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At least 271 records · Page 15Linked to original sources
PubMed1992

Characterization of mouse-hamster somatic cell hybrids by PCR: a panel of mouse-specific primers for each chromosome.

Mouse/hamster somatic cell hybrids form a valuable resource for mouse gene mapping. Characterization of these hybrids by isozyme analysis can be technically demanding and time-consuming. Species-specific polymerase chain reaction (PCR), where a mouse gene but not its homolog in the hamster is amplified, can provide an alternative means of characterization. Mouse-specific primers have been designed for at least one gene on each of the mouse autosomes and the X Chromosome (Chr). Primers are chosen to correspond to untranslated regions of the mouse gene concerned, in order to decrease the chance of cross-hybridization with the homologous hamster gene. These primer sequences are presented, together with the conditions for their use.

Animals↗
PubMed1990

Gene mapping of mouse laminin A and B2 subunits using mouse-Chinese hamster somatic cell hybrids.

Laminin is a multichain extracellular matrix glycoprotein found primarily in basement membranes. The molecule is made up of three subunits, designated as A, B1, and B2. Using an 850-base cDNA probe for the mouse laminin A-chain and a 1000-base cDNA probe for the mouse laminin B2 chain, we have screened mouse-Chinese hamster somatic cell hybrids in order to assign the genes for each of these polypeptides to their respective mouse chromosome. We have determined that the mouse laminin B2-chain gene is located on chromosome 1 (confirming this assignment) and the laminin A-chain gene is located on chromosome 17.

Animals↗
PubMed1994

Role of macrophages, interferon gamma and procoagulant activity in the resistance of genetic heterogeneous mouse populations to mouse hepatitis virus infection.

Genetic heterogeneous mouse populations selected for high (HIII) and low (LIII) antibody response were used to study some aspects of mouse hepatitis virus 3 (MHV3) infection, such as the resistance pattern, virus replication in the liver and peritoneal exudate or in cultured peritoneal macrophages, the interferon (IFN) synthesis in the serum and peritoneal exudate and the procoagulant activity (PCA) of the peritoneal exudate (PEC) and spleen cells (SC). The HIII mice, when compared to their LIII mice counterparts, were susceptible to MHV3 infection showing higher virus titres in the liver and peritoneal exudate, comparable IFN alpha/beta or IFN gamma titres in the peritoneal exudate or in the serum, and higher levels of PCA of PEC and SC. A higher virus titre was detected in the supernatants of HIII mouse macrophages infected with MHV3. The activation of HIII mouse macrophages with LPS, IFN alpha/beta or IFN gamma, in contrast to that of LIII mouse macrophages, did not induce an antiviral effect with partial restriction of the MHV3 replication. The LPS antiviral activity was shown to be partially exerted by IFN alpha/beta synthesis. The IFN gamma was shown to be more effective in inducing an antiviral state in LIII macrophages, when compared to IFN alpha/beta. The data obtained are consistent with the notion that the resistance mechanisms to the MHV3 infection involve the PCA and the sensitivity of macrophages to IFN.

Animals↗
PubMed1975

Chinese hamster X mouse hybrid cells segregating mouse chromosomes and isozymes.

Hybrid cells are readily formed by fusing clonal Chinese hamster cells to fresh, noncultured, adult mouse spleen cells followed by isolation in selective medium. The vast majority of such hybrids retain Chinese hamster chromosomes and isozymes while segregating mouse chromosomes and isozymes. The growth, plating efficiency, ease of karyology, and rapid segregation of mouse markers allows linkage tests in primary clones. Analysis of 13 isozymes showed 12 to be asyntenic and on epair (PGD-PGM2) to be syntenic This system will allow extensive somatic cell hybrid gene mapping in the mouse and permit a comparison of human and mouse linkage relationships.

Animals↗
PubMed1990

Production of a human monoclonal antibody recognising a determinant on mouse IgG2b from a patient receiving mouse monoclonal antibody for diagnostic imaging.

The development of human antibodies recognising mouse immunoglobulins represents an obstacle to effective antibody therapy. This study shows that patients produce modest titres of antibodies (predominantly anti-mouse rather than anti-idiotypic) after a single low-dose injection for immunoscintigraphy, suggesting that repeated imaging with the same or a different antibody could be a problem. Fusion of the lymphocytes from a patient who had been imaged twice previously resulted in a monoclonal antibody that specifically binds to an IgG2b isotypic determinant. Anti-IgG2b antibodies predominated in this patient's serum. Production of human monoclonal antibodies from patients given mouse monoclonal antibodies not only allows a finer dissection of the immune repertoire but also provides possible reagents for controlling the human anti-(mouse Ig) response, for selection of class-switch variants of mouse monoclonal antibodies and enhancing tumour imaging.

