://dx.doi.org/10.1128/mmbr.00012-07.

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SUMMARY High-affinity iron acquisition is mediated by siderophore-dependent pathways in the majority of pathogenic and nonpathogenic bacteria and fungi. Considerable progress has been made in characterizing and understanding mechanisms of siderophore synthesis, secretion, iron scavenging, and siderophore-delivered iron uptake and its release. The regulation of siderophore pathways reveals multilayer networks at the transcriptional and posttranscriptional levels. Due to the key role of many siderophores during virulence, coevolution led to sophisticated strategies of siderophore neutralization
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4

Conrad, Marcel E., and Jay N. Umbreit. "Iron absorption: Relative importance of iron transport pathways." American Journal of Hematology 67, no. 3 (2001): 215. http://dx.doi.org/10.1002/ajh.1114.

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5

Shakoury-Elizeh, Minoo, John Tiedeman, Jared Rashford, et al. "Transcriptional Remodeling in Response to Iron Deprivation inSaccharomyces cerevisiae." Molecular Biology of the Cell 15, no. 3 (2004): 1233–43. http://dx.doi.org/10.1091/mbc.e03-09-0642.

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The budding yeast Saccharomyces cerevisiae responds to depletion of iron in the environment by activating Aft1p, the major iron-dependent transcription factor, and by transcribing systems involved in the uptake of iron. Here, we have studied the transcriptional response to iron deprivation and have identified new Aft1p target genes. We find that other metabolic pathways are regulated by iron: biotin uptake and biosynthesis, nitrogen assimilation, and purine biosynthesis. Two enzymes active in these pathways, biotin synthase and glutamate synthase, require an iron-sulfur cluster for activity. I
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6

Perraud, Quentin, Paola Cantero, Béatrice Roche, et al. "Phenotypic Adaption of Pseudomonas aeruginosa by Hacking Siderophores Produced by Other Microorganisms." Molecular & Cellular Proteomics 19, no. 4 (2020): 589–607. http://dx.doi.org/10.1074/mcp.ra119.001829.

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Bacteria secrete siderophores to access iron, a key nutrient poorly bioavailable and the source of strong competition between microorganisms in most biotopes. Many bacteria also use siderophores produced by other microorganisms (exosiderophores) in a piracy strategy. Pseudomonas aeruginosa, an opportunistic pathogen, produces two siderophores, pyoverdine and pyochelin, and is also able to use a panel of exosiderophores. We first investigated expression of the various iron-uptake pathways of P. aeruginosa in three different growth media using proteomic and RT-qPCR approaches and observed three
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7

Spencer, Michelle J. S., Andrew Hung, Ian K. Snook, and Irene Yarovsky. "Iron Surfaces: Pathways to Interfaces." Surface Review and Letters 10, no. 02n03 (2003): 169–74. http://dx.doi.org/10.1142/s0218625x03005025.

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We have used density functional theory to examine the effects of avalanche in adhesion between Fe(100) surfaces, in registry and out of registry. When the central layers of the two surfaces are constrained the surface layers are attracted towards each other, forming a strained crystal region at intermediate interfacial separations. When the constraints in the z-direction are lifted, the surfaces avalanche together. In addition, when the surfaces are allowed to move sideways, we find that an interface initially out of registry will tend to avalanche towards an interface that is in registry.
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8

Theil, Elizabeth C. "Mining ferritin iron: 2 pathways." Blood 114, no. 20 (2009): 4325–26. http://dx.doi.org/10.1182/blood-2009-08-239913.

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9

Chen, Jen-Chih, Scott I. Hsieh, Janette Kropat, and Sabeeha S. Merchant. "A Ferroxidase Encoded by FOX1 Contributes to Iron Assimilation under Conditions of Poor Iron Nutrition in Chlamydomonas." Eukaryotic Cell 7, no. 3 (2008): 541–45. http://dx.doi.org/10.1128/ec.00463-07.

