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  • Articles  (91)
  • Mice  (91)
  • American Association for the Advancement of Science (AAAS)  (91)
  • American Institute of Physics
  • Elsevier
  • 2020-2022
  • 1985-1989  (91)
  • 1950-1954
  • 1945-1949
  • 1988  (91)
Collection
  • Articles  (91)
Source
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (91)
  • American Institute of Physics
  • Elsevier
  • Springer  (6)
Years
  • 2020-2022
  • 1985-1989  (91)
  • 1950-1954
  • 1945-1949
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  • 1
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    The ras oncogenes increase the intrinsic resistance of NIH 3T3 cells to ionizing radiation (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-05
    Description: Identification of genes that function to protect cells from radiation damage is an essential step in understanding the molecular mechanisms by which mammalian cells cope with ionizing radiation. The intrinsic radiation resistance (D0) of NIH 3T3 cells was markedly and significantly increased by transformation with ras oncogenes activated by missense mutations. This radiobiologic activity appeared to be a specific consequence of the ras mutations rather than of transformation, since revertant cells that contained functional ras genes (but were no longer phenotypically transformed) retained their increased D0's.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sklar, M D -- CA 41166/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 5;239(4840):645-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, University of Michigan Medical School, Ann Arbor 48109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3277276" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Survival/*radiation effects ; Cell Transformation, Neoplastic ; Cells, Cultured ; Clone Cells ; Dose-Response Relationship, Radiation ; *Genes, ras ; Mice ; Mice, Inbred Strains
    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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  • 2
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    Immunotherapy of the nonobese diabetic mouse: treatment with an antibody to T-helper lymphocytes (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-04-29
    Description: Spontaneous diabetes mellitus was blocked in nonobese diabetic mice by treatment with a monoclonal antibody against the L3T4 determinant present on the surface of T-helper lymphocytes. Sustained treatment with the monoclonal antibody led to cessation of the lymphocytic infiltration associated with the destruction of the insulin-producing beta cells. Moreover, the mice remained normoglycemic after the antibody therapy was stopped. These studies indicate that immunotherapy with monoclonal antibodies to the lymphocyte subset may not only halt the progression of diabetes, but may lead to long-term reversal of the disease after therapy has ended.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shizuru, J A -- Taylor-Edwards, C -- Banks, B A -- Gregory, A K -- Fathman, C G -- AI11313/AI/NIAID NIH HHS/ -- DK39959/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 29;240(4852):659-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Stanford University Medical Center, CA 94305-5111.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2966437" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*therapeutic use ; Antigens, Differentiation, T-Lymphocyte/*immunology ; Cyclosporins/therapeutic use ; Diabetes Mellitus, Experimental/pathology/*therapy ; Female ; *Immunotherapy ; Islets of Langerhans/pathology ; Lymphocytes/pathology ; Mice ; Mice, Inbred ICR ; T-Lymphocytes, Helper-Inducer/*immunology/pathology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Antisense RNA directed against the 3' noncoding region prevents dormant mRNA activation in mouse oocytes (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-05
    Description: Primary mouse oocytes contain untranslated stable messenger RNA for tissue plasminogen activator (t-PA). During meiotic maturation, this maternal mRNA undergoes a 3'-polyadenylation, is translated, and is degraded. Injections of maturing oocytes with different antisense RNA's complementary to both coding and noncoding portions of t-PA mRNA all selectively blocked t-PA synthesis. RNA blot analysis of t-PA mRNA in injected, matured oocytes suggested a cleavage of the RNA.RNA hybrid region, yielding a stable 5' portion, and an unstable 3' portion. In primary oocytes, the 3' noncoding region was susceptible to cleavage, while the other portions of the mRNA were blocked from hybrid formation until maturation occurred. Injection of antisense RNA complementary to 103 nucleotides of its extreme 3' untranslated region was sufficient to prevent the polyadenylation, translational activation, and destabilization of t-PA mRNA. These results demonstrate a critical role for the 3' noncoding region of a dormant mRNA in its translational recruitment during meiotic maturation of mouse oocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strickland, S -- Huarte, J -- Belin, D -- Vassalli, A -- Rickles, R J -- Vassalli, J D -- HD-17875/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 5;241(4866):680-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Histology and Embryology, University of Geneva Medical School, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2456615" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Mice ; Nucleic Acid Hybridization ; Oocytes/*metabolism ; Poly A/metabolism ; Protein Biosynthesis/drug effects ; RNA/*pharmacology ; RNA, Antisense ; RNA, Messenger/*antagonists & inhibitors/metabolism ; Tissue Plasminogen Activator/*genetics
