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At least 19 recordsLinked to original sources

PubMed2000

Mouse allergen. II. The relationship of mouse allergen exposure to mouse sensitization and asthma morbidity in inner-city children with asthma.

BACKGROUND: Although mouse allergen is known to cause occupational asthma in laboratory workers, its potential significance in home environments has never been studied. OBJECTIVE: This study was designed to define the prevalence of mouse sensitivity and its relationship to mouse allergen exposure and disease activity in inner-city children with asthma. METHODS: A subset of 499 subjects from the National Cooperative Inner-City Asthma Study had dust samples adequate for mouse allergen analysis, as well as valid puncture skin test (PST) results. Data were analyzed to relate mouse allergen exposure and other risk factors to mouse sensitization and asthma morbidity. RESULTS: Eighty-nine (18%) of the 499 children had a positive mouse skin test response. Children whose homes had mouse allergen levels above the median (1.60 microg/g) in the kitchen had a significantly higher rate of mouse sensitization (23% vs 11%, P =. 007). Atopy was also significantly related to mouse sensitization, with 40% of those with more than 4 positive PST responses having mouse sensitivity compared with 4% of those with no other positive PST responses (P <.0001). When atopy and exposure were considered together, 53% of those with more than 4 positive PST responses and allergen levels above the median had a positive PST response to mouse allergen compared with 22% of those with more than 4 positive PST responses and allergen levels below the median (P <.0001). The relationship among mouse allergen exposure, sensitization, and any measures of asthma morbidity was not statistically significant. CONCLUSIONS: Mouse allergen may be an important indoor allergen in inner-city children with asthma, with exposure and atopy contributing to mouse sensitization.

Allergens↗

PubMed1979

In vitro fertilization of two species of deer mouse eggs by homologous or heterologous sperm and penetration of laboratory mouse eggs by deer mouse sperm.

Newly ovulated eggs from immature deer mice (Peromyscus maniculatus and P. polionotus) and mature laboratory mice (Mus musculus) treated with PMSG and HCG were inseminated in vitro with spermatozoa recovered from the cauda epididymidis of mature males. The time required for capacitation of deer mouse sperm in culture was estimated to be about two to five hours based on the dispersal of sperm agglutination and increase of sperm motility. The rate of sperm penetration through the zona pellucida of deer mouse eggs by homologous or heterologous sperm was relatively high (72-91%) but that of laboratory mouse eggs by deer mouse sperm was low (20-21%). After penetration through the zona pellucida, a high proportion of deer mouse eggs (79-93%) were fertilized by homologous or heterologous deer mouse sperm but no laboratory mouse eggs were fertilized by sperm of two species of deer mice. The zona pellucida was dissolved in a higher proportion of laboratory mouse eggs cultured with P. maniculatus (45%) than with P. polionotus sperm (3.4%), but this did not happen by incubation of deer mouse eggs with homologous or heterologous sperm. It seems that there is little difference in sperm penetration and fertilization between these two closely related species of deer mice but the reactions between the mouse eggs and deer mouse sperm are quite different.

Animals↗

PubMed1986

Differential expression of mouse beta/goat beta c, mouse beta/goat beta F, and mouse beta/goat epsilon II hybrid globin genes in murine erythroleukemia cells.

We assembled three hybrid beta-globin genes by fusing the mouse beta-major promoter and initial transcribed region to one of three goat beta-like globin gene bodies: beta c (preadult), beta F (fetal), or epsilon II (embryonic). Thymidine kinase (tk)-deficient murine erythroleukemia (MEL) cells were cotransformed with one of these constructs and a separate plasmid bearing the tk gene. Half of the 24 cell lines containing either the mouse beta/goat beta c or mouse beta/goat beta F genes expressed the transferred genes at significant levels; in many cases the hybrid genes were, like the endogenous beta-globin genes, inducible with dimethyl sulfoxide. We obtained 13 cell lines containing the mouse beta/goat epsilon II hybrid gene, 6 of which were cotransfected with a mouse beta/human beta fusion gene known to function in MEL cells. In contrast to the results with the other fusion genes, the mouse beta/goat epsilon II hybrid was very poorly expressed: in two separate experiments, 0 of 13 and 2 of 13 lines showed significant mouse beta/goat epsilon II RNA levels after induction. In all these lines the endogenous mouse beta and cotransfected mouse beta/human beta genes were expressed. As an initial test of possible reasons for the inactivity of the mouse beta/goat epsilon II hybrid, we recloned this fusion gene into a tk-bearing plasmid, adjacent to the tk gene. Of 12 cell lines transformed with this plasmid, 11 produced mouse beta/goat epsilon II RNA; in 6 cases the expression was both strong and dimethyl sulfoxide inducible.