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ABSTRACT When the abundance of the FOX1 gene product is reduced, Chlamydomonas cells grow poorly in iron-deficient medium, but not in iron-replete medium, suggesting that FOX1-dependent iron uptake is a high-affinity pathway. Alternative pathways for iron assimilation, such as those involving ZIP family transporters IRT1 and IRT2, may be operational.
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10

Mercier, Alexandre, and Simon Labbé. "Iron-Dependent Remodeling of Fungal Metabolic Pathways Associated with Ferrichrome Biosynthesis." Applied and Environmental Microbiology 76, no. 12 (2010): 3806–17. http://dx.doi.org/10.1128/aem.00659-10.

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ABSTRACT The fission yeast Schizosaccharomyces pombe excretes and accumulates the hydroxamate-type siderophore ferrichrome. The sib1 + and sib2 + genes encode, respectively, a siderophore synthetase and an l-ornithine N5-oxygenase that participate in ferrichrome biosynthesis. In the present report, we demonstrate that sib1 + and sib2 + are repressed by the GATA-type transcriptional repressor Fep1 in response to high levels of iron. We further found that the loss of Fep1 results in increased ferrichrome production. We showed that a sib1Δ sib2Δ mutant strain exhibits a severe growth defect on ir
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11

Dinkla, Inez J. T., Esther M. Gabor, and Dick B. Janssen. "Effects of Iron Limitation on the Degradation of Toluene by Pseudomonas Strains Carrying the TOL (pWWO) Plasmid." Applied and Environmental Microbiology 67, no. 8 (2001): 3406–12. http://dx.doi.org/10.1128/aem.67.8.3406-3412.2001.

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ABSTRACT Most aerobic biodegradation pathways for hydrocarbons involve iron-containing oxygenases. In iron-limited environments, such as the rhizosphere, this may influence the rate of degradation of hydrocarbon pollutants. We investigated the effects of iron limitation on the degradation of toluene by Pseudomonas putida mt2 and the transconjugant rhizosphere bacterium P. putidaWCS358(pWWO), both of which contain the pWWO (TOL) plasmid that harbors the genes for toluene degradation. The results of continuous-culture experiments showed that the activity of the upper-pathway toluene monooxygenas
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12

Lönnerdal, Bo. "Alternative pathways for absorption of iron from foods." Pure and Applied Chemistry 82, no. 2 (2010): 429–36. http://dx.doi.org/10.1351/pac-con-09-06-04.

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Iron is known to be absorbed from foods in two major forms, heme iron and non-heme iron. Iron status as well as dietary factors known to affect iron absorption has limited effect on heme iron absorption, whereas inhibitors and enhancers of iron absorption have pronounced effects on non-heme iron absorption. The enterocyte transporter for non-heme iron, DMT1, is strongly up-regulated during iron deficiency and down-regulated during iron overload. A transporter for heme iron, HCP1, was recently characterized and is present on the apical membrane of enterocytes. Two other pathways for iron absorp
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13

Perraud, Quentin, Paola Cantero, Mathilde Munier, et al. "Phenotypic Adaptation of Pseudomonas aeruginosa in the Presence of Siderophore-Antibiotic Conjugates during Epithelial Cell Infection." Microorganisms 8, no. 11 (2020): 1820. http://dx.doi.org/10.3390/microorganisms8111820.

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Iron acquisition pathways have often been considered to be gateways for the uptake of antibiotics into bacteria. Bacteria excrete chelators, called siderophores, to access iron. Antibiotic molecules can be covalently attached to siderophores for their transport into pathogens during the iron-uptake process. P. aeruginosa produces two siderophores and is also able to use many siderophores produced by other bacteria. We investigated the phenotypic plasticity of iron-uptake pathway expression in an epithelial cell infection assay in the presence of two different siderophore–antibiotic conjugates,
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14

Zhang, Tianrui, Zhidan Xiao, Chuanliang Liu, et al. "Autophagy Mediates the Degradation of Plant ESCRT Component FREE1 in Response to Iron Deficiency." International Journal of Molecular Sciences 22, no. 16 (2021): 8779. http://dx.doi.org/10.3390/ijms22168779.