    Print ISSN: 0036-8075
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  • 4
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    A transcriptional enhancer 3' of C beta 2 in the T cell receptor beta locus (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-08
    Description: Run-on transcription experiments were used to demonstrate that transcription of T cell receptor beta chain V genes is activated by DNA rearrangement, in a manner similar to immunoglobulin genes. A transcriptional enhancer likely to be involved in this activation has been identified. A 25-kilobase region from J beta 1 to V beta 14 was tested for enhancer activity by transient transfections, and an enhancer was found 7.5 kilobases 3' of C beta 2. The beta enhancer has low activity relative to the simian virus 40 viral enhancer, does not display a preference for V beta promoters, has a T cell-specific activity, and binds two purified immunoglobulin heavy chain enhancer factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDougall, S -- Peterson, C L -- Calame, K -- GM29361/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 8;241(4862):205-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, UCLA School of Medicine 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2968651" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; Genes, Immunoglobulin ; Immunoglobulin Heavy Chains/genetics ; In Vitro Techniques ; Mice ; Nuclear Proteins/physiology ; Receptors, Antigen, T-Cell/*genetics ; Receptors, Antigen, T-Cell, alpha-beta ; *Regulatory Sequences, Nucleic Acid ; Transcription Factors/physiology ; Transcription, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Selection of variable-joining region combinations in the alpha chain of the T cell receptor (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-09
    Description: Most T lymphocytes express an antigen-specific receptor composed of two subunits, alpha and beta, each of which can exhibit structural variability. A complex selection process operates on T cells during development in the thymus such that cells expressing only particular alpha beta-receptors migrate to the periphery. The alpha-chain repertoire was dissected at different stages of the selection process by using the polymerase chain reaction (PCR) technique to amplify only those transcripts of a particular variable region gene (V58). Sequences from these V58 cDNAs reveal the predominant expression of four joining (J) segments by T cells in the adult thymus, suggesting that molecular or cellular processes select particular V alpha J alpha combinations during development. T cells expressing one of these V58J alpha chains appear to have been negatively selected at a later stage, since these transcripts were present in the spleen at approximately one-tenth the level in the thymus. Results also indicate that residues present at the V alpha J alpha junction may be important in an early selection process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roth, M E -- Lacy, M J -- McNeil, L K -- Kranz, D M -- AI24635/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 9;241(4871):1354-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Illinois, Urbana 61801.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2970673" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Genes ; *Major Histocompatibility Complex ; Mice ; Mice, Inbred Strains ; Molecular Sequence Data ; Receptors, Antigen, T-Cell/*genetics ; Receptors, Antigen, T-Cell, alpha-beta ; Recombination, Genetic ; Spleen/physiology ; T-Lymphocytes/*physiology ; Thymus Gland/physiology ; Tissue Distribution
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  • 6
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    Salivary gland lysates from the sand fly Lutzomyia longipalpis enhance Leishmania infectivity (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-03-11
    Description: Leishmaniasis is a parasitic disease transmitted by phlebotomine sand flies. The role of sand fly saliva in transmission of the disease was investigated by injecting mice with Leishmania major parasites in the presence of homogenized salivary glands from Lutzomyia longipalpis. This procedure resulted in cutaneous lesions of Leishmania major that were routinely five to ten times as large and contained as much as 5000 times as many parasites as controls. With inocula consisting of low numbers of Leishmania major, parasites were detected at the site of injection only when the inoculum also contained salivary gland material. This enhancing effect of sand fly salivary glands on cutaneous leishmaniasis occurred with as little as 10 percent of the contents of one salivary gland of one fly. Material obtained from other bloodsucking arthropods could not mediate the phenomenon.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Titus, R G -- Ribeiro, J M -- 1 R29 AI24511/AI/NIAID NIH HHS/ -- 5 P01 AI22794/AI/NIAID NIH HHS/ -- AI18694 0481/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1306-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Rheumatology and Immunology, Brigham and Women's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3344436" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthropods ; *Diptera ; Leishmania tropica/*pathogenicity ; Leishmaniasis/*physiopathology ; Mice ; Mice, Inbred CBA ; Salivary Glands ; Species Specificity ; Tissue Extracts/*pharmacology