Animals↗
PubMed1989

Cultivation of the exoerythrocytic stage of Plasmodium berghei in primary cultures of mouse hepatocytes and continuous mouse cell lines.

Plasmodium berghei exoerythrocytic (EE) stages have been cultured in vitro in human continuous cell lines and primary cultures of both human and rat hepatocytes. Although the predominant experimental model of irradiated sporozoite-induced protective immunity is the mouse, P. berghei has not been cultivated in primary mouse hepatocytes or in continuous mouse lines. Because of this, target cells are not available for determining if these immunized mice produce cytotoxic T lymphocytes (CTLs) that recognize P. berghei antigens expressed on hepatocytes in the context of class I major histocompatability (MHC) antigens. We report the development of methods for cultivating the (EE) stage of P. berghei in murine hepatocytes and in two cell lines derived from the livers of BALB/c mice; one line produced from a primary hepatocyte culture and the other produced by fusion of mouse hepatocytes with a continuous rat liver line. Mature parasites were detected by microscopy and by DNA probe in both cell lines, each of which supported complete development of P. berghei liver stages and production of infectious merozoites. Since class I MHC antigens are present on the surface of primary hepatocytes and the mouse X rat hybrid line, these cells can be used to detect cytotoxic T cells against liver stage parasites.

Animals↗
PubMed1998

Bile salt-stimulated lipase (BSSL) distribution in rat, mouse and transgenic mouse expressing human BSSL.

In some species, including man and mouse, bile salt-stimulated lipase (BSSL) in milk catalyzes the hydrolysis of triacylglycerides into glycerol and free fatty acids, a reaction that is of particular importance during suckling. The enzyme is also secreted by the pancreas (referred to as carboxyl-ester hydrolase, CEH). We wished to localize sources and storage sites for BSSL/CEH in rats, in wild-type mice, and in transgenic mice producing recombinant human BSSL in milk. Immunoreactivity against several BSSL fragments was strong in the pancreatic acinar cells and moderate in the absorptive cells of the small intestine and in salivary duct cells of the mice, as well as in rats. Sections from lactating mammary glands of mouse, but not rat, also showed immunoreactivity for BSSL; the signal was strongest in the transgenic mice. Radioactive riboprobes for BSSL mRNA hybridized on sections of rat and mouse pancreatic acinar cells, and mouse mammary glands (both wild-type and transgenic). Using RT-PCR, it was possible to amplify BSSL mRNA from wild-type mouse pancreas and mammary gland, from rat submandibular glands, and, in a few cases, from rat liver. In transgenic mice, the BSSL mRNA was highly expressed only in lactating mammary gland, but could be detected in a few other organs as well.

Animals↗
PubMed2004

Dlx5, the mouse homologue of the human-imprinted DLX5 gene, is biallelically expressed in the mouse brain.

The mouse Dlx5 gene encodes a distal-less-related DNA-binding homeobox protein first expressed during early embryonic development in anterior regions of mouse embryo and is located on chromosome 6, which is the syntenic region to the human chromosome 7q21-q31 imprinting cluster. Recently, its human homologue, DLX5, was identified to be imprinted and maternally expressed, at least in normal human lymphoblasts and in brain tissues. In our study, we analyzed the imprinting status of mouse Dlx5 by RT-PCR, first in the F1 of a reciprocal cross between two different mouse strains, and second in heterozygous Dlx5 mutant mice. Both approaches revealed that mouse Dlx5 followed a biallelic pattern of expression in brain tissue and in testis. Our findings suggest that the Dlx5 gene escapes genomic imprinting, at least in mice of certain genetic backgrounds.

3' Untranslated Regions↗
PubMed1989

The occurrence of mouse-type oligosaccharides in mouse-human chimeric immunoglobulin G.