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Multivesicular body (MVB)-mediated endosomal sorting and macroautophagy are the main pathways mediating the transport of cellular components to the vacuole and are essential for maintaining cellular homeostasis. The interplay of these two pathways remains poorly understood in plants. In this study, we show that FYVE DOMAIN PROTEIN REQUIRED FOR ENDOSOMAL SORTING 1 (FREE1), which was previously identified as a plant-specific component of the endosomal sorting complex required for transport (ESCRT), essential for MVB biogenesis and plant growth, can be transported to the vacuole for degradation i
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15

Lin, Min-Yu, Yen-Hua Chen, Jey-Jau Lee, and Hwo-Shuenn Sheu. "Reaction pathways of iron-sulfide mineral formation: an in situ X-ray diffraction study." European Journal of Mineralogy 30, no. 1 (2018): 77–84. http://dx.doi.org/10.1127/ejm/2017/0029-2681.

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16

Aring, Luisa, Eun-kyeong Choi, and Young-Ah Seo. "WDR45 Contributes to Iron Accumulation Through Dysregulation of Neuronal Iron Homeostasis." Current Developments in Nutrition 4, Supplement_2 (2020): 1188. http://dx.doi.org/10.1093/cdn/nzaa057_004.

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Abstract Objectives Neurodegeneration with brain iron accumulation (NBIA) is a clinically and genetically heterogeneous group of neurodegenerative diseases characterized by an abnormal accumulation of brain iron and progressive degeneration of the nervous system. β-propeller protein-associated neurodegeneration (BPAN) (OMIM #300,894) is a recently identified subtype of NBIA. BPAN is caused by de novo mutations in the WD repeat domain 45 (WDR45) gene. WDR45 deficiency in BPAN patients and animal models has shown defects in autophagic flux, suggesting a role for WDR45 in autophagy. How WDR45 def
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17

van Beers, Eduard J., Yanqin Yang, Susan Yuditskaya, Nalini Raghavachari, and Gregory J. Kato. "Turnover of Heme-Bound Iron Is Associated with Activation of TLR4 and Chemokine Receptor Pathways in the Peripheral Blood Mononuclear Cell Transcriptome in Sickle Cell Anemia." Blood 120, no. 21 (2012): 819. http://dx.doi.org/10.1182/blood.v120.21.819.819.

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Abstract Abstract 819 Introduction It is widely accepted that inflammation plays an important role in the pathophysiology of Sickle Cell Anemia (SCA). Recently a number of studies indicated that peripheral blood mononuclear cell (PBMC) iron may contribute to inflammation in some diseases In SCA, PBMCs are continuously exposed to high turnover of iron in haptoglobin/hemoglobin complexes and free heme due to severe intravascular hemolysis. Therefore, we hypothesized that PBMC iron flux is marked by altered expression of iron-regulated genes, and in turn associated with the up regulation of genes
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18

Lenoir, Anne, Jean-Christophe Deschemin, Léon Kautz, et al. "Iron-deficiency anemia from matriptase-2 inactivation is dependent on the presence of functional Bmp6." Blood 117, no. 2 (2011): 647–50. http://dx.doi.org/10.1182/blood-2010-07-295147.

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Abstract Hepcidin is the master regulator of iron homeostasis. In the liver, iron-dependent hepcidin activation is regulated through Bmp6 and its membrane receptor hemojuvelin (Hjv), whereas, in response to iron deficiency, hepcidin repression seems to be controlled by a pathway involving the serine protease matriptase-2 (encoded by Tmprss6). To determine the relationship between Bmp6 and matriptase-2 pathways, Tmprss6−/− mice (characterized by increased hepcidin levels and anemia) and Bmp6−/− mice (exhibiting severe iron overload because of hepcidin deficiency) were intercrossed. We showed th
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19

Chhabra, Ravneet, Aishwarya Saha, Ashkon Chamani, Nicole Schneider, Riya Shah, and Meera Nanjundan. "Iron Pathways and Iron Chelation Approaches in Viral, Microbial, and Fungal Infections." Pharmaceuticals 13, no. 10 (2020): 275. http://dx.doi.org/10.3390/ph13100275.