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  • 7
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    Two mechanisms for the extinction of gene expression in hybrid cells (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-02
    Description: When two different mammalian cell types are fused to generate a stable hybrid cell line, genes that are active in only one of the parents are frequently shut off, a phenomenon called extinction. In this study two distinct, complementary mechanisms for such extinction of growth hormone gene expression were identified. In hybrids formed by fusing fibroblasts to pituitary cells, pituitary-specific proteins that bind to the growth hormone promoter were absent. In addition, a negative regulatory element located near the rat growth hormone promoter was specifically activated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tripputi, P -- Guerin, S L -- Moore, D D -- New York, N.Y. -- Science. 1988 Sep 2;241(4870):1205-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital, Boston.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2842865" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Animals ; Avian Sarcoma Viruses/genetics ; Chloramphenicol O-Acetyltransferase ; Enhancer Elements, Genetic ; Fibroblasts/metabolism ; *Gene Expression Regulation ; Growth Hormone/*genetics ; Herpesviridae/genetics ; Hybrid Cells/*metabolism ; Hypoxanthine Phosphoribosyltransferase/genetics ; L Cells (Cell Line) ; Mice ; Pituitary Gland/metabolism ; Plasmids ; Promoter Regions, Genetic ; Rats ; Thymidine Kinase/genetics ; Transfection
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  • 8
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    Nuclear factors in B lymphoma enhance splicing of mouse membrane-bound mu mRNA in Xenopus oocytes (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-01-29
    Description: Regulation of the synthesis of membrane-bound and secreted immunoglobulin mu heavy chains at the level of RNA processing is an important element for B cell development. The precursor mu RNA is either polyadenylated at the upstream poly(A) site (for the secreted form) or spliced (for the membrane-bound form) in a mutually exclusive manner. When the mouse mu gene linked to the SV40/HSV-TK hybrid promoter was microinjected into Xenopus oocytes, the mu messenger RNA (mRNA) was altered by coinjection of nuclei of mouse surface IgM-bearing B-lymphoma cells to include the synthesis of the membrane-bound form. An increase in the membrane-bound form was not observed when nuclei of IgM-secreting hybridoma cells or fibroblast cells were coinjected. Deletion of the upstream poly(A) site did not eliminate the effect of B-lymphoma nuclei suggesting that membrane-specific splicing is stimulated. Further, splicing of other mu gene introns was not affected by coinjection of B-lymphoma nuclei. These results suggest that mature B cells contain one or more transacting nuclear factors that stimulate splicing specific for membrane-bound mu mRNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsurushita, N -- Ho, L -- Korn, L J -- AI21298/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 29;239(4839):494-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3124268" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology/ultrastructure ; Cell Membrane/metabolism ; Cell Nucleus/*physiology ; DNA, Recombinant ; Female ; Hybridomas/ultrastructure ; Immunoglobulin M/genetics ; Immunoglobulin mu-Chains/*genetics ; Introns ; Lymphoma/*immunology/ultrastructure ; Mice ; Microinjections ; Nuclear Transfer Techniques ; Oocytes/*metabolism ; Plasmids ; Promoter Regions, Genetic ; *RNA Splicing ; RNA, Messenger/*genetics ; Tumor Cells, Cultured ; Xenopus
    Print ISSN: 0036-8075
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  • 9
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    Reshaping human antibodies: grafting an antilysozyme activity (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-03-25