The asparagine-linked sugar chains of mouse-human chimeric IgG which is composed of the variable regions derived from mouse and the constant regions derived from human and produced in mouse cells were quantitatively released as tritium-labelled oligosaccharides by hydrazinolysis followed by N-acetylation and NaB3H4-reduction. Paper electrophoresis in combination with sialidase digestion indicated that more than 70% of the oligosaccharides were neutral and the rest was sialylated oligosaccharides. Their structures were determined by sequential exoglycosidase digestions. The mouse-human chimeric IgG was shown to have same sugar chains as those of mouse IgG.

Animals↗
PubMed1988

Structural organization of the mouse cytosolic malate dehydrogenase gene: comparison with that of the mouse mitochondrial malate dehydrogenase gene.

We cloned and characterized a mouse cytosolic malate dehydrogenase (cMDHase) (EC 1.1.1.37) gene, which is about 14 x 10(3) base-pairs long and is interrupted by eight introns. The 5' and 3' flanking regions and the exact sizes and boundaries of the exon blocks, including the transcription-initiation sites, were determined. The 5' end of the gene lacks the TATA and CAAT boxes characteristic of eukaryotic promoters, but contains G + C-rich sequences, one putative binding site for a cellular transcription factor, Sp1, and at least two major transcription-initiation sites. The sequences around the transcription-initiation sites are compatible with the formation of a number of potentially stable stem-loop structures. We compared structural organization of the mouse cMDHase gene with that of the previously characterized mouse mitochondrial MDHase (mMDHase) gene, and found that the conservation of intron positions spreads across much of the two genes. This result suggests that a common ancestral gene for the cytosolic MDHase and the mitochondrial MDHase was broken up by introns, before the divergence. We also compared the nucleotide sequence of the promoter region of the mouse cytosolic MDHase gene with that of the other three mouse genes coding for isoenzymes participating in the malate-aspartate shuttle, i.e. mitochondrial MDHase, cytosolic and mitochondrial aspartate aminotransferases (cAspATase and mAspATase). We found that highly conserved regions are present in the promoter region of the cAspATase gene.

Amino Acid Sequence↗
PubMedDate not supplied

Activation of nitrosamines and other carcinogens by mouse-liver S9, mouse hepatocytes and in the host-mediated assay produces different mutagenic responses in Salmonella TA1535.

5 indirect alkylating carcinogens, namely, dimethylnitrosamine (DMNA), methylethylnitrosamine (MENA), diethylnitrosamine (DENA), 1,2-dimethylhydrazine (DMH) and cyclophosphamide (CP), were tested in liquid incubation assays for their mutagenic activity towards Salmonella TA1535 in the presence of mouse-liver homogenate (S9) or freshly isolated, single liver-cell preparations. The capacity of these mouse-liver preparations to activate the compounds to mutagens for TA1535 was compared with the mutagenic effect of low doses of the carcinogens in intrasanguineous host-mediated assays, with the same strain of mice as host. Although the mouse hepatocytes retained their activating capacity longer than S9 preparations did during incubation at 37 degrees C, the latter gave much higher yields of mutants with 10 mM (DMNA, MENA, DMH) and 5 mM (CP) of 4 out of the 5 compounds. DENA was not mutagenic in either assay. These differences between whole cell and disrupted cell preparations were reduced or absent when the concentrations of the test compounds were reduced by a factor of 10. It was concluded that hepatocytes at the maximal concentration of cells have a limited capacity to metabolize the mutagens. On the basis of protein concentration, hepatocytes are more effective (nitrosamines) or equally effective (CP and DMH) in activating the compounds. Compared with the host-mediated assays, both liver fractions have only a marginal potential to activate equal low amounts of the carcinogens. The present results do not indicate that hepatocytes take an 'intermediate' position between existing in vitro and in vivo activation systems, although they do suggest that these mouse hepatocyte preparations activate the nitrosamines DMNA and MENA in a quantitatively or qualitatively different way than do mouse-liver homogenates.

1,2-Dimethylhydrazine↗
PubMed1992

Recombinant mouse monoclonal antibodies with single amino acid substitutions affecting Clq and high affinity Fc receptor binding have identical serum half-lives in the BALB/c mouse.