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Iron is an essential element required to support the health of organisms. This element is critical for regulating the activities of cellular enzymes including those involved in cellular metabolism and DNA replication. Mechanisms that underlie the tight control of iron levels are crucial in mediating the interaction between microorganisms and their host and hence, the spread of infection. Microorganisms including viruses, bacteria, and fungi have differing iron acquisition/utilization mechanisms to support their ability to acquire/use iron (e.g., from free iron and heme). These pathways of iron
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20

Adhikari, Bishwo N., Kenneth A. Callicott, and Peter J. Cotty. "Conservation and Loss of a Putative Iron Utilization Gene Cluster among Genotypes of Aspergillus flavus." Microorganisms 9, no. 1 (2021): 137. http://dx.doi.org/10.3390/microorganisms9010137.

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Iron is an essential component for growth and development. Despite relative abundance in the environment, bioavailability of iron is limited due to oxidation by atmospheric oxygen into insoluble ferric iron. Filamentous fungi have developed diverse pathways to uptake and use iron. In the current study, a putative iron utilization gene cluster (IUC) in Aspergillus flavus was identified and characterized. Gene analyses indicate A. flavus may use reductive as well as siderophore-mediated iron uptake and utilization pathways. The ferroxidation and iron permeation process, in which iron transport d
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21

Adhikari, Bishwo N., Kenneth A. Callicott, and Peter J. Cotty. "Conservation and Loss of a Putative Iron Utilization Gene Cluster among Genotypes of Aspergillus flavus." Microorganisms 9, no. 1 (2021): 137. http://dx.doi.org/10.3390/microorganisms9010137.

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Iron is an essential component for growth and development. Despite relative abundance in the environment, bioavailability of iron is limited due to oxidation by atmospheric oxygen into insoluble ferric iron. Filamentous fungi have developed diverse pathways to uptake and use iron. In the current study, a putative iron utilization gene cluster (IUC) in Aspergillus flavus was identified and characterized. Gene analyses indicate A. flavus may use reductive as well as siderophore-mediated iron uptake and utilization pathways. The ferroxidation and iron permeation process, in which iron transport d
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22

Montejano-Ramírez, Vicente, Ernesto García-Pineda, and Eduardo Valencia-Cantero. "Bacterial Compound N,N-Dimethylhexadecylamine Modulates Expression of Iron Deficiency and Defense Response Genes in Medicago truncatula Independently of the Jasmonic Acid Pathway." Plants 9, no. 5 (2020): 624. http://dx.doi.org/10.3390/plants9050624.

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Plants face a variety of biotic and abiotic stresses including attack by microbial phytopathogens and nutrient deficiencies. Some bacterial volatile organic compounds (VOCs) activate defense and iron-deficiency responses in plants. To establish a relationship between defense and iron deficiency through VOCs, we identified key genes in the defense and iron-deprivation responses of the legume model Medicago truncatula and evaluated the effect of the rhizobacterial VOC N,N-dimethylhexadecylamine (DMHDA) on the gene expression in these pathways by RT-qPCR. DMHDA increased M. truncatula growth 1.5-
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23

Mangani, S., I. Bertini, D. Lalli, C. Pozzi, C. Rosa, and P. Turano. "Structural insight into iron pathways in ferritin." Acta Crystallographica Section A Foundations of Crystallography 67, a1 (2011): C772. http://dx.doi.org/10.1107/s0108767311080482.

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24

Williams, Gregory M., and Mark J. Pino. "Isomerization pathways of (acylcycloheptatriene)iron tricarbonyl complexes." Organometallics 11, no. 1 (1992): 345–49. http://dx.doi.org/10.1021/om00037a058.

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25

Szabo, Robert, Cristina Petrișor, Constantin Bodolea, et al. "Effects of Tocilizumab on Inflammation and Iron Metabolism in Critically Ill Patients with COVID-19." Pharmaceutics 15, no. 2 (2023): 646. http://dx.doi.org/10.3390/pharmaceutics15020646.

