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  • 11
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    Prevention of allogeneic bone marrow graft rejection by H-2 transgene in donor mice (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-11-03
    Description: Rejection of bone marrow grafts in irradiated mice is mediated by natural killer (NK) cells and is controlled by genes linked to the major histocompatibility complex (MHC). It has, however, not been possible to identify the genes or their products. An MHC class I (Dd) transgene introduced in C57BL donors prevented the rejection of their bone marrow by NK cells in irradiated allogeneic and F1 hybrid mice expressing the Dd gene. Conversely, H-2Dd transgenic C57BL recipients acquired the ability to reject bone marrow from C57BL donors but not from H-2Dd transgenic C57BL donors. These results provide formal evidence that NK cells are part of a system capable of rejecting cells because they lack normal genes of the host type, in contrast to T cells, which recognize cells that contain abnormal or novel sequences of non-host type.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ohlen, C -- Kling, G -- Hoglund, P -- Hansson, M -- Scangos, G -- Bieberich, C -- Jay, G -- Karre, K -- 1 ROI CA 44882-01/CA/NCI NIH HHS/ -- 5 ROI CA-25250-06/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1989 Nov 3;246(4930):666-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Tumor Biology, Karolinska Institute, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2814488" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Marrow Transplantation ; *Genes, MHC Class I ; *Graft Rejection ; H-2 Antigens/*genetics ; Killer Cells, Natural/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; Transplantation, Homologous
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 12
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    Function of myosin-V in filopodial extension of neuronal growth cones (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-02
    Description: The molecular mechanisms underlying directed motility of growth cones have not been determined. The role of myosin-V, an unconventional myosin, in growth cone dynamics was examined by chromophore-assisted laser inactivation (CALI). CALI of purified chick brain myosin-V absorbed onto nitrocellulose-coated cover slips inhibited the ability of myosin-V to translocate actin filaments. CALI of myosin-V in growth cones of chick dorsal root ganglion neurons resulted in rapid filopodial retraction. The rate of filopodial extension was significantly decreased, whereas the rate of filopodial retraction was not affected, which suggests a specific role for myosin-V in filopodial extension.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, F S -- Wolenski, J S -- Cheney, R E -- Mooseker, M S -- Jay, D G -- NS-29007/NS/NINDS NIH HHS/ -- NS-34699/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Aug 2;273(5275):660-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662560" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/pharmacology ; Animals ; Axons/*physiology/ultrastructure ; Calmodulin-Binding Proteins/antagonists & inhibitors/immunology/*physiology ; Cells, Cultured ; Chick Embryo ; Dendrites/*physiology/ultrastructure ; Fluorescent Antibody Technique, Indirect ; Ganglia, Spinal/cytology ; Lasers ; Microinjections ; Myosin Light Chains/antagonists & inhibitors/immunology/*physiology ; *Myosin Type V ; Nerve Tissue Proteins/antagonists & inhibitors/immunology/*physiology ; Pseudopodia/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    Functional insertion of an Alu type 2 (B2 SINE) repetitive sequence in murine class I genes (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-23
    Description: The regulation of expression of the family of MHC (major histocompatibility complex) class I genes is complex. Sequence analysis has revealed that class I genes from the H-2D subregion of the MHC (which includes the D and L genes) differ from the class I gene from the H-2K subregion (the K gene) by the insertion of a type 2 Alu-like repetitive element (the murine B2 sequence) within the 3' noncoding region of the D and L genes. The consequence of this insertion in the D and L genes is the introduction of a novel polyadenylation signal, which is preferentially used over the more distal signal, the analog of that found in the K gene. The insertion of the type 2 Alu-like sequence results in a change in the preferred site for endonucleolytic cleavage which is necessary for generating a correct 3' terminus for polyadenylation. The data demonstrate that the type 2 Alu-like sequence has a function; the data also suggest a possible regulatory role of this sequence in the expression of class I genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kress, M -- Barra, Y -- Seidman, J G -- Khoury, G -- Jay, G -- AI 19148/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1984 Nov 23;226(4677):974-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6095445" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Deletion ; *Cloning, Molecular ; DNA/*metabolism ; DNA Restriction Enzymes ; *DNA Transposable Elements ; Genes, MHC Class II ; Genetic Linkage ; *Major Histocompatibility Complex ; Mice ; Protein Biosynthesis ; Repetitive Sequences, Nucleic Acid
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 14
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    Reversal of oncogenesis by the expression of a major histocompatibility complex class I gene (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-05
    Description: The classical transplantation antigens (the major histocompatibility complex class I antigens) play a key role in host defense against cells expressing foreign antigens. Several naturally occurring tumors and virally transformed cells show an overall suppression of these surface antigens. Since the class I molecules are required in the presentation of neoantigens on tumor cells to the cytotoxic T lymphocytes, their absence from the cell surface may lead to the escape of these tumors from immunosurveillance. To test this possibility, a functional class I gene was transfected into human adenovirus 12-transformed mouse cells that do not express detectable levels of class I antigens; the transformants were tested for expression of the transfected gene and for changes in oncogenicity. The expression of a single class I gene, introduced by DNA-mediated gene transfer into highly tumorigenic adenovirus 12-transformed cells, was sufficient to abrogate the oncogenicity of these cells. This finding has important implications for the regulation of the malignant phenotype in certain tumors and for the potential modulation of oncogenicity through derepression of the endogenous class I genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanaka, K -- Isselbacher, K J -- Khoury, G -- Jay, G -- New York, N.Y. -- Science. 1985 Apr 5;228(4695):26-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975631" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/immunology ; Cell Line ; Immunization ; *Major Histocompatibility Complex ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neoplasm Transplantation ; Neoplasms, Experimental/genetics/*immunology ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 15