The serum half-lives of three recombinant mouse monoclonal antibodies, differing radically in their ability to bind to Clq or FcRI but only minimally in structure, were determined in the BALB/c mouse following intravenous administration. The wild-type antibody, a chimaeric antibody comprising variable domains binding 3-iodo-4-hydroxy-5-nitrophenylacetate and constant domains of the mouse IgG2b isotype, was eliminated from the bloodstream with biphasic kinetics: alpha-phase, 0.5 days; beta-phase, 7.0 days. The alpha- and beta-phase half-lives of mutant recombinant antibodies with single amino acid substitutions, either Glu 235-Leu allowing binding to the mouse FcRI, or Lys 322-Ala reducing Clq binding 30-fold, were indistinguishable from those of the wild-type antibody demonstrating that the biological half-life of intact mouse IgG is independent of the ability to bind Clq or FcRI. The major implication of the present study is that IgG molecules which have been genetically engineered to eliminate interaction with other components of the immune system should retain the long half-life typical of natural antibodies.

Animals↗
PubMed1995

Expression in mouse embryos and in adult mouse brain of three members of the amyloid precursor protein family, of the alpha-2-macroglobulin receptor/low density lipoprotein receptor-related protein and of its ligands apolipoprotein E, lipoprotein lipase, alpha-2-macroglobulin and the 40,000 molecular weight receptor-associated protein.

We have analysed by northern blotting and by in situ hybridization the expression patterns of eight different genes during the second half of mouse embryonic development and in adult mouse brain: we compared the messenger RNA levels of amyloid precursor protein and of the two amyloid precursor protein-like proteins 1 and 2 and we have analysed expression of apolipoprotein E and of its main receptor in brain, the alpha-2-macroglobulin/low density lipoprotein receptor-related protein and three other ligands: the proteinase inhibitor alpha-2-macroglobulin, the modifying enzyme lipoprotein lipase and the 44,000 molecular weight heparin binding protein, a ligand of unknown function. During embryogenesis the temporal expression pattern differs considerably for the three members of the amyloid precursor proteins. Total embryo messenger RNA levels of amyloid precursor protein and amyloid precursor protein-like protein 2 increased progressively, while amyloid precursor protein-like protein 1 messenger RNA showed a burst of synthesis between days 10 and 13 post-coitum. Significantly, expression of the alpha-2-macroglobulin/low density lipoprotein receptor-related protein and of its associated protein, the 44,000 molecular weight heparin binding protein, exhibited their most important increase very similar to that of amyloid precursor protein-like protein 1, between days 10 and 13 post-coitum. Apolipoprotein E, lipoprotein lipase and alpha-2-macroglobulin messenger RNA levels in total embryos increased progressively, beginning most pronounced at days 13, 15 and 17, respectively. In mouse embryos, in situ hybridization established amyloid precursor protein, amyloid precursor protein-like protein 2 and alpha-2-macroglobulin/low density lipoprotein receptor-related protein messenger RNA to be expressed in most organs, with the notable exception of the liver, while expression of the other studied proteins was much more restricted. Among adult mouse tissues, the genes investigated were expressed very prominently in brain, except for lipoprotein lipase and for the complete absence of alpha-2-macroglobulin messenger RNA. In adult mouse brain, the cortex and hippocampus exhibited strong signals for most genes analysed. Exceptions are lipoprotein lipase and apolipoprotein E messenger RNAs, and the absent alpha-2-macroglobulin messenger RNA. Several interesting features, similarities as well as differences, between brain tissue sections hybridized with probes for amyloid precursor protein, amyloid precursor protein-like proteins 1 and 2 and between alpha-2-macroglobulin/low density lipoprotein receptor-related protein and heparin binding protein-44 were observed and are described. The results are further discussed in view of the known or anticipated physiological functions of the proteins examined and of their possible role in the etiology of Alzheimer's disease.

Amyloid beta-Protein Precursor↗
PubMed1994

Waardenburg syndrome in man and splotch mutants in the mouse: a paradigm of the usefulness of linkage and synteny homologies in mouse and man for the genetic analysis of human congenital malformations.

The use of chromosomal segments with conserved homologous linkage groups found in different species provides one method of predicting the location of genes causing congenital malformations in man. For example, homology between man and mouse involves 241 homologous autosomal genes spread on 68 homologous chromosomal segments. In addition, the similarities of phenotypic expression of human congenital malformations and mouse mutations indicate the possible involvement of an homologous gene implicated during ontogeny of the two species. The identification of a single gene defect in the mouse and comparative mouse-human gene mapping provides therefore another approach for selecting candidate loci for inborn error of morphogenesis in man. Further molecular studies can then be performed to show that the loci are identical. The human Waardenburg syndrome and the splotch (Sp) mouse mutant represent the first example of the potential of this approach for the understanding of human congenital malformations at the molecular level.