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COVID-19 produces cytokine-mediated persistent inflammation and is associated with elevated iron stores and low circulating iron. It is believed that central to the pathophysiological mechanism is interleukin 6 and hepcidin. A state of iron overload, termed hyperferritinemia, and inflammatory anemia take place. Both conditions are linked to a worse result in critically ill patients. Blocking the interleukin 6—hepcidin pathway with Tocilizumab could present favorable outcomes. The aim of this study was to evaluate if Tocilizumab influences survival, the occurrence of sepsis, anemia and transfus
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Hwang, Lena H., Erica Seth, Sarah A. Gilmore, and Anita Sil. "SRE1Regulates Iron-Dependent and -Independent Pathways in the Fungal Pathogen Histoplasma capsulatum." Eukaryotic Cell 11, no. 1 (2011): 16–25. http://dx.doi.org/10.1128/ec.05274-11.

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ABSTRACTRegulation of iron acquisition genes is critical for microbial survival under both iron-limiting conditions (to acquire essential iron) and iron-replete conditions (to limit iron toxicity). In fungi, iron acquisition genes are repressed under iron-replete conditions by a conserved GATA transcriptional regulator. Here we investigate the role of this transcription factor, Sre1, in the cellular responses of the fungal pathogenHistoplasma capsulatumto iron. We showed that cells in whichSRE1levels were diminished by RNA interference were unable to repress siderophore biosynthesis and utiliz
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27

Tan, Xuelian, Timothy Cody Ashby, Yuqi Zhu, et al. "Iron Trafficking through Macrophages Regulates Signaling Pathways in Myeloma." Blood 136, Supplement 1 (2020): 2. http://dx.doi.org/10.1182/blood-2020-140372.

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Background Iron is an essential element for cell growth, including cancer cells, and is present in the microenvironment. We have shown that multiple myeloma (MM) cells have abnormal iron metabolism and harbor increased intracellular iron. However, the mechanism by which MM cells retain iron has remained largely elusive. Methods Expression and clinical relevance of the transferrin receptor in MM samples were analyzed in publicly available microarray and RNA-sequencing databases. Macrophages were isolated from C57BL/6J mice and were induced to specific subtypes by cytokines or culturing with MM
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28

Gelvan, D., E. Fibach, EG Meyron-Holtz, and AM Konijn. "Ferritin uptake by human erythroid precursors is a regulated iron uptake pathway." Blood 88, no. 8 (1996): 3200–3207. http://dx.doi.org/10.1182/blood.v88.8.3200.bloodjournal8883200.

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Iron delivery to mammalian cells is traditionally ascribed to diferric transferrin (Tf). We recently reported that human erythroid precursor cells possess specific membranes receptors that bind and internalize acid isoferritin. Here we show that ferritin uptake by these cells is highly regulated and that the internalized ferritin-iron is used for home synthesis and thus, this process could constitute a physiological pathway for iron assimilation. Ferritin was internalized by a specific, saturable process, distinct from the uptake of iron associated with albumin. Ferritin uptake downregulated t
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29

Mladěnka, Přemysl, Radomír Hrdina, Mojmír Hübl, and Tomáš Šimůnek. "The Fate of Iron in The Organism and Its Regulatory Pathways." Acta Medica (Hradec Kralove, Czech Republic) 48, no. 3-4 (2005): 127–35. http://dx.doi.org/10.14712/18059694.2018.40.

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Iron is an essential element involved in many life-necessary processes. Interestingly, in mammals there is no active excretion mechanism for iron. Therefore iron kinetics has to be meticulously regulated. The most important step for regulation of iron kinetics is absorption. The absorption takes place in small intestine and it is implicated that it requires several proteins. Iron is then released from enterocytes into the circulation and delivered to the cells. Iron movement inside the cell is only partially elucidated and its traffic to mitochondia is not known. Surprisingly, the regulation o
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Lehmann, C., S. Islam, S. Jarosch, et al. "The Utility of Iron Chelators in the Management of Inflammatory Disorders." Mediators of Inflammation 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/516740.