Animals↗

PubMed2005

A new mouse model for infantile neuroaxonal dystrophy, inad mouse, maps to mouse chromosome 1.

Infantile neuroaxonal dystrophy (INAD) is a rare autosomal recessive hereditary neurodegenerative disease of humans. So far, no responsible gene has been cloned or mapped to any chromosome. For chromosome mapping and positional cloning of the responsible gene, establishment of an animal model would be useful. Here we describe a new mouse model for INAD, named inad mouse. In this mouse, the phenotype is inherited in an autosomal recessive manner, symptoms occur in the infantile period, and the mouse dies before sexual maturity. Axonal dystrophic change appearing as spheroid bodies in central and peripheral nervous system was observed. These features more closely resembled human INAD than did those of the gad mouse, the traditional mouse model for INAD. Linkage analysis linked the inad gene to mouse Chromosome 1, with the highest LOD score (=128.6) at the D1Mit45 marker, and haplotype study localized the inad gene to a 7.5-Mb region between D1Mit84 and D1Mit25. In this linkage area some 60 genes exist: Mutation of one of these 60 genes is likely responsible for the inad mouse phenotype. Our preliminary mutation analysis in 15 genes examining the nucleotide sequence of exons of these genes did not find any sequence difference between inad mouse and C57BL/6 mouse.

Animals↗

PubMed2004

Mouse allergen exposure and immunologic responses: IgE-mediated mouse sensitization and mouse specific IgG and IgG4 levels.

BACKGROUND: Although there is evidence that contact with mice is associated with IgE-mediated mouse sensitization and mouse specific antibody responses, the exposure-response relationships remain unclear. OBJECTIVE: To determine whether IgE-mediated mouse sensitization and mouse specific IgG (mIgG) and mIgG4 levels increase with increasing Mus m 1 exposure. METHODS: One hundred fifty-one workers at a mouse research and production facility were studied. Exposure assignments were made by linking participants to airborne Mus m 1 concentrations in their respective work areas. Cumulative exposure was estimated by multiplying airborne Mus m 1 concentration by duration of employment. Serum mIgG and mIgG4 levels were quantified by antigen-binding assays, and IgE-mediated mouse sensitization was evaluated by skin prick testing (SPT). RESULTS: Prevalence rates of mouse SPT sensitivity and of high levels of mIgG and mIgG4 were increasingly higher by quintiles of increasing cumulative exposure (P < .01 for SPT, mIgG, and mIgG4). After adjusting for age, sex, and atopy, the log odds ratio (OR) of having positive mouse SPT results was linearly related to cumulative exposure (r2 = 0.87), as was the log OR of having a high mIgG level (r2 = 0.86). Quintile of cumulative exposure was an independent predictor of both SPT sensitivity (OR, 1.7; 95% confidence interval, 1.2-2.5) and a high mIgG level (OR, 1.7; 95% confidence interval, 1.2-2.4). CONCLUSIONS: IgE-mediated mouse sensitization and mIgG and mIgG4 levels were related to cumulative exposure in a dose-dependent manner. Thus, strategies to prevent allergy to mice should remain focused on reducing mouse allergen exposure.

Adult↗

PubMed1992

Cross-species transplantation tolerance: rat bone marrow-derived cells can contribute to the ligand for negative selection of mouse T cell receptor V beta in chimeras tolerant to xenogeneic antigens (mouse + rat----mouse).