    Description: The production of therapeutic human monoclonal antibodies by hybridoma technology has proved difficult, and this has prompted the "humanizing" of mouse monoclonal antibodies by recombinant DNA techniques. It was shown previously that the binding site for a small hapten could be grafted from the heavy-chain variable domain of a mouse antibody to that of a human myeloma protein by transplanting the hypervariable loops. It is now shown that a large binding site for a protein antigen (lysozyme) can also be transplanted from mouse to human heavy chain. The success of such constructions may be facilitated by an induced-fit mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Verhoeyen, M -- Milstein, C -- Winter, G -- New York, N.Y. -- Science. 1988 Mar 25;239(4847):1534-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Laboratory of Molecular Biology, Cambridge, England.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2451287" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibodies, Monoclonal/genetics/immunology ; Base Sequence ; Binding Sites, Antibody ; Binding, Competitive ; Cloning, Molecular ; DNA, Recombinant ; Epitopes/immunology ; Humans ; Immunoglobulin G/genetics/immunology ; Immunoglobulin Variable Region/genetics ; Mice ; Molecular Sequence Data ; Muramidase/*immunology ; Plasmids ; Recombinant Proteins ; Transfection
    Print ISSN: 0036-8075
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  • 10
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    Familial imprinting determines H-2 selective mating preferences (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-06-03
    Description: Inbred male mice typically prefer to mate with females of a different, non-self H-2 haplotype. To determine whether this natural preference is irrevocable or results from familial imprinting, a test system was used which relied on previous observations that B6 males (H-2b) mate preferentially with congenic B6-H-2k rather than B6 females, and B6-H-2k males with B6 females. This preference was reversed in B6 males fostered by B6-H-2k parents and in B6-H-2k males fostered by B6 parents, preference in these cases favoring the same H-2 type. Thus, H-2 selective mating preference is acquired by imprinting on familial H-2 types.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamazaki, K -- Beauchamp, G K -- Kupniewski, D -- Bard, J -- Thomas, L -- Boyse, E A -- CA-39827/CA/NCI NIH HHS/ -- GMCA-32096/GM/NIGMS NIH HHS/ -- NS-22623/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 3;240(4857):1331-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Monell Chemical Senses Center, Philadelphia, PA 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3375818" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; H-2 Antigens/*genetics ; *Imprinting (Psychology) ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Odors ; *Sexual Behavior, Animal ; Smell/physiology
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  • 11
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    Reconstruction of an immune system (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yancopoulos, G D -- Alt, F W -- New York, N.Y. -- Science. 1988 Sep 23;241(4873):1581-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3262236" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/physiology ; *Chimera ; Immune System/cytology/*physiology/surgery ; Immune Tolerance ; Immunoglobulin Variable Region/genetics ; Immunologic Deficiency Syndromes/etiology/genetics ; Lymphoid Tissue/transplantation ; Mice ; Mice, Mutant Strains/*immunology ; *Models, Biological ; T-Lymphocytes/physiology ; Transplantation, Heterologous
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  • 12
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    Cells process exogenous proteins for recognition by cytotoxic T lymphocytes (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-05
    Description: Cells exposed to intact, noninfectious influenza virus were shown to be recognized by class I-restricted anti-influenza cytotoxic T lymphocytes (CTLs). Both internal and external proteins derived from virions were processed by cells for CTL recognition. Sensitization required the inactivation of viral neuraminidase activity and could be inhibited by preventing fusion of viral and cellular membranes. These findings are important in designing vaccines to elicit CTL responses, since they demonstrate that cells can process intact, exogenous proteins for recognition by CTLs and suggest that such processing depends on introduction of exogenous proteins into the cytoplasm.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yewdell, J W -- Bennink, J R -- Hosaka, Y -- AI-14162/AI/NIAID NIH HHS/ -- AI-22114/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 5;239(4840):637-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wistar Institute for Anatomy and Biology, Philadelphia, PA 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3257585" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytotoxicity, Immunologic ; Influenza A virus/*immunology/radiation effects ; Mice ; Mice, Inbred CBA ; T-Lymphocytes, Cytotoxic/*immunology ; Ultraviolet Rays ; Viral Proteins/*immunology ; Virion/*immunology
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  • 13
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    2-Aminopurine selectively inhibits the induction of beta-interferon, c-fos, and c-myc gene expression (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-04-08
