33 results about "Ferroportin" patented technology

Positional cloning has been carried out to identify the gene responsible for the hypochromic anemia of the zebrafish mutant weissherbst. The gene, ferroportin1, encodes a novel multiple-transmembrane domain protein, expressed in the yolk sac. Zebrafish ferroportin1 is required for the transport of iron from maternally-derived yolk stores to the circulation, and functions as an iron exporter when expressed in Xenopus oocytes. Human and mouse homologs of the ferroportin1 gene have been identified. The invention includes isolated polynucleotides, vectors and host cells comprising nucleotide sequences encoding Ferroportin1 proteins and variants thereof, including those having iron transport function. The invention also includes polypeptides encoded by ferroportin1 genes and variants of such polypeptides, and fusion polypeptides comprising a Ferroportin1 or a portion thereof. Methods to produce a Ferroportin1, methods to produce antibodies to a Ferroportin1 and methods to identify agents binding to a Ferroportin1, which can be inhibitors or enhancers of Ferroportin1 iron transport activity, are also described. Inhibitors of Ferroportin1 activity can be used in a therapy for hemochromatosis.

An L-amino acid is produced by culturing an L-amino acid-producing bacterium which belongs to the Enterobacteriaceae family and which has been modified so that the activity of an iron transporter is increased by enhancing expression of one or more genes of the following genes: tonB gene, fepA gene, and fecA.

Provided is a megakaryocyte and/or platelet production method, enabling to produce a megakaryocyte and/or platelet from mesenchymal cells such as preadipocytes in a relatively short period of time, simply, in a large amount and at lower cost or more efficiently in vitro and a method for producing TPO simply and in a larger amount. A first invention is a method for producing a megakaryocyte and/or platelet, comprising culturing a mesenchymal cell in a mesenchymal cell culturing basic medium containing an iron ion and an iron transporter and collecting megakaryocytes and/or platelets from a culture. A second invention is a method for producing thrombopoietin, comprising culturing a mesenchymal cell or mesenchymal cell-derived megakaryocyte in a mesenchymal cell culturing basic medium containing an iron ion and an iron transporter and collecting thrombopoietin from a culture. A third invention is a method for producing thrombopoietin, comprising culturing a preadipocyte in a preadipocyte culturing basic medium containing dexamethasone, 3-isobutyl-1-methylxanthine and insulin and collecting thrombopoietin from a culture.

Disclosed herein S-alkylated hepcidin peptides and methods of making and using thereof. In some embodiments, the present invention is directed to an S-alkylated hepcidin peptide having the following Structural Formula IA or IB. In some embodiments, the present invention is directed to a composition comprising at least one S-alkylated hepcidin peptide of the present invention. In some embodiments, the present invention is directed to a method of binding a ferroportin or inducing ferroportin internalization and degradation which comprises contacting the ferroportin with at least one S-alkylated hepcidin peptide of the present invention. In some embodiments, the present invention is directed to a kit comprising at least one S-alkylated hepcidin peptide.

The invention discloses an application of a ferroptosis inhibitor in preparation of a preparation for improving the motion function of aged individuals. Through transcriptome sequencing analysis, Tfr1 expression in skeletal muscle and muscle satellite cells is reduced along with age increase. The specific knockout of the Tfr1 muscle satellite cells leads to irreversible inactivation of the muscle satellite cells. The skeletal muscle regeneration process of the Tfr1 muscle satellite cell specific mouse is accompanied by amyotrophy, iron ion accumulation and increase of unsaturated fatty acid biosynthesis, and then skeletal muscle ferroptosis is induced. The senescent skeletal muscle shows that the expression of Tfr1 is reduced, and the surface of an Slc39a14 membrane is enriched, so that the absorption of non-iron transporter binding iron is promoted to be increased, and the occurrence of ferroptosis is promoted. By intraperitoneal injection of the Ferrostatin-1 into aged mice, muscle aplastic disorder and dyskinesia caused by skeletal muscle ferroptosis can be remarkably improved.

The invention provides a Chorispora bungeana ferroportin gene CbIRT which has a base sequence shown as SEQ ID NO:1. The invention also provides an encoding product CbIRT of the Chorispora bungeana ferroportin gene CbIRT, wherein the encoding product CbIRT has an amino acid sequence shown as SEQ ID NO:2.

