73 results about "CD59" patented technology

The invention involves assays, diagnostics, kits, and assay components for determining levels of K41-glycated CD59 in subjects. Treatments for subjects based upon levels of K41-glycated CD59 also are provided.

Compositions comprising menstrual stem cells (MSCs) and methods, processes, and system therefor are provided by the invention. MSCs are processed from menstrual flow collected during menses. MSCs may be cryopreserved, processed through various culturing and selection steps in preparation for cryopreservation, or processed for therapeutic or cosmeceutical use. Cryopreserved MSCs may be thawed in preparation for therapeutic and cosmeceutical use. MSCs express CD9, CD10, CD13, CD29, CD44, CD49e, CD49f, CD59, CD81, CD105, CD166, and HLA class I, and have low or no expression of CD3 and HLA class II.

The invention includes antibodies or antigen-binding fragments thereof which bind specifically to glycated CD59, compositions containing one or a combination of such antibodies or antigen-binding fragments thereof, hybridoma cell lines that produce the antibodies, and methods of producing and using the antibodies or antigen-binding fragments thereof for diagnosis and treatment of diabetic conditions and diabetic-associated conditions.

The invention provides for isolated population of pulp marrow similar cells (DPMSCs) and methods for isolating and using these cells. The population of DPMSCs are highly homogenous for CD1O, CD29, CD13, CD44, CD49a, CD49d, CD59, CD73, CDw90, CD105, Oct-4 Isoform A and B, Nanog, Sox-2, and SSEA-4.

This invention relates to the diagnosis and treatment of cancerous diseases, particularly to the mediation of cytotoxicity of tumor cells; and most particularly to the use of cancerous disease modifying antibodies (CDMAB), optionally in combination with one or more chemotherapeutic agents, as a means for initiating the cytotoxic response. The invention further relates to binding assays which utilize the CDMAB of the instant invention.

The present invention relates to recombinant antibody molecules and functional fragments thereof, useful for neutralizing the complement regulatory proteins CD55 and CD59, compositions comprising the recombinant molecules and methods of using the recombinant molecules for controlling complement resistance in cancer. The present invention further relates to heterodimeric diabody molecules comprising variable regions specific for CD55/CD59 and CD20.

This document provides methods and materials involved in reducing cardiac xenograft rejection. For example, methods and materials for preparing transgenic pigs expressing reduced or no endogenous Sd^a or SDa-like glycans derived from the porcine β1,4 N-acetyl-galactosaminyl transferase 2 (B4GALNT2) glycosyltransferase and/or reduced or no endogenous α-Gal antigens, methods and materials for modifying the xenograft recipient's immunological response to non-Gal antigens (e.g. CD46, CD59, CD9, PROCR, and ANXA2) to reduce cardiac xenograft rejection, and methods and materials for monitoring the progress of xenotransplant immunologic rejection are provided.

The present invention relates to a method of producing a parthenocarpic, and optionally male sterile, tomato plant comprising introgressing into said plant a genetic region from Chromosome 4, 5 and/or 12 of S. habrochaites LYC4/78, a representative sample of seed of which was deposited on 13 Nov. 2007 with the NCIMB under Accession number 41517, wherein the genetic region from Chromosome 4 of S. habrochaites LYC4/78 includes at least one marker selected from Marker CD59, RFLP Marker CT229, and COS Marker T1068, and wherein the genetic region from Chromosome 5 of S. habrochaites LYC4/78 includes at least one marker selected from COS Marker T1181, RFLP Marker TG441 and/or RFLP Marker CD31(A).

This invention relates to the staging, diagnosis and treatment of cancerous diseases (both primary tumors and tumor metastases), particularly to the mediation of cytotoxicity of tumor cells; and most particularly to the use of cancerous disease modifying antibodies (CDMAB), optionally in combination with one or more CDMAB/chemotherapeutic agents, as a means for initiating the cytotoxic response. The invention further relates to binding assays, which utilize the CDMAB of the instant invention. The anti-cancer antibodies can be conjugated to toxins, enzymes, radioactive compounds, cytokines, interferons, target or reporter moieties and hematogenous cells.