    Description: The protein kinase inhibitor 2-aminopurine (2AP) blocks the induction of the human beta-interferon gene by virus or poly(I)-poly(C) at the level of transcription. This inhibition is specific, since 2AP does not inhibit induction of either the hsp70 heat-shock gene by high temperature or the metallothionein gene by cadmium or dexamethasone. However, 2AP does block the induction of the c-fos and c-myc proto-oncogenes by serum growth factors or virus, suggesting that a protein kinase may be involved in the regulation of these genes, as well as of the beta-interferon gene. However, different factors must be required for the induction of these three genes, since they are not coordinately regulated by the same inducers in most of the cell lines examined.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zinn, K -- Keller, A -- Whittemore, L A -- Maniatis, T -- AI20642/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 8;240(4849):210-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, MA 02138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3281258" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Aminopurine/*pharmacology ; Adenine/*analogs & derivatives ; Animals ; Cells, Cultured ; Gene Expression Regulation/*drug effects ; Heat-Shock Proteins/genetics ; Humans ; Interferon Type I/*genetics ; Mice ; Protein Kinase Inhibitors ; Proto-Oncogene Proteins/*genetics ; *Proto-Oncogenes ; Regulatory Sequences, Nucleic Acid ; Transcription, Genetic/drug effects
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  • 14
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    Independent molecular pathways in initiation and loss of hormone responsiveness of breast carcinomas (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-04-22
    Description: These studies were set up to determine whether those oncogenes participating in the initiation of mammary carcinogenesis (for example, ras oncogenes) play a direct role in the outcome of events associated with the late stages of tumor development such as loss of hormone dependency. Mammary carcinomas induced by a single carcinogenic insult in pubescent rats was selected as an in vivo model system with direct relevance to human breast cancer. Acquisition of hormone-independent growth in these carcinogen-induced tumors was found to be independent of the activation of ras oncogenes during the early stages of carcinogenesis. In agreement with these observations, introduction of a human ras oncogene into human MCF-7 breast carcinoma cells did not abrogate their hormonal dependency for growth in vivo. These findings suggest that those events responsible for the critical stages of breast cancer development occur independently and in an uncoordinated manner.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sukumar, S -- Carney, W P -- Barbacid, M -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 22;240(4851):524-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Oncology Section, Basic Research Program, Frederick Cancer Research Facility, MD 21701.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3282307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*physiopathology ; Cell Line ; Estrogens/*physiology ; Gene Expression Regulation ; *Genes, ras ; Humans ; Mammary Neoplasms, Experimental/*physiopathology ; Methylnitrosourea ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Rats ; Receptors, Estrogen/*physiology
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  • 15
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    Progress reported on mouse models for AIDS (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1638.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3059496" target="_blank"〉PubMed〈/a〉
    Keywords: *Acquired Immunodeficiency Syndrome/genetics/immunology/microbiology ; Animals ; Bone Marrow Transplantation ; *Disease Models, Animal ; HIV/genetics ; Humans ; Mice ; Mice, Transgenic ; National Institutes of Health (U.S.) ; United States
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  • 16
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    AIDS mice die in NIH accident (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1988 Dec 16;242(4885):1502.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201235" target="_blank"〉PubMed〈/a〉
    Keywords: Accidents ; *Acquired Immunodeficiency Syndrome ; Animals ; Disease Models, Animal ; HIV/genetics ; Mice ; National Institutes of Health (U.S.) ; Transfection ; United States
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  • 17
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    Gene transfer is coming on target (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-10-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1988 Oct 14;242(4876):191-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175649" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chimera ; DNA/genetics ; Drug Resistance/genetics ; *Genetic Therapy ; Globins/genetics ; Growth ; Hypoxanthine Phosphoribosyltransferase/genetics ; Mice ; *Transfection
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  • 18