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Since iron can contribute to detrimental radical generating processes through the Fenton and Haber-Weiss reactions, it seems to be a reasonable approach to modulate iron-related pathways in inflammation. In the human organism a counterregulatory reduction in iron availability is observed during inflammatory diseases. Under pathological conditions with reduced or increased baseline iron levels different consequences regarding protection or susceptibility to inflammation have to be considered. Given the role of iron in development of inflammatory diseases, pharmaceutical agents targeting this pa
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31

Ayala-Castro, Carla, Avneesh Saini, and F. Wayne Outten. "Fe-S Cluster Assembly Pathways in Bacteria." Microbiology and Molecular Biology Reviews 72, no. 1 (2008): 110–25. http://dx.doi.org/10.1128/mmbr.00034-07.

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SUMMARY Iron-sulfur (Fe-S) clusters are required for critical biochemical pathways, including respiration, photosynthesis, and nitrogen fixation. Assembly of these iron cofactors is a carefully controlled process in cells to avoid toxicity from free iron and sulfide. Multiple Fe-S cluster assembly pathways are present in bacteria to carry out basal cluster assembly, stress-responsive cluster assembly, and enzyme-specific cluster assembly. Although biochemical and genetic characterization is providing a partial picture of in vivo Fe-S cluster assembly, a number of mechanistic questions remain u
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Cheng, Ching-Feng, and Wei-Shiung Lian. "Prooxidant Mechanisms in Iron Overload Cardiomyopathy." BioMed Research International 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/740573.

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Iron overload cardiomyopathy (IOC), defined as the presence of systolic or diastolic cardiac dysfunction secondary to increased deposition of iron, is emerging as an important cause of heart failure due to the increased incidence of this disorder seen in thalassemic patients and in patients of primary hemochromatosis. At present, although palliative treatment by regular iron chelation was recommended; whereas IOC is still the major cause for mortality in patient with chronic heart failure induced by iron-overloading. Because iron is a prooxidant and the associated mechanism seen in iron-overlo
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Pantopoulos, K., G. Weiss, and M. W. Hentze. "Nitric oxide and oxidative stress (H2O2) control mammalian iron metabolism by different pathways." Molecular and Cellular Biology 16, no. 7 (1996): 3781–88. http://dx.doi.org/10.1128/mcb.16.7.3781.

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Several cellular mRNAs are regulated posttranscriptionally by iron-responsive elements (IREs) and the cytosolic IRE-binding proteins IRP-1 and IRP-2. Three different signals are known to elicit IRP-1 activity and thus regulate IRE-containing mRNAs: iron deficiency, nitric oxide (NO), and the reactive oxygen intermediate hydrogen peroxide (H2O2). In this report, we characterize the pathways for IRP-1 regulation by NO and H2O2 and examine their effects on IRP-2. We show that the responses of IRP-1 and IRP-2 to NO remarkably resemble those elicited by iron deficiency: IRP-1 induction by NO and by
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34

Mardini, Louay, Jadwiga Gasiorek, Anna Derjuga, et al. "Antagonistic roles of the ERK and p38 MAPK signalling pathways in globin expression, haem biosynthesis and iron uptake1." Biochemical Journal 432, no. 1 (2010): 145–51. http://dx.doi.org/10.1042/bj20100541.

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Late-stage erythroid cells synthesize large quantities of haemoglobin, a process requiring the co-ordinated regulation of globin and haem synthesis as well as iron uptake. In the present study, we investigated the role of the ERK (extracellular-signal-regulated kinase) and p38 MAPK (mitogen-activated protein kinase) signalling pathways in MEL (mouse erythroleukaemia) cell differentiation. We found that treatment of HMBA (hexamethylene bisacetamide)-induced MEL cells with the ERK pathway inhibitor UO126 results in an increase in intracellular haem and haemoglobin levels. The transcript levels o
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35

Mancinelli, Romina, Luigi Rosa, Antimo Cutone, et al. "Viral Hepatitis and Iron Dysregulation: Molecular Pathways and the Role of Lactoferrin." Molecules 25, no. 8 (2020): 1997. http://dx.doi.org/10.3390/molecules25081997.

