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At least 1,279 records · Page 71Linked to original sources
PubMedDate not supplied

Antitumor potential of interferon-gamma: retroviral expression of mouse interferon-gamma cDNA in two kinds of highly metastatic mouse tumor lines reduces their tumorigenicity.

The antitumor effects of interferon (IFN)-gamma were examined in two types of malignant metastatic mouse tumor cell lines following their transfection with the IFN-gamma gene by retroviral gene transfer. In both ovarian and lung tumor lines, but more markedly in the latter, subcutaneous (s.c.) tumor progression of the IFN-gamma-producing cells was profoundly suppressed in the normal syngeneic as well as in athymic nude mice. In addition, experimental metastasis via the tail vein of the IFN-gamma producers was also suppressed. Lung tumor suppression was abolished by X-irradiation of the syngeneic mice or by the administration of antiasialoganglioside GM1 antibodies into the nude mice. These results suggest that tumor suppression is due to the effect of the tumor-derived IFN-gamma on the host antitumor mechanisms including natural killer cells. Moreover, tumorigenicity of several unrelated tumor cells was significantly reduced when s.c. injected as a mixture with the apparently benign IFN-gamma-producing lung tumor cells, so that such 'non-malignant' IFN-gamma-producing cells may have therapeutic benefit against certain other malignant tumors.

Animals↗
PubMedDate not supplied

Studies on sperm chromatin structure alterations and cytogenetic damage of mouse sperm following in vitro incubation. Studies on in vitro-incubated mouse sperm.

Mouse epididymal sperm incubated in Tyrode's T6 fertilization media were analyzed over time for chromosome damage by two methods. First, cytogenetic analysis was done on paternal pronuclei metaphase chromosomes. After 6 hours incubation 11% of the cells demonstrated chromosome structural abnormalities. Secondly, sperm nuclei were measured by the sperm chromatin structure assay, which is a measure of the susceptibility of sperm DNA to the nuclei demonstrated an increased susceptibility to DNA denaturation, reaching near 100% by 48 hours. Changes in chromatin structure at the molecular level may lead to chromosome breaks seen in pronuclear chromosomes.

Animals↗
PubMed1996

Inactivation of mouse alpha-globin gene by homologous recombination: mouse model of hemoglobin H disease.

We have disrupted the 5' locus of the duplicated adult alpha-globin genes by gene targeting in the mouse embryonic stem cells and created mice with alpha-thalassemia syndromes. The heterozygous knockout mice (.alpha/alpha alpha) are asymptomatic like the silent carriers in humans whereas the homozygous knockout mice (.alpha/.alpha) show hemolytic anemia. Mice with three dysfunctional alpha-globin genes generated by breeding the 5' alpha-globin knockouts (.alpha/alpha alpha) and the deletion type alpha-thalassemia mice (../alpha alpha) produce severe hemoglobin H disease and they die in utero. These results indicate that the 5' alpha-globin gene is the predominant locus in mice, and suggest that it is even more dominant than its human homologue.

Animals↗
PubMed1997

[Knockout mouse--its characteristics and application (1): NMDA receptor subunit knockout mouse].

The N-methyl-D-aspartate (NMDA) type of glutamate receptors is thought to be essential in many central actions of neurotransmitter glutamate, including learning, memory, neurodevelopment and neurodegenerative disorders. Recent molecular cloning has revealed that the NMDA receptor has multiple subunits with distinct distribution, properties and regulation. This implies that NMDA receptors are different in molecular architecture and functional properties, depending on the brain region and developmental stage. To clarify the significance of the molecular diversity of NMDA receptors in vivo, a gene-targeting technique was applied to NMDA receptor subunit genes and several strains of mutant mice lacking targeted NMDA receptor subunit molecules were created. Using these NMDA receptor subunit knockout mice, various physiological, histological and behavioral analyses were performed. In this article, after briefly reviewing recent findings, we discuss the advantages and disadvantages of the NMDA receptor subunit knockout mouse as a tool for the studies of NMDA receptors and synaptic plasticity.