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    Gene-watcher's feast served up in Toronto (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-10-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1988 Oct 7;242(4875):32-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175634" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; *Genes ; *Genetic Engineering ; Humans ; Mice ; Mice, Mutant Strains ; Swine
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
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    A parent's sex may affect gene expression (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-01-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1988 Jan 22;239(4838):352-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3336789" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA/metabolism ; Female ; *Gene Expression Regulation ; Genes ; Humans ; Male ; Methylation ; Mice ; Mice, Transgenic ; *Sex Characteristics ; Tissue Distribution
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  • 20
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    Sexual responses are--almost--all in the brain (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1988 Aug 19;241(4868):903-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3043664" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Female ; Humans ; Male ; Menopause/*physiology ; Mice ; Pituitary Hormone-Releasing Hormones/*biosynthesis ; Puberty/*physiology ; Rats ; Sexual Maturation
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  • 21
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    Carboxyl terminal domain of Gs alpha specifies coupling of receptors to stimulation of adenylyl cyclase (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-07-22
    Description: The alpha subunits of Gs and Gi link different sets of hormone receptors to stimulation and inhibition, respectively, of adenylyl cyclase. A chimeric alpha i/alpha s cDNA was constructed that encodes a polypeptide composed of the amino terminal 60% of an alpha i chain and the carboxyl terminal 40% of alpha s. The cDNA was introduced via a retroviral vector into S49 cyc- cells, which lack endogenous alpha s. Although less than half of the hybrid alpha chain is derived from alpha s, its ability to mediate beta-adrenoceptor stimulation of adenylyl cyclase matched that of the normal alpha s polypeptide expressed from the same retroviral vector in cyc- cells. This result indicates that carboxyl terminal amino acid sequences of alpha s contain the structural features that are required for specificity of interactions with the effector enzyme, adenylyl cyclase, as well as with the hormone receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Masters, S B -- Sullivan, K A -- Miller, R T -- Beiderman, B -- Lopez, N G -- Ramachandran, J -- Bourne, H R -- New York, N.Y. -- Science. 1988 Jul 22;241(4864):448-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2899356" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/*physiology ; Animals ; Cell Line ; Cell Membrane/physiology ; Cholera Toxin/pharmacology ; Colforsin/pharmacology ; Enzyme Activation ; GTP-Binding Proteins/*physiology ; Guanosine Triphosphate/pharmacology ; Isoproterenol/pharmacology ; Mice ; Receptors, Adrenergic, beta/*physiology ; Recombinant Proteins ; Somatostatin/pharmacology ; Structure-Activity Relationship
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  • 22
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    Mitogenesis in response to PDGF and bombesin abolished by microinjection of antibody to PIP2 (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-02-05
    Description: The turnover of phosphatidylinositol 4,5-bisphosphate (PIP2) is believed to constitute a crucial step in the signaling pathways for stimulation of cells by a variety of bioactive substances, including mitogens, but decisive evidence for the idea has not been obtained. In the present study, a monoclonal antibody to PIP2 was microinjected into the cytoplasm of NIH 3T3 cells before or after exposure to mitogens. The antibody completely abolished nuclear labeling with [3H]thymidine induced by platelet-derived growth factor and bombesin, but not by fibroblast growth factor, epidermal growth factor, insulin, or serum. The findings strongly suggest that PIP2 breakdown is crucial in the elicitation and sustaining of cell proliferation induced by some types of mitogens such as platelet-derived growth factor and bombesin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matuoka, K -- Fukami, K -- Nakanishi, O -- Kawai, S -- Takenawa, T -- New York, N.Y. -- Science. 1988 Feb 5;239(4840):640-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Tokyo Metropolitan Institute of Gerontology, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2829356" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibodies, Monoclonal ; Antigen-Antibody Complex ; Bombesin/*pharmacology ; Cell Division/*drug effects ; Cells, Cultured ; Insulin/pharmacology ; Kinetics ; Mice ; Mice, Inbred Strains ; Phosphatidylinositol 4,5-Diphosphate ; Phosphatidylinositols/immunology/*physiology ; Platelet-Derived Growth Factor/*pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 23
