Tomas Ganz americký lékař
Ganz, Tomáš, 1948-
VIAF ID: 54168590422718222063 (Personal)
Permalink: http://viaf.org/viaf/54168590422718222063
Preferred Forms
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- 100 0 _ ‡a Tomas Ganz ‡c americký lékař
4xx's: Alternate Name Forms (11)
Works
Title | Sources |
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Mice lacking liver-specific β-catenin develop steatohepatitis and fibrosis after iron overload | |
Microanalysis of antimicrobial properties of human fluids | |
Microbicidal/cytotoxic proteins of neutrophils are deficient in two disorders: Chediak-Higashi syndrome and "specific" granule deficiency | |
Microbiology: Gut defence | |
Minihepcidin peptides as disease modifiers in mice affected by β-thalassemia and polycythemia vera | |
Minihepcidins are rationally designed small peptides that mimic hepcidin activity in mice and may be useful for the treatment of iron overload | |
Minihepcidins prevent iron overload in a hepcidin-deficient mouse model of severe hemochromatosis | |
A model for antimicrobial gene therapy: demonstration of human beta-defensin 2 antimicrobial activities in vivo | |
Modulation of hepcidin production during hypoxia-induced erythropoiesis in humans in vivo: data from the HIGHCARE project | |
Molecular and clinical correlates in iron overload associated with mutations in ferroportin. | |
The molecular basis of ferroportin-linked hemochromatosis | |
Molecular cloning and tissue expression of porcine beta-defensin-1. | |
Molecular control of iron transport | |
The molecular mechanism of hepcidin-mediated ferroportin down-regulation | |
Molecular pathogenesis of anemia of chronic disease | |
Monocyte-chemotactic activity of defensins from human neutrophils | |
Mouse models of anemia of cancer | |
Murine 32D c13 cells--a transfectable model of phagocyte granule formation | |
Mutations in HFE2 cause iron overload in chromosome 1q-linked juvenile hemochromatosis | |
The N-terminus of hepcidin is essential for its interaction with ferroportin: structure-function study | |
Neutrophil alpha-defensins cause lung injury by disrupting the capillary-epithelial barrier | |
Neutrophil defense in patients undergoing bone marrow transplantation: bactericidal/permeability-increasing protein (BPI) and defensins in graft-derived neutrophils. | |
Newborn rabbit alveolar macrophages are deficient in two microbicidal cationic peptides, MCP-1 and MCP-2. | |
The NMR structure of human beta-defensin-2 reveals a novel alpha-helical segment | |
Novel Oral Iron Therapies for Iron Deficiency Anemia in Chronic Kidney Disease | |
The opsonizing ligand on Salmonella typhimurium influences incorporation of specific, but not azurophil, granule constituents into neutrophil phagosomes | |
Overexpression and structural study of the cathelicidin motif of the protegrin-3 precursor. | |
Oxygen-independent bactericidal systems. Mechanisms and disorders | |
P105 Decrease in intra- and extra-cellular free iron species and oxidative stress parameters and increase in serum and urinary hepcidin during treatment with deferasirox in iron-loaded patients with MDS | |
Paneth cell trypsin is the processing enzyme for human defensin-5. | |
Paneth cells--guardians of the gut cell hatchery | |
Polymorphic expression of defensins in neutrophils from outbred rats | |
Porcine epithelial beta-defensin 1 is expressed in the dorsal tongue at antimicrobial concentrations | |
Porcine polymorphonuclear leukocytes generate extracellular microbicidal activity by elastase-mediated activation of secreted proprotegrins | |
A Portuguese patient homozygous for the -25G>A mutation of the HAMP promoter shows evidence of steady-state transcription but fails to up-regulate hepcidin levels by iron | |
Posttranslational processing of hepcidin in human hepatocytes is mediated by the prohormone convertase furin | |
Preface: iron and cancer | |
Primary iron overload with inappropriate hepcidin expression in V162del ferroportin disease | |
Primary structures of three human neutrophil defensins | |
The pro region of human neutrophil defensin contains a motif that is essential for normal subcellular sorting. | |