Methods of identifying specific target molecules for design of anti-angiogenic and vascular targeting approaches are disclosed. Transcriptional profiles of tumor endothelial cells were compared with that of normal resting endothelial cells, normal but angiogenically activated placental endothelial cells, and cultured endothelial cells. Although the majority of transcripts were classified as general angiogenesis markers, 17 genes were identified that show specific overexpression in tumor endothelium. Antibody targeting of four cell-surface expressed or secreted products (vimentin, CD59, HMGB1 and IGFBP7) inhibited angiogenesis in vitro and in vivo. Finally, targeting endothelial vimentin in a mouse tumor model significantly inhibited tumor growth and reduced microvessel density. The results demonstrate the utility of the identification and subsequent targeting of specific tumor endothelial markers for anticancer therapy.

The invention discloses a fusion protein of a single-chain antibody of a human anti-complement C3d molecule and a complement inhibitor CD59. The antibody has excellent antigen binding activity. Biological distribution experiments prove that the fusion protein provided by the invention can be rapidly and highly aggregated at an arthritis part after entering a rheumatoid arthritis mouse model, and has an excellent anti-adhesion/anti-inflammation targeting inhibition effect. In treatment of MRL/lpr lupus erythematosus mice, the fusion protein provided by the invention can obviously improve the survival rate of the mice, and symptoms of proteinuria, glomerular score, interstitial inflammation, vasculitis, crescent/necrosis and the like of a treatment group are obviously improved, so that the fusion protein provided by the invention has an excellent application prospect in preparation of medicaments for treating autoimmune diseases.

An antigenic and immunogenic composition of predetermined inactivated strains of human immunodeficiency virus (HIV) is disclosed. Inactivation is through psoralen and ultraviolet radiation; the composition is rendered more effective by the removal of structural features of HIV that interfere with immune response. In particular, sialic acid is removed to enhance immune recognition of the composition and to impair Complement Factor H binding. CD55 and CD59 are also removed to prevent the binding of Complement Factor H. Determination of strains for inactivation may be though immunotherapeutic genotyping or probabilistic assessment of risk of exposure.

The invention relates to novel cyclic compounds (cyclic peptides), linkers useful as beta-turn promoters in cyclic peptides, and methods for treatment of malignant cells in vitro or in vivo using one or more linear and cyclic peptides. The peptides can act as integrin interaction inhibitors and may be used in the treatment of cancers as monotherapies or in combination with other anti-cancer agents, such as proteasome inhibitors, inhibitors of autophagy, alkylating agents, MEK inhibitors, FAK/PYK2 inhibitors, and EGFR inhibitors. The invention further concerns a method of predicting the binding of a cyclic or linear HYD1 peptide to a cancer cell by assessing overexpression of biomarkers such as CD44, VLA-4 integrin, basigin, CD138 (syndecan 1), NCAM, ICAM1, ICAM3, and CD59. The invention further concerns a method of detecting one or more members of a complex comprising CD44, VLA-4 integrin, basigin, CD138 (syndecan 1), NCAM, ICAM1, ICAM3, and CD59, using a linear or cyclic HYD1 peptide bearing a detectable moiety.

The invention discloses an anti-P-selectin single-chain antibody targeted complement inhibitor ScFv-CD59 and application thereof. The invention aims to provide an anti-P-selectin single-chain antibody targeted complement inhibitor ScFv-CD59 with specific targeting and the application thereof in preparing medicaments for treating systemic inflammations. The anti-P-selectin single-chain antibody targeted complement inhibitor ScFv-CD59 is a fusion protein obtained by connecting the amino terminal of the anti-P-selectin single-chain antibody ScFv with the complement inhibitor CD59 by using a connecting peptide. The experiment proves that the ScFv-CD59 can obviously improve the efficiency of inhibiting the complement-mediated cell cracking, can achieve high-degree accumulation at the immune injury part, can obviously inhibit the occurrence and degeneration of inflammations and can obviously reduce the side effect of infection caused by the complement inhibitor. Therefore, the ScFv-CD59 can be used as an active ingredient to be prepared into a novel gene engineering targeted protein medicament with a targeted P-selectin complement inhibitor for treating inflammations. The invention plays an important role in the pharmaceutical field and has wide application prospects.

The invention provides an agent comprising: (i) a T cell antigen, and (ii) a binding partner for any of CD22, CD23, CD30, CD74, CD70, CD43, CD44, CD47, CD54, CD58, CD62L, CD95, HLA-DR, CD59, CD55, wherein, following binding of the agent to a cell that expresses any of CD22, CD23, CD30, CD74, CD70, CD43, CD44, CD47, CD54, CD58, CD62L, CD95, HLA-DR, CD59, CD55, the agent is internalised and the T cell antigen is presented on the surface of the cell in a form that can be recognised by a T cell.