The invention relates to the use of ferroportin inhibitor compounds of the general formula (I) for preventing and treating kidney injuries, such as in particular acute kidney injuries, and the symptoms and pathological conditions associated therewith.

The invention relates to novel salts of compounds of the general formula (I), pharmaceutical compositions comprising them and the use thereof as medicaments, in particular for the use as ferroportin inhibitors, more particularly for the use in the prophylaxis and/or treatment of diseases caused by a lack of hepcidin or iron metabolism disorders, such as particularly iron overload states such as in particular thalassemia, sickle cell disease and hemochromatosis.

A mutant, human ferroportin-1 protein and encoding nucleic acid are provided. The mutant ferroportin-1 protein has a deletion of valine 162 compared to wild-type ferroportin-1 protein. The mutant protein and nucleic acid may be useful in detection of a predisposition to iron overload disorders such as haemochromatosis. Furthermore, it is proposed that the valine 162 deletion is a loss-of-function mutation that may underlie iron overload disorders such as haemochromatosis. Therefore, methods of both diagnosis and treatment of haemochromatosis are provided.

The subject matter described herein is directed to Ferroportin inhibitor compounds of Formula I and pharmaceutical salts thereof, methods of preparing the compounds, pharmaceutical compositions comprising the compounds and methods of administering the compounds for prophylaxis and/or treatment of diseases caused by a lack of hepcidin or iron metabolism disorders, particularly iron overload states, such as thalassemia, sickle cell disease and hemochromatosis.

The present invention is based on the discovery of autoantibodies in cancer patients specific for a number of antigens that are normally intracellular, including homeobox protein HOXA7, homeobox protein HOXB7, ADP-ribosylation factor 1 (Arf-1), ATP-dependent iron transporter ABC-7, and a novel protein encoded by a EcoRI/XhoI fragment of bacteriophage λ clone 44B.1 deposited under ATCC accession No. ______. The presence of these autoantibodies can be correlated with neoplastic processes in patients, and therefore detection of autoantibodies (or detection of expression of the antigens by other means) can be used as a component of a cancer screening program. The present invention provides such screening assays. In addition, the studies leading to the identification of the predictive autoantigens have also succeeded in identifying a hitherto unknown antigen that is disclosed herein.

The invention discloses an application of SPD_0310 protein as a target spot in preparation of a medicine for preventing and treating streptococcus pneumoniae infection. The invention finds that the expression quantity of the SPD_0310 in three mutant strains with three main iron transport genes of streptococcus pneumoniae knocked out at the same time is increased, and the SPD_0310 can normally grow, which indicates that the SPD_0310 protein may participate in the interaction of various iron transport proteins. The invention also finds that the infectivity of the SPD_0310 gene-knockout strain tomice is reduced, and on the basis, the SPD_0310 can be used for preparing an antibody of the protein, so that antibody drugs can be researched and developed. Besides, the invention also finds that the active center of the protein can be combined with heme, and proves that porphyrin drugs can be used as a substrate to compete with the heme, which indicates that the porphyrin drugs can be used as an inhibitor of the SPD_0310 to inhibit the toxicity of the streptococcus pneumoniae, so that the porphyrin drugs have wide application prospects in the field of antibacterial drugs.

The invention chimeric organism comprises a chimeric surface integrin-like fusion protein in which the I domain has been replaced by an antibody fragment that binds a disease-associated antigen on a cell. Binding of the antibody fragment to the disease-associated antigen triggers virulent transformation of the chimeric pathogenic organism so as to cause the organism to infiltrate the target cell with specificity. Preferably, the chimeric organism is a chimeric pathogenic C. albicans having an INT1 fusion protein in which the I domain is replaced by an antibody fragment, preferably a single chain antibody, and in which expression of an iron transporter gene necessary for infiltration of a target cell is triggered under the control of a EFG1p response element. Binding of the antibody to the disease-associated antigen causes filamentous transformation in the chimeric pathogenic C. albicans and specific infiltration of target cells. The invention chimeric pathogenic organisms are used in therapeutic methods to specifically infiltrate and destroy diseased cells to which the antibody fragment binds while remaining non-pathogenic to normal cells.