Mixed xenogeneic bone marrow reconstitution (mouse + rat----mouse) results in stable mixed lymphopoietic chimerism (1-48% rat), long-term survival, and the induction of stable functional donor-specific transplantation tolerance to xenoantigens in vivo. To examine the role of negative selection of potentially xenoreactive T lymphocytes during tolerance induction across a species barrier, mixed xenogeneic chimeras (mouse + rat----mouse) were prepared and analyzed using a mixture of mouse and rat bone marrow cells for relative T cell receptor (TCR)-V beta expression on mouse T cells. In mixed xenogeneic chimeras (B10 mouse + rat----B10 mouse), T cell maturation proceeded normally in the presence of rat bone marrow-derived elements, and functional donor-specific tolerance to rat xenoantigens was present when assessed by mixed lymphocyte reactivity in vitro. V beta 5, which is expressed at high (undeleted) levels in normal B10 mice, was consistently deleted in B10 recipients of Wistar Furth (WF), but not F344 rat bone marrow, whereas the coadministration of either F344 rat or WF rat bone marrow with B10 mouse bone marrow cells resulted in a significant decrease in expression of TCR-V beta 11. Taken together, these data demonstrate for the first time that rat bone marrow-derived cells can contribute in a strain-specific manner to the ligand for negative selection of specific mouse TCR-V beta during tolerance induction across a species barrier.

Animals↗

PubMed2002

Molecular cloning and characterization of mouse Wnt14b, clustered with mouse Wnt3 in mouse chromosome 11.

WNTs are a family of secreted-type glycoproteins implicated in embryogenesis and carcinogenesis. We have previously cloned and characterized human WNT2B/WNT13, WNT3, WNT3A, WNT5B, WNT6, WNT7B, WNT8A, WNT8B, WNT10A, WNT10B, WNT11, WNT14, and WNT14B/WNT15. WNT14B gene is clustered with WNT3 gene in human chromosome 17q21, and mRNA expression of WNT14B is significantly up-regulated by retinoic acid during the early phase of neuronal differentiation in human NT2 cells. Here, we identified mouse Wnt14b gene fragments in mouse genome draft sequence AL596108.5 by using bioinformatics, and isolated mouse Wnt14b cDNAs by using cDNA-PCR. Mouse Wnt14b was found to encode a 359-amino-acid WNT family protein with the N-terminal signal peptide, an N-linked glycosylation site, and 24 conserved cysteine residues. Mouse Wnt14b showed 92.5% total-amino-acid identity with human WNT14B, and 64.2% total-amino-acid identity with human WNT14. Mouse Wnt14b gene, consisting of 4 exons, was clustered with mouse Wnt3 gene in mouse chromosome 11. Mouse Wnt14b mRNA was relatively highly expressed in 17-day embryo, and also expressed in adult brain, kidney, liver, 7-day embryo, and 11-day embryo. This is the first report on molecular cloning and characterization of mouse Wnt14b.

Amino Acid Sequence↗

PubMed1982

More than one-third of the discernible mouse polypeptides are not expressed in a Chinese hamster-mouse embryo fibroblast hybrid that retains all mouse chromosomes.

Gene expression at the level of polypeptide synthesis has been investigated in a somatic cell hybrid (20 BW-4) isolated after fusion of spontaneously transformed, tumorigenic Chinese hamster lung fibroblasts with mouse embryo fibroblasts. This hybrid exhibited suppression of tumorigenicity and retained--in addition to the parental Chinese hamster genome--copies of all mouse chromosomes as demonstrated by direct karyotype analysis and confirmed for 18 different mouse chromosomes by analysis of 18 different mouse isozymes. Two-dimensional gel electrophoresis of [35S]methionine-labeled polypeptides from hybrid 20 BW-4 showed that the overall polypeptide pattern corresponded to that of the hamster parent. All polypeptides detected in the hamster parental cells were also expressed in the hybrid although some of them were expressed in altered amounts. Of approximately 1200 labeled polypeptides revealed in the parental cells, 115 mouse polypeptides could be clearly distinguished from the hamster polypeptides due to their different electrophoretic mobilities. Forty-two of these (i.e., 37%) were not expressed in the hybrid 20 BW-4. These observations were confirmed by analysis of another independently isolated hybrid (2W 23) of the same parental cells that also exhibited suppression of malignancy and that retained copies of all mouse chromosomes except no. 5. The results suggest that the genome of the tumorigenic cell after hybridization can suppress expression of more than one-third of the normal parental genome. The suppressed mouse genetic information is probably located on many, if not all, different mouse chromosomes. Even if the level of genetic suppression is high the mouse genome is able to reduce the tumorigenicity of the hamster parental cell.

