63 results about "Murine cell" patented technology

A substantially enriched mammalian hematopoietic cell subpopulation is provided, which is characterized by progenitor cell activity for lymphoid lineages, but lacking the potential to differentiate into myeloid and erythroid lineages. Methods are provided for the isolation and culture of this common lymphoid progenitor cell (CLP). The cell enrichment methods employ reagents that specifically recognize CDw127 (IL-7 receptor α); CD117 (c-kit) protein, in conjunction with other markers expressed on lineage committed cells. The murine cells are also characterized as expressing low levels of sca-1 (Ly-6E and Ly-6A). The CLPs are predominantly cycling, blast cells. These cells give rise to B cells, T cells and natural killer cells, as evidenced by their growth and differentiation in vitro and in vivo.

Surfaces useful for cell culture comprise a support to which is bound a CAR material, and, bound to the CAR material, collagen VI or a biologically active fragment or variant thereof and, optionally, one or more other ECM proteins (or fragments or variants thereof) such as elastin, fibronectin, vitronectin, tenascin, laminin, entactin, aggrecan, decorin, collagen I, collagen III, and collagen IV. Also, optionally present on the surface is one or more polycationic polymers, such as poly-D-lysine or poly-D-ornithine. This surface is used in cell culture to promote cell attachment, survival, and/or proliferation of a number of different cell types such as (a) liver cells (e.g., HepG2 tumor cells, and a newly discovered line of rat liver epithelial stem cells) (b) osteoblasts, such as the murine cell line MC3T3 cell line and (c) primary bone marrow cells. Kits comprising the surfaces and additional reagents are also disclosed.

The invention relates to a conditioned cell culture medium and a corresponding method to obtain it. The invention also refers to methods of using this cellconditioned medium for the maintenance, proliferation and differentiation of mammalian cells. The culture medium produced in accordance with the present invention is conditioned by the cell secretion activity of murine cells, in particular, those differentiated and immortalized transgenic hepatocytes, named MMH (Met Murine Hepatocyte). These media are employed in in vitro cell culture systems to induce maintenance, proliferation and differentiation of mammalian cells. The cells named MMH are differentiated non transformed murine hepatocytes that produce important biological molecules (e.g cytokines and growth factors) and, in accordance with the present invention, they are used in in vitro cell culture systems for the maintenance, proliferation and differentiation of mammalian cells.

The present invention relates to the engineering of animal cells, preferably mammalian, more preferably rat, that are deficient due to the disruption of gene(s) or gene product(s) resulting in cytokine-cytokine mediated autoimmune and inflammatory disease. In another aspect, the invention relates to genetically modified rats, as well as the descendants and ancestors of such animals, which are animal models of human autoimmune and inflammatory disease and methods of their use. Specifically, the invention pertains to a genetically altered rat, or a rat cell in culture, that is defective in at least one of two alleles of a cytokine gene such as the Faslg gene, the Fas gene, etc. In one embodiment, the cytokine gene is the Faslg gene. In another embodiment, the cytokine gene is one of several known cytokine genes, such as Fas, IFNγ, TNF-α, IL-2, IL-10, and IL-12. The inactivation of at least one of these cytokine alleles results in an animal with a higher susceptibility to cytokine-cytokine mediated autoimmune and inflammatory disease induction. In one embodiment, the genetically altered animal is a rat of this type and is able to serve as a useful model for cytokine-cytokine mediated autoimmune and inflammatory disease and as a test animal for autoimmune and other studies.

This invention relates to a genetically modified or chimeric rat cell whose genome comprises chromosomal alleles of an obesity-diabetes gene (especially, the Mc4r gene or Lep gene), wherein at least one of the two alleles contains a mutation, or the progeny of this cell. The obesity or diabetes gene may affect any of the pathways of obesity and diabetes. The obesity or diabetes gene may predispose the rat to a phenotype of obese and diabetic, lean and diabetic, obese and non-diabetic, non-obese and diabetic or any of the combinations thereof. In another aspect, the invention relates to a desired rat or a rat cell which contains a predefined, specific and desired alteration rendering the rat or rat cell predisposed to obesity or diabetes.

Preparations comprising an enriched population of extracellular vesicles (nEVs) having a negatively charged surface, and that are CD81+ and CD9−, are provided. Improved processes and methods for producing an enriched population of nEVs from non-murine cells, especially human origin cells and/or tissues, are disclosed. Therapeutic methods for using the preparations, including for reducing brain inflammation and treatment of various pathologies associated with brain inflammation, such as by intravenous or intranasal administration, are also described. Methods and preparations for reducing brain inflammation associated with traumatic brain injury (TBI) are also disclosed. A method for treating a patient having suffered a mild traumatic injury (mTMI), or concussion, such as a sports-related head injury, is also disclosed. The nEVs are also demonstrated to reduce the expression level of IL-Iβ in brain tissue of an animal having had traumatic brain injury. Methods for improving cognitive function and performance in animals after a traumatic brain injury is also demonstrated using the preparations of nEVs disclosed herein.