Animals↗
PubMed1992

The Mouse Genome Project and human genetics. A report from the 5th International Mouse Genome Mapping Workshop, Lunteren, Holland.

Genome-wide mapping efforts are moving toward the establishment of a 1-cM genetic map of the entire mouse genome. The bulk of linkage groups conserved between the mouse and the human genomes has been identified. Microsatellite mapping has had a major impact on the development of genome-wide genetic maps and, in particular, on genome-wide searches for polygenic disease loci. Some substantial regions of the mouse genome have a marker density of 1 cM or less and many of these regions are now physically mapped. Embryonic YAC contigs have been established in some physically mapped regions. A unitary, global mouse mapping database--the Mouse Genome Database--is under development along with associated software tools. Chromosome committees are having a major impact on the establishment and verification of chromosome maps through the preparation of published annual reports.

Animals↗
PubMed2004

Mouse neural progenitor cells differentiate into oligodendrocytes in the brain of a knockout mouse model of Canavan disease.

Canavan disease (CD) is an autosomal recessive disorder that leads to spongy degeneration in the white matter of the brain. Aspartoacylase (ASPA) synthesizing cells, oligodendrocytes, are lost in CD. Transplantation of neural progenitor cells (NPCs) offers an interesting therapeutic approach for treating neurodegenerative diseases by replacing the lost cells. Therefore, the NPCs transplantation to the brain of the CD mouse was studied. Injection of mouse NPCs to the striatum and cerebellum of juvenile CD mouse showed numerous BrdU positive cells at 1 month after injection. The same result was also observed in the adult CD mouse brain after 5 weeks of post-transplantation period. The implanted cells differentiated into oligodendrocytes and fibrous astrocytes, as observed using glial cell marker. This is the first report to describe the survival, distribution and differentiation of NPCs within the brain of CD mouse and a first step toward the potential clinical use of cell therapy to treat CD.

Amidohydrolases↗
PubMed2004

Expression of the mouse WNK1 gene in correlation with ganglioside GD3 and functional analysis of the mouse WNK1 promoter.

WNK1 is one of WNK (With No K=Lysine) protein kinases which comprise a newly described subfamily. Our studies showed that expression of the mouse WNK1 gene was dramatically suppressed in a tumor cell line when its phenotype was altered by suppression of the GD3-synthase gene expression. The mouse WNK1 gene was expressed at a high level at early stage of embryonic brain and its expression decreased as brain developed, similar to the expression pattern of the GD3-synthase gene. To study transcriptional regulation, we cloned a 5'-flanking 1239-bp fragment of the mouse WNK1 gene. This fragment contains a number of potential consensus binding sites for transcription factors, including Sp1, AP2, CCAAT, Est-1, Oct-1, CNBP, and NFkB, but lacks a TATA box. Primer extension identified multiple putative transcriptional initiation sites, including several sites downstream of the ATG codon. Activities of the promoter fragments were assessed in mouse breast Sa/R-MT cells by transient transfection and the results showed that the promoter elements between -700 and -977 is required for maintaining a high level of promoter activity of the TATA-less mouse WNK1 gene.

5' Flanking Region↗
PubMed2004

Mouse model characterisation for anthrax vaccine development: comparison of one inbred and one outbred mouse strain.

In order to evaluate the immunogenicity and protective efficacy of anthrax vaccine candidates a suitable small animal model is required. The inbred A/J strain of mouse has been selected as a potential model, and its immune response to immunisation with recombinant protective antigen (rPA) vaccine characterised, by assessment of rPA specific antibody production, and protection against injected challenge, with the unencapsulated STI strain of Bacillus anthracis. Studies were conducted to determine the time required post immunisation to develop a protective immune response, to define the minimum protective dose of vaccine required and to assess the long-term immune response to immunisation. From the results of these studies it was possible to establish that the A/J mouse is a consistent and robust small animal model for rPA vaccine testing. A comparison of the immune response to rPA vaccine immunisation in the Turner Outbred (TO) mouse strain was also conducted. Both inbred and outbred mouse strains displayed a predominantly Th2 biased immune response and showed a comparable antibody response to rPA immunisation. An assessment of protection in the TO mouse against aerosol challenge with the fully virulent strain of B. anthracis, Ames, was also made.

Animals↗