Animals↗

PubMed1990

Structure, expression, and genetic linkage of the mouse BCM1 (OX45 or Blast-1) antigen. Evidence for genetic duplication giving rise to the BCM1 region on mouse chromosome 1 and the CD2/LFA3 region on mouse chromosome 3.

The mouse BCM1 (OX45, Blast-1) antigen has been cDNA cloned and sequenced to provide data supporting the view that BCM1, LFA3, and CD2 constitute a subgroup within the Ig superfamily. Mouse BCM1 is widely expressed on leukocytes and is likely to be anchored to the cell surface by a glycosyl-phosphatidylinositol anchor, as is the case for rat and human BCM1 antigen. Genetic linkage studies by recombination and pulse field analysis showed the BCM1 locus (Bcm-1) to be on distal mouse chromosome 1 and to be linked within 1,600 kb to the locus for an ATPase alpha chain gene (Atpa-3). A similar relationship was established between the human BCM1 locus (BCM1) and ATP1A2, and other markers on chromosome 1q. Conservation of genomic organization within a segment of human chromosome 1q and mouse chromosome 1 was demonstrated. A similar situation is seen in the region of the CD2 and LFA3 genes between mouse chromosome 3 and human chromosome 1p. Furthermore, the CD2/LFA3 genes are linked within 580 kb to Atpa-1/ATP1A1 genes to provide a parallel situation to the linkage between Bcm-1/BCM1 and Atpa-3/ATP1A2 on chromosomes 1 (mouse) and 1q (human). Taken together, the data suggest duplication of a chromosome region including the precursors of the genes for BCM1, CD2, and LFA3, and the ATPase genes to give rise to the linkage groups now observed. The duplicated regions may have stayed together on chromosome 1 in the human (with the insertion of a centromere), while in the mouse, the genetic regions are proposed to have become dispersed in the formation of chromosomes 1 and 3. CD2 and LFA3 are more dissimilar in sequence than BCM1 and LFA3, and if the precursors of the CD2 and LFA3 loci formed before the proposed chromosome segment duplication, then a gene encoding a recognizer molecule for BCM1 may exist in linkage with Bcm-1/BCM1 on chromosome 1 (mouse) and 1q (human).

Amino Acid Sequence↗

PubMed1999

Use of a repetitive mouse B2 element to identify transplanted mouse cells in mouse-chick chimeras.

Monitoring the migrations of cells during embryonic development requires a system in which cells can be identified in situ during locomotion. One promising system involves the generation of chimeras by transplanting mouse cells into chick embryos in ovo to exploit the wealth of mouse genetic variants. The success of this technique relies on the ability to detect individual mouse cells in a chick environment with high specificity. The murine B2 family of short interspersed elements is present in the mouse genome at copy numbers in excess of 10(5), whereas this sequence is absent in the chick genome based on hybridization techniques. This differential of five orders of magnitude produces signals in mouse cells that are easily identified, even in an environment that is predominantly chick. Thus, the B2 repeat probe is highly effective for the purpose of identifying mouse cells in mouse-chick chimeras.

Animals↗

PubMed2006

A mouse monoclonal antibody specific for mouse apoB48 and apoB100 produced by immunizing "apoB39-only" mice with mouse apoB48.

We have generated and characterized a murine monoclonal antibody (mAb) that binds to both mouse apolipoprotein (apo) B48 and apoB100. We immunized "apoB39-only" mice (mice that synthesize a truncated form of apoB, apoB39, but no apoB48 or apoB100) with lipoproteins containing mouse apoB48 and then used splenocytes from the immunized mice to create hybridomas. We identified a hybridoma, 2G11, that secretes a mAb that binds to mouse apoB48 and apoB100 but not to apoB39. Antibody 2G11 also binds apoB48 and apoB100 from rats and hamsters but not from humans. The mAb recognizes mouse apoB equally in very low and low density lipoproteins and was used to quantify apoB in wild-type, apoE-deficient and low-density lipoprotein receptor-deficient mice and in mice treated with an antisense drug that lowers plasma apoB levels. The antibody will be an important reagent for studying mouse models of atherosclerosis. The study also underscores the utility of genetically modified mice for generating mouse mAbs against mouse proteins.