Novel mutated mammalian cells are provided that have been characterized by identifying the sequence of the genes that have been mutated. Preferably, novel mutated cells are murine ES cells that stably incorporate retroviral gene trap constructs in the specifically identified genes. The novel mutated cells and animals are useful in functional genomic analysis, and in the discovery and development of new therapeutic and diagnostics agents and methods.

The invention provides a sesterterpene compound, a preparation method thereof and an application thereof in preparation of anti-inflammatory drugs and immunosuppressive drugs, and relates to the technical field of natural pharmaceutical chemistry. The sesterterpene compound provided by the invention has any one of structures shown in formulas 1 to 12. The sesterterpene compound provided by the invention is a sesterterpene compound with a very rare skeleton, has anti-inflammatory and immunosuppressive effects, and can be applied to preparation of anti-inflammatory drugs and immunosuppressive drugs. Results of embodiments show that the sesterterpene compounds provided by the invention have obvious inhibition effects on CD3 and CD28 monoclonal antibodies for stimulating mouse T cell proliferation and generating cytokine IFN-gamma. The invention further provides a pharmaceutical composition. The pharmaceutical composition comprises pharmaceutically acceptable pharmaceutical excipients andone or more of the sesterterpene compounds in the scheme.

The present invention relates to a purified polypeptide, which is capable of mediating infection of a cell, by use of the polytropicixenotropic receptor encoded by the Rmc1 locus from a NIH Swiss inbred NFS/N mouse for entry, and unable of mediating infection of a cell by use of a human polytropic/xenotropic receptor encoded by the human RMC1 locus. The present invention especially relates to an envelope protein from the Murine leukaemia Virus (MLV) strain SL3-2, which is capable of infecting murine cells through usega of the polytropic receptor encoded by the Rruc1 locus, but lacks the ability of infecting human cells expressing the corresponding xenotropic receptor encoded by the RMC locus. The present invention furthermore demonstrate that replacements of at least one specified amino acid in the polypeptide can alter the tropism and enable the SL3-2 envelope to infect a human cell by use of the human polytropic/xenotropic receptor encoded by the RMC1 locus for entry.

Rat cells and rats comprising an inactivated Cfh locus and methods of making and using such rat cells and rats are provided. The rats comprising an inactivated Cfh locus model C3 glomerulopathy (C3G). Methods are provided for using such rats comprising an inactivated Cfh locus to assess in vivo efficacy of putative C3G therapeutic agents.

A method for treating tumors. Through infusion or xenotransplantation of xenogeneic cells, such as infusion of murine cells into the peritoneal cavity of humans, a hyperacute rejection response to the cells is induced. This in turn creates a bystander effect to the tumor. This effect creates tumor regression. This treatment can be used alone or in conjunction with gene therapy or chemotherapy treatments.

The invention discloses a variable region sequence of a specific anti-chlorothalonil antibody. The amino acid sequence of a heavy chain variable region coding gene is shown in SEQ ID NO: 2. The invention also discloses an anti-chlorothalonil recombinant full-length IgG antibody. The invention also discloses a recombinant antibody expression plasmid. The heavy chain variable region and light chain variable region sequences of the anti-chlorothalonil recombinant full-length IgG antibody are derived from a monoclonal cell strain which secretes a high-affinity and high-specificity anti-chlorothalonil antibody and is obtained by immunizing mice for multiple times, performing cell fusion and screening. The sequence genes are respectively connected to expression vectors containing a mouse IgG1 heavy chain constant region gene and a mouse kappa light chain constant region gene, the recombinant full-length IgG antibody is obtained by expression of mammalian cells of a double-plasmid system, the recognition activity of the recombinant full-length IgG antibody is very close to that of a mouse-derived parent antibody, large-scale standardized production of the anti-chlorothalonil antibody can be realized, and reliable core raw materials are provided for various immunoassay methods for rapid detection of chlorothalonil residues.

The invention discloses a construction method and an application of an NK (natural killer) cell activation testing receptor signal path NKG2D fluorescence report system. A human NKG2D extracellular region gene sequence and mouse NKG2D transmembrane region and cytoplasmic region gene sequences are obtained by the aid of PCR (polymerase chain reaction) technology, the human and mouse NKG2D gene sequences are connected together by the aid of overlapping PCR technology, and the constructed human and mouse heterozygous NKG2D sequences are inserted into a pLXSN16E6E7 vector to form a vector pLXSN16E6E7-mhNKG2D. A human DAP12 gene sequence is constructed by the aid of the PCR technology and inserted into the pLXSN16E6E7 vector to form a vector pLXSN16E6E7-hDAP12. Plasmids of the two vectors and helper plasmids pCL-ECO of a retrovirus system are co-transfected with HEK293T cells to obtain virus particles containing reinfected mouse cells 3A9. Cell supernatants containing virus particles infect the cells 3A9, a cell line 12A9 steadily expressing mouse and human infusion NKG2D and human DAP12 is screened out by means of repeated flow sorting and re-culture, and downstream signals of NKG2D can be activated under the stimulus of human NKG2D ligand MICA/MICB, so that green fluorescence emitted by the cells can be detected by GFP (green fluorescent protein) expression.