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The liver is a frontline immune site specifically designed to check and detect potential pathogens from the bloodstream to maintain a general state of immune hyporesponsiveness. One of the main functions of the liver is the regulation of iron homeostasis. The liver detects changes in systemic iron requirements and can regulate its concentration. Pathological states lead to the dysregulation of iron homeostasis which, in turn, can promote infectious and inflammatory processes. In this context, hepatic viruses deviate hepatocytes’ iron metabolism in order to better replicate. Indeed, some viruse
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36

Lagaditis, Paraskevi O., Peter E. Sues, Alan J. Lough, and Robert H. Morris. "Exploring the decomposition pathways of iron asymmetric transfer hydrogenation catalysts." Dalton Transactions 44, no. 27 (2015): 12119–27. http://dx.doi.org/10.1039/c4dt02799j.

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37

Kontoghiorghes, George, and Christina Kontoghiorghe. "Iron and Chelation in Biochemistry and Medicine: New Approaches to Controlling Iron Metabolism and Treating Related Diseases." Cells 9, no. 6 (2020): 1456. http://dx.doi.org/10.3390/cells9061456.

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Iron is essential for all living organisms. Many iron-containing proteins and metabolic pathways play a key role in almost all cellular and physiological functions. The diversity of the activity and function of iron and its associated pathologies is based on bond formation with adjacent ligands and the overall structure of the iron complex in proteins or with other biomolecules. The control of the metabolic pathways of iron absorption, utilization, recycling and excretion by iron-containing proteins ensures normal biologic and physiological activity. Abnormalities in iron-containing proteins,
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38

Varga, Edit, Ramóna Pap, Gergely Jánosa, Katalin Sipos, and Edina Pandur. "IL-6 Regulates Hepcidin Expression Via the BMP/SMAD Pathway by Altering BMP6, TMPRSS6 and TfR2 Expressions at Normal and Inflammatory Conditions in BV2 Microglia." Neurochemical Research 46, no. 5 (2021): 1224–38. http://dx.doi.org/10.1007/s11064-021-03322-0.

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AbstractThe hormone hepcidin plays a central role in controlling iron homeostasis. Iron-mediated hepcidin synthesis is triggered via the BMP/SMAD pathway. At inflammation, mainly IL-6 pro-inflammatory cytokine mediates the regulation of hepcidin via the JAK/STAT signalling pathway. Microglial cells of the central nervous system are able to recognize a broad spectrum of pathogens via toll-like receptors and initiate inflammatory response. Although the regulation of hepcidin synthesis is well described in many tissues, little is known about the inflammation mediated hepcidin regulation in microg
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Kotla, Nikhil Kumar, Priyata Dutta, Sanjana Parimi, and Nupur K. Das. "The Role of Ferritin in Health and Disease: Recent Advances and Understandings." Metabolites 12, no. 7 (2022): 609. http://dx.doi.org/10.3390/metabo12070609.

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Systemic iron homeostasis needs to be tightly controlled, as both deficiency and excess iron cause major global health concerns, such as iron deficiency anemia, hemochromatosis, etc. In mammals, sufficient dietary acquisition is critical for fulfilling the systemic iron requirement. New questions are emerging about whether and how cellular iron transport pathways integrate with the iron storage mechanism. Ferritin is the intracellular iron storage protein that stores surplus iron after all the cellular needs are fulfilled and releases it in the face of an acute demand. Currently, there is a su
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40

Maru, Devangkumar, Akhil Hothi, Chintan Bagariya, and Anmol Kumar. "Targeting Ferroptosis Pathways: A Novel Strategy for Cancer Therapy." Current Cancer Drug Targets 22, no. 3 (2022): 234–44. http://dx.doi.org/10.2174/1568009622666220211122745.