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    Prevention of type I diabetes in nonobese diabetic mice by virus infection (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-01-29
    Description: The nonobese diabetic (NOD) mouse is an animal model of type I diabetes and develops a characteristic autoimmune lesion in the islets of Langerhans with lymphocytic infiltration and destruction of pancreatic beta cells. The result is hypoinsulinemia, hyperglycemia, ketoacidosis, and death. Diabetes usually begins by the sixth month of age but can occur earlier when young NOD mice are infused with lymphocytes from older NOD donors. When newborn or adult NOD mice were infected with a lymphotropic virus they did not become diabetic. The interaction between viruses and lymphocytes is pivotal in aborting diabetes, as established by experiments in which lymphocytes from virus-infected donors failed to transfer diabetes. In contrast, lymphocytes from age- and sex-matched uninfected donors caused disease. Therefore, viruses and, presumably, their products can be developed to be beneficial and may have potential as a component for treatment of human diseases. Further, these results point to the utility of viruses as probes for dissecting the pathogenesis of a nonviral disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oldstone, M B -- AG-04342/AG/NIA NIH HHS/ -- AI-09484/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 29;239(4839):500-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Research Institute of Scripps Clinic, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3277269" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/pathology ; Bone Marrow/pathology ; Diabetes Mellitus, Experimental/immunology/pathology/*prevention & control ; Diabetes Mellitus, Type 1/immunology/pathology/*prevention & control ; Female ; Islets of Langerhans/pathology ; Lymphocyte Transfusion ; Lymphocytes/immunology ; Lymphocytic Choriomeningitis/*immunology/pathology ; Mice ; Spleen/pathology ; T-Lymphocytes/immunology
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  • 24
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    Activation of developmentally mutated human globin genes by cell fusion (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-11-18
    Description: Human fetal globin genes are not expressed in hybrid cells produced by the fusion of normal human lymphocytes with mouse erythroleukemia cells. In contrast, when lymphocytes from persons with globin gene developmental mutations (hereditary persistence of fetal hemoglobin) are used for these fusions, fetal globin is expressed in the hybrid cells. Thus, mutations of developmental origin can be reconstituted in vitro by fusing mutant lymphoid cells with differentiated cell lines of the proper lineage. This system can readily be used for analyses, such as globin gene methylation, that normally require large numbers of pure nucleated erythroid cells, which are difficult to obtain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papayannopoulou, T -- Enver, T -- Takegawa, S -- Anagnou, N P -- Stamatoyannopoulos, G -- DK30852/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 18;242(4881):1056-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2461587" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Fusion ; Chromosome Deletion ; Fetal Hemoglobin/*genetics ; Gene Expression Regulation ; Globins/*genetics ; Hemoglobinopathies/*genetics ; Humans ; Leukemia, Erythroblastic, Acute ; Mice ; Mutation ; Promoter Regions, Genetic ; RNA, Messenger/genetics
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  • 25
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    Interferon-gamma: the major mediator of resistance against Toxoplasma gondii (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-04-22
    Description: Mice were injected with a monoclonal antibody to interferon-gamma to examine the importance of endogenous production of this lymphokine in resistance against infection with the sporozoan parasite Toxoplasma gondii. Mice with intraperitoneal infections of T. gondii that received no antibody survived and developed chronic T. gondii infection, whereas the infected mice that received the monoclonal antibody died of toxoplasmosis. The activation of macrophages, which kill T. gondii in vivo, was inhibited by administration of the monoclonal antibody, but the production of antibodies to T. gondii was not suppressed. The fact that an antibody to interferon-gamma can eliminate resistance to acute Toxoplasma infection in mice suggests that this lymphokine is an important mediator of host resistance to this parasite.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzuki, Y -- Orellana, M A -- Schreiber, R D -- Remington, J S -- A104717/PHS HHS/ -- A107089/PHS HHS/ -- CA43059/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Apr 22;240(4851):516-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Infectious Diseases, Research Institute, Palo Alto Medical Foundation, CA 94301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3128869" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antibodies, Protozoan/biosynthesis ; Immunity, Cellular ; Immunologic Techniques ; Interferon-gamma/*physiology ; Macrophage Activation ; Macrophages/immunology ; Mice ; Toxoplasmosis, Animal/*immunology