Animals↗

PubMed1988

Feeder cells from different sources and conditioned media for recloning of human--mouse and mouse--mouse hybridomas.

The use of different feeder cell layers (peritoneal macrophages from mice and rats, spleen cells and thymocytes from mice) for recloning of human--mouse and mouse--mouse hybridomas has been described. Optimal numbers of feeder cells from different sources required for high cloning efficiencies were determined. It was possible to use cryopreserved rat and mouse macrophages as feeders for cell cloning. However, the resulting cloning efficiency was much lower in comparison to the fresh material. Culture supernatants from human endothelial cells (added in a final concentration of 40% v/v) and from chicken embryo fibroblasts (25%) could replace the feeder cell layer in recloning experiments with both human--mouse and mouse--mouse hybridomas. Therefore, conditioned media (prepared in large quantities) may be used for generating standardized conditions for high-efficient cloning and recloning of hybridoma cell lines.

Animals↗

PubMed1980

Coordinate secretion of mouse alphafetoprotein, mouse albumin and rat albumin by mouse hepatoma-rat hepatoma hybrid cells.

Mouse heptoma cells that secrete large amounts of alpha-fetoprotein (AFP) and albumin have been crossed with rat hepatoma cells that secret only albumin, and in relatively small amounts, to investigate the influence of each parental genome upon the expression of serum proteins. All of the ten independent hybrid clones examined produce mouse AFP and both mouse and rat albumin; none produces rat AFP. The absence of production of rat AFP by the hybrids suggests that different mechanisms are involved in the initiation and in the maintenance of expression of this function. The secretion of the three proteins by the hybrid cells is coordinate: Whatever the growth phase (exponential or stationary) and irrespective of the amounts produced over a wide range, the ratio secreted of mouse AFP to mouse albumin is near to one, and that of mouse albumin to rat albumin is near to five. In addition, even though the pattern of protein secretion during the growth cycle of hybrid cells is different from those of both parents, the products of both parental genomes conform to the new hybrid pattern. Finally, some hybrids secrete less of the proteins with increasing numbers of cell generations, yet all three continue to be secreted in coordinate fashion. Since the rates of secretion of serum proteins probably reflect their rates of synthesis, we conclude that coordinate secretion indicates coordinate synthesis, and may reflect coordinate transcription of the relevant genes.

Albumins↗

PubMed2000

The Mouse Genome Database (MGD): expanding genetic and genomic resources for the laboratory mouse. The Mouse Genome Database Group.

The Mouse Genome Database (MGD) is a comprehensive public database of mouse genomic, genetic and phenotypic information (http://www. informatics.jax.org). This community database provides information about genes, serves as a mapping resource of the mouse genome, details mammalian orthologs, integrates experimental data, represents standardized mouse nomenclature for genes and alleles, incorporates links to other genomic resources such as sequence data, and includes a variety of additional information about the laboratory mouse. MGD scientists and annotators work cooperatively with the research community to provide an integrated, consensus view of the mouse genome while also providing experimental data including data conflicting with the consensus representation. Recent improvements focus on the representation of phenotypic information and the enhancement of gene and allele descriptions.

Animals↗

PubMed1984

Effect of mouse lymphokines and cloned mouse interferon-gamma on the interaction of Rickettsia prowazekii with mouse macrophage-like RAW264.7 cells.