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Abstract: Ferroptosis is an iron-dependent nonapoptotic kind of regulated cell death resulting from the destruction of redox balance in the cytosol. Unlike apoptosis, ferroptosis is caused by an increase in intracellular iron and lipid peroxides that causes significant damage to the membrane lipid bilayer and mitochondria leading to cell death. Increased iron level in the cell promotes ROS production. Ferroptosis inducer molecules increase ROS production and inhibit the antioxidant defence mechanism to facilitate ferroptosis in cancer cells. Inhibition of GPX4, redox-active iron availability,
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41

Meneghetti, Fiorella, Stefania Villa, Arianna Gelain, et al. "Iron Acquisition Pathways as Targets for Antitubercular Drugs." Current Medicinal Chemistry 23, no. 35 (2016): 4009–26. http://dx.doi.org/10.2174/0929867323666160607223747.

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42

Schmidt, Wolfgang. "Iron Homeostasis in Plants: Sensing and Signaling Pathways." Journal of Plant Nutrition 26, no. 10-11 (2003): 2211–30. http://dx.doi.org/10.1081/pln-120024276.

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Martins, Telma S., Vítor Costa, and Clara Pereira. "Signaling pathways governing iron homeostasis in budding yeast." Molecular Microbiology 109, no. 4 (2018): 422–32. http://dx.doi.org/10.1111/mmi.14009.

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Monti, M., B. Santos, A. Mascaraque, et al. "Oxidation Pathways in Bicomponent Ultrathin Iron Oxide Films." Journal of Physical Chemistry C 116, no. 21 (2012): 11539–47. http://dx.doi.org/10.1021/jp300702d.

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45

Flannery, Andrew R., Rebecca L. Renberg, and Norma W. Andrews. "Pathways of iron acquisition and utilization in Leishmania." Current Opinion in Microbiology 16, no. 6 (2013): 716–21. http://dx.doi.org/10.1016/j.mib.2013.07.018.

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Conroy, Brigid S., Jason C. Grigg, Maxim Kolesnikov, L. Daniela Morales, and Michael E. P. Murphy. "Staphylococcus aureus heme and siderophore-iron acquisition pathways." BioMetals 32, no. 3 (2019): 409–24. http://dx.doi.org/10.1007/s10534-019-00188-2.

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Xiao, Yuanyou, Guocheng Wang, Hong Lei, and Seetharaman Sridhar. "Formation pathways for MgO·Al2O3 inclusions in iron melt." Journal of Alloys and Compounds 813 (January 2020): 152243. http://dx.doi.org/10.1016/j.jallcom.2019.152243.

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48

Chepelev, Nikolai L., and William G. Willmore. "Regulation of iron pathways in response to hypoxia." Free Radical Biology and Medicine 50, no. 6 (2011): 645–66. http://dx.doi.org/10.1016/j.freeradbiomed.2010.12.023.

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Li, Yikun, Xiali Huang, Jingjing Wang, Ruiling Huang, and Dan Wan. "Regulation of Iron Homeostasis and Related Diseases." Mediators of Inflammation 2020 (May 2, 2020): 1–11. http://dx.doi.org/10.1155/2020/6062094.

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The liver is the organ for iron storage and regulation; it senses circulating iron concentrations in the body through the BMP-SMAD pathway and regulates the iron intake from food and erythrocyte recovery into the bloodstream by secreting hepcidin. Under iron deficiency, hypoxia, and hemorrhage, the liver reduces the expression of hepcidin to ensure the erythropoiesis but increases the excretion of hepcidin during infection and inflammation to reduce the usage of iron by pathogens. Excessive iron causes system iron overload; it accumulates in never system and damages neurocyte leading to neurod
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Novikova, I. A. "IRON AND IMMUNE RESPONSE." Health and Ecology Issues, no. 4 (December 28, 2011): 42–48. http://dx.doi.org/10.51523/2708-6011.2011-8-4-7.

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The present-day data on possible pathways of iron influence on human immune response and susceptibility to infections have been considered. The article describes changes of immunologic resistance in conditions of low iron level and mechanisms of iron status disturbance as a consequence of immunostimulation.
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