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    A transgenic mouse model for human neurofibromatosis (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-09-11
    Description: Human T-lymphotropic virus type 1 (HTLV-1) has been associated with the neurologic disorder tropical spastic paraparesis and possibly with multiple sclerosis. The tat gene of HTLV-1 under control of its own long terminal repeat is capable of inducing tumors in transgenic mice. The morphologic and biologic properties of these tumors indicate their close resemblance to human neurofibromatosis (von Recklinghausen's disease), the most common single gene disorder to affect the nervous system. The high spontaneous incidence of this disease, together with the diverse clinical and pathologic features associated with it, suggests that environmental factors may account for some of the observed cases. Multiple tumors developed simultaneously in the transgenic tat mice at approximately 3 months of age, and the phenotype was successfully passed through three generations. The tumors arise from the nerve sheaths of peripheral nerves and are composed of perineural cells and fibroblasts. Tumor cells from these mice adapt easily to propagation in culture and continue to express the tat protein in significant amounts. When transplanted into nude mice, these cultured cells efficiently induce tumors. Evidence of HTLV-1 infection in patients with neural and other soft tissue tumors is needed in order to establish a link between infection by this human retrovirus and von Recklinghausen's disease and other nonlymphoid tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hinrichs, S H -- Nerenberg, M -- Reynolds, R K -- Khoury, G -- Jay, G -- New York, N.Y. -- Science. 1987 Sep 11;237(4820):1340-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2888191" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Deltaretrovirus Infections/*genetics/pathology ; Disease Models, Animal ; Fluorescent Antibody Technique ; Genetic Engineering ; Humans ; Mice ; Mice, Nude ; Neurofibromatosis 1/*genetics/microbiology/pathology ; Viral Fusion Proteins/analysis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    The tat gene of human T-lymphotropic virus type 1 induces mesenchymal tumors in transgenic mice (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-09-11
    Description: Human T-lymphotropic virus type 1 (HTLV-1) is a suspected causative agent of adult T-cell leukemia. One of the viral genes encodes a protein (tat) that not only results in transactivation of viral gene expression but may also regulate the expression of certain cellular genes that are important for cell growth. Transgenic mice that expressed the authentic tat protein under the control of the HTLV-1 long terminal repeat were generated, and cell types that are permissive for the viral promoter and the effects of the tat gene on these cells were studied. Three of eight founder mice with high levels of expression of the transgene in muscle were bred and then analyzed. All developed soft tissue tumors at multiple sites between 13 to 17 weeks of age. This phenotype was transmitted to nine of nine offspring that inherited the tat gene and were available for analysis. The remaining five founders expressed the transgene in the thymus, as well as in muscle. This second group of mice all exhibited extensive thymic depletion and growth retardation; in all of these mice, death occurred between 3 to 6 weeks of age before tumors became macroscopically visible. The tat gene under the control of the HTLV-1 regulatory region showed tissue-specific expression and the tat protein efficiently induced mesenchymal tumors. The data establish tat as an oncogenic protein and HTLV-1 as a transforming virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nerenberg, M -- Hinrichs, S H -- Reynolds, R K -- Khoury, G -- Jay, G -- New York, N.Y. -- Science. 1987 Sep 11;237(4820):1324-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2888190" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Deltaretrovirus/*genetics ; Deltaretrovirus Infections/*genetics ; Female ; *Genes, Viral ; Genetic Engineering ; Genetic Vectors ; Male ; Mesenchymoma/genetics/*microbiology ; Mice ; Pedigree ; Plasmids ; Protein Biosynthesis ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Neoplastic transformation of human epidermal keratinocytes by AD12-SV40 and Kirsten sarcoma viruses (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-08
    Description: Recent investigations have begun to dissect the number and nature of genetic alterations associated with cancer cells. In the present study, primary human epidermal keratinocytes acquired indefinite life-span in culture but did not undergo malignant conversion in response to infection with a hybrid of adenovirus 12 and simian virus 40. Addition of Kirsten murine sarcoma virus, which contains a K-ras oncogene, to these cells induced morphological alterations associated with the acquisition of neoplastic properties. These findings demonstrate the malignant transformation of human primary epithelial cells in culture and support a multiple-step process for neoplastic conversion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rhim, J S -- Jay, G -- Arnstein, P -- Price, F M -- Sanford, K K -- Aaronson, S A -- New York, N.Y. -- Science. 1985 Mar 8;227(4691):1250-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2579430" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviruses, Human/*metabolism ; Animals ; Cell Transformation, Neoplastic/*metabolism ; Epithelial Cells ; Humans ; Keratins ; Kirsten murine sarcoma virus/*metabolism ; Mice ; Mice, Inbred C3H ; Mice, Nude ; Sarcoma Viruses, Murine/*metabolism ; Sarcoma, Experimental/metabolism ; Simian virus 40/*metabolism ; Skin/*cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Distribution, composition, and orientation of down deadwood in riparian old-growth woodlands of Zoar Valley Canyon, western New York State, USA (2007)
    Elsevier
    Details
    Publication Date: 2007-02-01
    Print ISSN: 0378-1127
    Electronic ISSN: 1872-7042
    Topics: Biology , Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
    Published by Elsevier
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  • 19
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    The lake breeze-ground-level ozone connection in eastern Wisconsin: a climatological perspective (2002)
    Wiley
    Details
    Publication Date: 2002-01-01
    Print ISSN: 0899-8418
    Electronic ISSN: 1097-0088
    Topics: Geosciences , Physics
    Published by Wiley
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  • 20
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    Diatom assemblages in a reservoir sediment core track land-use changes in the watershed (2015)
    Springer
    Details
    Publication Date: 2015-09-26
    Print ISSN: 0921-2728
    Electronic ISSN: 1573-0417
    Topics: Biology , Geosciences
    Published by Springer
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