82 results about "Midkine" patented technology

MK (midkine) was found to rise in the blood or urine of patients with various types of cancers at early stage. Based on this finding, a method for detecting early cancer, comprising the step of measuring MK in blood or urine was completed.

Heparin-binding regions of several proteins, such as neural cell adhesion molecule, fibronectin, laminin, midkine, and anti-thrombin III have been shown to promote neurite extension on two-dimensional surfaces. The effect of heparin-binding peptides on neurite extension through three-dimensional matrices was investigated by culturing embryonic chick dorsal root ganglia (DRG) within fibrin gels containing chemically attached heparin-binding peptide (HBP). The length of neurites within fibrin gels containing cross-linked HBP was increased by more than 70% over extension through fibrin gels containing no peptide. The HBP sequence of antithrombin III was incorporated into the fibrin gel as the C-terminal domain of a bidomian, chimeric peptide; the N-terminal second domain of this peptide contained the ∀2-plasmin inhibitor substrate for Factor XIIIa. Factor XIIIa, a transglutaminase, was used to chemically attach the HBP-containing chimeric peptide to the fibrin gels during polymerization. The amount of HBP cross-linked into the fibrin gels was determined, after degradation by plasmin using gel permeation chromatography, to be approximately 8 moles of peptide per mole fibrinogen. A peptide (HBP), where the cross-linking glutamine was replaced with glycine, showed no increase in extension in comparison with fibrin gels. The additional of heparin to the gel percursors resulted in no increase in neurite extension in comparison with fibrin gels. HBPs promote neurite extension by binding to cell surface proteoglycans on the DRG.

The invention provides an ELISA kit to detect the concentration of Midkine and a method of application thereof. The kit comprises monoclonal antibodies of mouse anti-human MK coated on an enzyme marker; polyclonal antibodies of rabbit anti-human; polyclonal antibodies of goatanti rabbit IgG marked with horse radish peroxidase (HRP); His-MK expressed with procaryon in colibacillus E.coli and affinity purified with N ends having six His labels. The application method comprises coating a microlon ELISA plate with commercial monoclonal antibodies of Midkine of mouse anti-human; adding specimens to be detected, and multiple resistance of Midkine of rabbit anti-human and rabbit anti-human IgG marked with HRP for joint incubation after the plate is sealed; adding substrate solution of TMB for reaction and visualization; finally, terminating the reaction with vitriol, and detecting the absorbance at the position of 450nm. A standard curve is drawn with the concentration of standard samples and corresponding absorbance. In this way, the concentration of Midkine in the specimens to be detected can be got through the absorbance and the corresponding standard curve.

The invention relates to the field of biomedical research, and in particular to a construction method of an LM3 stable cell line with Midkine low expression. The LM3 cell line with Midkine stable low expression is constructed by virtue of an RNA interference technology. The construction method comprises the following steps: conducting primer design and target fragment amplification, and constructing Midkine shRNA recombinant plasmid; then, collecting a liquid medium containing viruses, filtering the liquid medium, adding the filtered liquid medium to a culture dish inoculated with LM3 cells in advance and conducting co-culture; and finally, conducting Puromycin resistance screening and sub-culturing on the LM3 cells accepting transfection, so that the LM3 stable cell line with Midkine low expression is finally obtained. With the establishment of the cell line, a new experimental material is provided for researching a molecular action mechanism of Midkine in tumors and a regulatory effect of the Midkine in tumor energy metabolism.

This invention relates to the discovery that midkine modulates pulmonary vasculature development and smooth muscle cell development. Modulation of midkine activity thus alters pulmonary vasculature development and smooth muscle cell development. The invention provides methods of modulating pulmonary disorders, smooth muscle cell related disorders, and pulmonary smooth muscle cell disorders. Disorders of particular interest include, but are not limited to, asthma and pulmonary hyperplasia. Further the invention relates to the discovery that TTF1 and HIF1 -α exhibit midkine modulating activity. The invention pertains to the discovery that midkine modulates myocardin activity.

The present invention relates to methods and compositions for monitoring, diagnosis, prognosis, and determination of treatment regimens in subjects suffering from or suspected of having a renal injury. In particular, the invention relates to using assays that detect one or more markers selected from the group consisting of Clusterin, Heart-type fatty acid binding protein, Hepatocyte growth factor, Interferon gamma, Interleukin-12 subunit beta, Interleukin-16, Interleukin-2, 72 kDa type IV collagenase, Matrix metalloproteinase-9, Midkine, and Serum amyloid P-component as diagnostic and prognostic biomarkers in renal injuries.

The present invention relates to a monoclonal antibody or a fragment thereof specific to truncated Midkine (tMK) protein, hybridoma producing the monoclonal antibody, a method of detecting truncated Midkine protein (tMK) by use of the monoclonal antibody, a method of detecting a tumor cell, and a kit containing the monoclonal antibody for detecting truncated Midkine (tMK) protein.

Embodiments provided herein relate to methods and compositions for treating mesothelioma and/or a small cell lung cancer that express midkine.

Cells within liver tumour mass comprise a unique set of proteins/tumour antigens when compared to the normal liver tissues epithelial cells juxtaposed to the tumour. The presence of tumour antigens couples the production of auto-antibodies against these tumour antigens. The present invention relates to the identification and elucidation of a protein set that can act as a novel marker set for liver cancer diagnosis and prognosis. Specifically, it relates to a kit that enables diagnostic and prognostic measurement of auto-antibodies in serum of liver cancer patients. The present invention provides a non-invasive, specific, sensitive, and cost effective detection and quantification method by evaluating a set of validated liver cancer proteins/tumour antigens, which includes Bmi-1, VCC1, SUMO-4, RhoA, TXN, ET-1, UBE2C, HDGF2, FGF21, LECT2, SOD1, STMN4, Midkine, IL-17A or IL26, to complement the conventional diagnostic methods.