Proinflammatory state, hepcidin, and anemia in older persons | |
Protegrins: new antibiotics of mammalian origin | |
Psychological stress downregulates epidermal antimicrobial peptide expression and increases severity of cutaneous infections in mice | |
Purification and antimicrobial properties of three defensins from rat neutrophils | |
Purification and characterization of defensins from cystic fibrosis sputum | |
Redox cycling metals: Pedaling their roles in metabolism and their use in the development of novel therapeutics | |
Reduced Paneth cell alpha-defensins in ileal Crohn's disease | |
Reduced serum hepcidin levels in patients with chronic hepatitis C. | |
Reduction of serum hepcidin by hemodialysis in pediatric and adult patients | |
Regulation of human beta-defensins by gastric epithelial cells in response to infection with Helicobacter pylori or stimulation with interleukin-1. | |
Regulation of iron acquisition and iron distribution in mammals | |
Results of the first international round robin for the quantification of urinary and plasma hepcidin assays: need for standardization | |
Retraction Notice to: The Hepcidin-Binding Site on Ferroportin Is Evolutionarily Conserved | |
Reversible deficiency of antimicrobial polypeptides in bacterial vaginosis | |
Rings of destruction | |
The role of hepcidin in iron metabolism | |
The role of inflammation, iron, and nutritional status in cancer-related anemia: results of a large, prospective, observational study | |
The role of protegrins and other elastase-activated polypeptides in the bactericidal properties of porcine inflammatory fluids. | |
Sequential evaluation of serum hepcidin in anemic myeloma patients: Study of correlations with myeloma treatment, disease variables, and anemia response | |
Serum hepcidin as a diagnostic test of iron deficiency in premenopausal female blood donors | |
Severe hemochromatosis in a Portuguese family associated with a new mutation in the 5'-UTR of the HAMP gene | |
Small cyclic agonists of iron regulatory hormone hepcidin | |
Soluble hemojuvelin is released by proprotein convertase-mediated cleavage at a conserved polybasic RNRR site | |
The solution structure of human hepcidin, a peptide hormone with antimicrobial activity that is involved in iron uptake and hereditary hemochromatosis | |
Stripline coupling to Josephson oscillators | |
Structure and mapping of the human beta-defensin HBD-2 gene and its expression at sites of inflammation | |
Structure-function analysis of ferroportin defines the binding site and an alternative mechanism of action of hepcidin | |
The structure of porcine protegrin genes | |
Structures of genes for two cathelin-associated antimicrobial peptides: prophenin-2 and PR-39. | |
Suppression of hepcidin during anemia requires erythropoietic activity | |
Synergistic activity of rabbit granulocyte peptides against Candida albicans | |
Synergistic cytolysis mediated by hydrogen peroxide combined with peptide defensins | |
Synthetic hepcidin causes rapid dose-dependent hypoferremia and is concentrated in ferroportin-containing organs | |
Systemic iron homeostasis | |
Testing the iron hypothesis in a mouse model of atherosclerosis | |
Testosterone perturbs systemic iron balance through activation of epidermal growth factor receptor signaling in the liver and repression of hepcidin | |
Testosterone suppresses hepcidin in men: a potential mechanism for testosterone-induced erythrocytosis | |
TGF-alpha regulates TLR expression and function on epidermal keratinocytes | |
Therapeutic recommendations in HFE hemochromatosis for p.Cys282Tyr (C282Y/C282Y) homozygous genotype. | |
Thiol-derivatized minihepcidins retain biological activity. | |
A time course of hepcidin response to iron challenge in patients with HFE and TFR2 hemochromatosis | |
Understanding the structure/activity relationships of the iron regulatory peptide hepcidin | |
Urinary hepcidin excretion in patients with myelodysplastic syndrome and myelofibrosis | |
Urinary hepcidin in congenital chronic anemias | |
Wound healing and expression of antimicrobial peptides/polypeptides in human keratinocytes, a consequence of common growth factors |