We studied the effects of crude mouse lymphokines and cloned mouse interferon-gamma on the interaction of Rickettsia prowazekii with mouse macrophage-like RAW264.7 cells. Treatment of RAW264.7 cells with lymphokines before infection, after infection, or both before and after infection with R. prowazekii led to killing of a substantial proportion of the RAW264.7 cells. Such cytotoxicity required both lymphokines and viable R. prowazekii and did not occur in mouse fibroblastic L929 cells. Untreated cultures of RAW264.7 cells supported good growth of the Breinl strain of R. prowazekii, but in lymphokine-treated cultures, little or no rickettsial growth occurred in the cells that survived the cytotoxic reaction. In addition, treatment of RAW264.7 cells with lymphokines before rickettsial infection was associated with suppression of the initial infection. The effects of cloned mouse interferon-gamma were similar to the effects of crude mouse lymphokines. Assessment of cytotoxicity, inhibition of the initial infection, and inhibition of rickettsial growth in RAW264.7 cells pretreated with various concentrations of interferon-gamma indicated that the effects of the lymphokines could be explained by the interferon-gamma that was present in these preparations. Treatment of RAW264.7 cells with interferon-gamma makes them unsuitable host cells for R. prowazekii.

Animals↗

PubMed1977

Rejection of mouse-derived Schistosoma japonicum and serum lethality of host immunized with mouse globulin or mouse erythrocytes.

Fourteen-day-old, mouse-derived Schistosoma japonicum schistosomula survived, matured, and deposited viable eggs following surgical transfer to the hepatic portal system of rabbits. The survival of such schistosomula is essentially eliminated in rabbits immunized with either mouse erythrocytes or mouse gamma globulin. Sera from rabbits immunized with either mouse erthrocytes or mouse gamma globulin in the presence of normal leukocytes is lethal for mouse-derived schistosomula 14 days of age or older. These sera have no significant effect on newly transformed schistosomula or those derived from rabbits. It is suggested that these results give additional evidence that immunological enhancement is one of the mechanisms involved in parasite survival.

Animals↗

PubMed2002

Infertility of CD9-deficient mouse eggs is reversed by mouse CD9, human CD9, or mouse CD81; polyadenylated mRNA injection developed for molecular analysis of sperm-egg fusion.

CD9 is a membrane protein belonging to the tetraspanin family. Despite CD9's broad tissue distribution, the only abnormality observed in CD9-deficient mice was infertility of females, which was responsible for a defect in the sperm-egg fusion process. However, the function of CD9 in sperm-egg fusion is not clear at all because the technique to analyze the activity of molecules in sperm-egg fusion has not been established. We demonstrated that the exogenous mouse CD9, expressed by polyadenylated mRNA injection at the germinal-vesicle stage oocytes, was precisely localized to the egg plasma membrane, and the expression reversed the infertility of CD9(-/-) eggs. Then, two other tetraspanins, human CD9 and mouse CD81, overexpressed with this technique on CD9(-/-) eggs restored the fertilization rate up to approximately 90 and approximately 50% against that of wild type eggs, respectively. Moreover, in the presence of an anti-mouse CD9 mAb, which blocks sperm-egg fusion, expression of human CD9 or mouse CD81 on eggs also rescued the fusibility. These results suggested that human CD9 plays a crucial role in human fertilization, and mouse CD81 has the potential to compensate for CD9 function in sperm-egg fusion. In addition, the polyadenylated mRNA injection is effective for molecular analysis of sperm-egg fusion.

Animals↗

PubMed1988

Effect of a monoclonal anti-mouse sperm antibody (OBF13) on the interaction of mouse sperm with zona-free mouse and hamster eggs.

Mouse eggs freed from zonae by chymotrypsin were mixed with sperm and pronuclear formation was observed. When anti-mouse sperm monoclonal antibody (OBF 13) from ascites fluid was added to the medium (at a final concentration of 0.05%), fertilization was significantly inhibited (9.7 +/- 4.3% compared to control 56.7 +/- 7.4%, P less than 0.01). This was based on the inhibition of sperm binding to the egg. However, when similar experiments were performed using zona-free hamster eggs, addition of the OBF 13 antibody caused no significant reduction in fertilization rate (91 +/- 7.1% compared to control 97 +/- 3.2%). It was also observed that binding of mouse sperm to hamster eggs was not inhibited by the antibody. It is therefore suggested that mouse sperm and mouse egg recognize each other in a species-specific manner.

Animals↗