The invention relates to a method for massively preparing midkine antisense oligodeoxynucleotide nano-liposomes for injection. The method comprises the following steps: dissolving a mixture of cationic liposomes and lecithoid liposomes in an organic solvent to obtain a liposome liquor; then, initially dispersing the liposomes by an ultrasonic instrument, and ultrafiltering to remove the organic solvent, and finally squeezing by a squeezer at a high pressure to uniform grain size to obtain blank nano-liposomes; and then, mixing with an MK-ASODN liquor to obtain MK-ASODN nano-liposomes. The grain size of the midkine antisense oligodeoxynucleotide nano-liposomes for injection produced by the method is within 100-500nm, and the midkine antisense oligodeoxynucleotide nano-liposomes for injection is stable in property and the anti-hepatoma effect of the midkine antisense oligodeoxynucleotide nano-liposomes for injection is remarkably enhanced. The method is simple in process, easy to realize, very easy to amplify, and suitable for industrial production.

Cells within liver tumor mass comprise a unique set of proteins/tumor antigens when compared to the normal liver tissues epithelial cells juxtaposed to the tumor. The presence of tumor antigens couples the production of auto-antibodies against these tumor antigens. The present invention relates to the identification and elucidation of a protein set that can act as a novel marker set for liver cancer diagnosis and prognosis. Specifically, it relates to a kit that enables diagnostic and prognostic measurement of auto-antibodies in serum of liver cancer patients. The present invention provides a non-invasive, specific, sensitive, and cost effective detection and quantification method by evaluating a set of validated liver cancer proteins/tumor antigens, which includes Bmi-1, VCC1, SUMO-4, RhoA, TXN, ET-1, UBE2C, HDGF2, FGF21, LECT2, SOD1, STMN4, Midkine, IL-17A, IL26, or DCP to complement the conventional diagnostic methods.

The invention relates to an application of human midkine protein blocking peptide for preparing antineoplastic medicine, wherein the human midkine protein blocking peptide comprises the following amino acid sequence: CTSTAMDNC. The invention provides an application of human midkine protein blocking peptide for preparing antineoplastic medicine, the polypeptide can inhibit the growth of malignant tumor cells, particularly for inhibiting the generation of malignant tumor neovascularization, provides foundation for screening new medicines, and has great clinical significance.

The present invention provides a method of stimulating angiogenesis in a human or animal in need thereof, and also provides a composition comprising an angiogenic factor and a pharmaceutically acceptable carrier. In one embodiment, the method comprises administering to a human or other animal a therapeutically effective amount of an angiogenic factor, such as pleiotropin or a midkine protein, contained in a pharmaceutically acceptable carrier. In one embodiment, the carrier includes a controlled release matrix, such as a polymer, that allows the controlled release of angiogenic factors. The polymer is biodegradable and/or bioerodible, preferably biocompatible. Polymers useful for controlled release include, for example, poly(esters), poly(anhydrides) and poly(amino acids). Polymers include, for example, silk elastin poly(amino acid) block copolymers and poly-lactide-co-glycolide. In another embodiment, angiogenic factors may be provided in a carrier comprising liposomes, such as heterocystic liposomes. Carriers such as liposomes may contain targeting ligands capable of targeting the liposomes to predetermined sites in vivo. Angiogenic factors may be administered to the vasculature, such as the cardiovascular system or the peripheral vasculature. In preferred embodiments, the angiogenic factor is a pleiotrophin or a midkine protein. In another embodiment, there is provided a method of stimulating angiogenesis in a human or animal, the method comprising administering to the human or animal a therapeutically effective amount of a gene transfer vector contained in a pharmaceutically acceptable carrier, the gene transfer vector Can encode pleiotropin or midkine protein. Gene transfer vectors can be, for example, naked DNA or viral vectors, and can be used, for example, in combination with liposomes.

A method of anticipating risk of the onset of cancer in an individual, including (1) obtaining a sample derived from the individual, (2) analyzing a polymorphism of a Midkine gene concerning the sample of (1), and (3) anticipating risk of the onset of cancer based on the polymorphism determined in (2) above.

The invention discloses a method for in vitro collecting Midkine proteins and treating cells with the collected Midkine proteins. Cells for highly expressing Midkine proteins are cultured, through thesecretion characteristics of the Midkine proteins, the Midkine proteins are collected in culture mediums, and the secretion quantity of the Midkine proteins is detected through Western blot experiment; through detection with the Western blot experiment, the inventor finds that MK proteins can be transferred into the cells, and the phosphorylation level of AMPK is restrained; when the Midkine proteins are applied outside the cells, heparin (heparin) is added, through detection with the Western blot experiment, the inventor finds that Heparin restrains the Midkine proteins from entering the cells, and the activity of the AMPK proteins is improved. The method provides a novel method for researching the action mechanism of the Midkine.

A peptide is derived from the Midkine protein, comprising at least one CD4<+>T or CD8<+>T epitope restricted by the HLA molecules predominant in the Caucasian population, or a polynucleotide encoding said peptide, as an anticancer vaccine or as a reagent for immunomonitoring of the cellular response against Midkine over the course of a cancer or of an anticancer treatment.

Provided is a therapeutic method targeting midkine for treating mammalian kidney disorders, primary kidney disorders, hypertension that follows secondary kidney disorders such as diabetic nephropathy, and hypertension secondary to chronic kidney disease.