Animals↗
PubMed1999

Reconstitution of the functional mouse oncostatin M (OSM) receptor: molecular cloning of the mouse OSM receptor beta subunit.

Oncostatin M (OSM) is a member of the interleukin-6 (IL-6) family of cytokines that share the gp130 receptor subunit. Of these family members, leukemia inhibitory factor (LIF) is most closely related to OSM, and various overlapping biologic activities have been described between human LIF and OSM (hLIF and hOSM). Two types of functional hOSM receptors are known: the type I OSM receptor is identical to the LIF receptor that consists of gp130 and the LIF receptor beta subunit (LIFRbeta), and the type II OSM receptor consists of gp130 and the OSM receptor beta subunit (OSMRbeta). It is thus conceivable that common biologic activities between hLIF and hOSM are mediated by the shared type I receptor and OSM-specific activities are mediated by the type II receptor. However, in contrast to the human receptors, recent studies have demonstrated that mouse OSM (mOSM) does not activate the type I receptor and exhibits unique biologic activity. To elucidate the molecular structure of the functional mOSM receptor, we cloned a cDNA encoding mOSMRbeta, which is 55.5% identical to the hOSMRbeta at the amino acid level. mOSM-responsive cell lines express high-affinity mOSM receptors, as well as mOSMRbeta, whereas embryonic stem cells, which are responsive to LIF but not to mOSM, do not express mOSMRbeta. mOSMRbeta alone binds mOSM with low affinity (kd = 13.0 nmol/L) and forms a high-affinity receptor (kd = 606 pmol/L) with gp130. Ba/F3 transfectants expressing both mOSMRbeta and gp130 proliferated in response to mOSM, but failed to respond to LIF and human OSM. Thus, the cloned mOSMRbeta constitutes an essential and species-specific receptor component of the functional mOSM receptor. Reminiscent of the colocalization of the mOSM and mLIF genes, the mOSMRbeta gene was found to be located in the vicinity of the LIFRbeta locus in the proximal end of chromosome 15.

Amino Acid Sequence↗
PubMed1983

Integration of new endogenous mouse mammary tumor virus proviral DNA at common sites in the DNA of mammary tumors of C3Hf mice and hypomethylation of the endogenous mouse mammary tumor virus proviral DNA in C3Hf mammary tumors and spleens.

To understand the molecular mechanisms by which the endogenous murine mammary tumor virus (MuMTV) proviruses are expressed and produce late-occurring mammary tumors in C3Hf mice, we analyzed, by the use of restriction enzymes and the Southern transfer procedure, genomic DNA from normal organs of mammary tumor-bearing and tumor-free mice and from 12 late-occurring C3Hf mammary tumors. We found, by using the restriction enzymes EcoRI and HindIII, that in addition to the preexisting endogenous MuMTV proviruses, new MuMTV-specific proviral DNA was integrated into new sites in the host genome in all 12 of the tumors that we examined. PstI digests of C3Hf tumor DNA revealed that the new proviral DNA found in C3Hf tumors was of endogenous origin. Moreover, the respective sizes of at least one of the new DNA fragments generated by EcoRI or HindIII digestion were the same in at least 50% of the C3Hf tumors analyzed, suggesting that the integration site of this new proviral DNA could be at the same location in the host genome of these tumors. Our results may imply that mammary tumorigenesis in C3Hf mice results from activation of cellular oncogenes by an MuMTV proviral DNA promoter. Specific hypomethylation of MuMTV proviral DNA was detected in the mammary tumors and spleens of C3Hf tumor-bearing mice. Our results indicated that most, if not all, of the hypomethylated MuMTV proviral DNA sequences were derived from the endogenous MuMTV provirus located at the MTV-1 locus, a locus responsible for the production of MuMTV antigens and increased incidence of mammary carcinoma in C3Hf mice. In spleens of non-tumor-bearing mice of ages 3, 6, 9, and 12 months, there was progressive hypomethylation of proviral DNA with increasing age, suggesting a possible correlation between demethylation of MuMTV proviral DNA in the spleens of C3Hf mice and the expression of endogenous MuMTV.

Aging↗