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  • 26
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    MyoD1: a nuclear phosphoprotein requiring a Myc homology region to convert fibroblasts to myoblasts (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-10-21
    Description: Expression of a complementary DNA (cDNA) encoding the mouse MyoD1 protein in a variety of fibroblast and adipoblast cell lines converts them to myogenic cells. Polyclonal antisera to fusion proteins containing the MyoD1 sequence show that MyoD1 is a phosphoprotein present in the nuclei of proliferating myoblasts and differentiated myotubes but not expressed in 10T1/2 fibroblasts or other nonmuscle cell types. Functional domains of the MyoD1 protein were analyzed by site-directed deletional mutagenesis of the MyoD1 cDNA. Deletion of a highly basic region (residues 102 to 135) interferes with both nuclear localization and induction of myogenesis. Deletion of a short region (residues 143 to 162) that is similar to a conserved region in the c-Myc family of proteins eliminates the ability of the MyoD1 protein to initiate myogenesis but does not alter nuclear localization. Deletions of regions spanning the remainder of MyoD1 did not affect nuclear localization and did not inhibit myogenesis. Furthermore, expression of only 68 amino acids of MyoD1, containing the basic and the Myc similarity domains, is sufficient to activate myogenesis in stably transfected 10T1/2 cells. Genetic analysis maps the MyoD1 gene to mouse chromosome 7 and human chromosome 11.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tapscott, S J -- Davis, R L -- Thayer, M J -- Cheng, P F -- Weintraub, H -- Lassar, A B -- New York, N.Y. -- Science. 1988 Oct 21;242(4877):405-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Fred Hutchinson Cancer Research Center, Seattle, WA 98104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175662" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Chromosome Mapping ; DNA/genetics ; Fibroblasts/cytology ; *Genes ; Humans ; Mice ; Muscles/cytology ; *MyoD Protein ; Nuclear Proteins/*genetics/physiology ; *Oncogenes ; Phosphoproteins/*genetics/physiology
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  • 27
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    Amiloride selectively blocks the low threshold (T) calcium channel (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-04-08
    Description: More than one type of voltage-gated calcium channel has been identified in muscle cells and neurons. Many specific organic and inorganic blockers of the conventional, slowly inactivating high threshold (L) calcium channel have been reported. No specific blockers of the low threshold (T) channel have been as yet identified. Amiloride, a potassium sparing diuretic, has now been shown to selectively block the low threshold calcium channel in mouse neuroblastoma and chick dorsal root ganglion neurons. The selective blockade of the T-type calcium channel will allow identification of this channel in different tissues and characterization of its specific physiological role.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, C M -- Presser, F -- Morad, M -- 1 K08 NS-01104/NS/NINDS NIH HHS/ -- R01 HL-16152/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 8;240(4849):213-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Pennsylvania, Department of Physiology, Philadelphia 19104-6085.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2451291" target="_blank"〉PubMed〈/a〉
    Keywords: Amiloride/*pharmacology ; Animals ; Calcium/*physiology ; Chickens ; Dose-Response Relationship, Drug ; Electric Conductivity ; In Vitro Techniques ; Ion Channels/*drug effects ; Mice ; Neurons/*physiology ; Sodium/physiology ; Tumor Cells, Cultured
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  • 28
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    Oral Salmonella typhimurium vaccine expressing circumsporozoite protein protects against malaria (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-04-15
    Description: Immunization with radiation-attenuated malaria sporozoites induces potent cellular immune responses, but the target antigens are unknown and have not previously been elicited by subunit vaccines prepared from the circumsporozoite (CS) protein. A method is described here for inducing protective cell-mediated immunity to sporozoites by immunization with attenuated Salmonella typhimurium transformed with the Plasmodium berghei CS gene. These transformants constitutively express CS antigens and, when used to immunize mice orally, colonize the liver, induce antigen-specific cell-mediated immunity, and protect mice against sporozoite challenge in the absence of antisporozoite antibodies. These data indicate that the CS protein contains T cell epitopes capable of inducing protective cell-mediated immunity, and emphasize the importance of proper antigen presentation in generating this response. Analogous, orally administered vaccines against human malaria might be feasible.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sadoff, J C -- Ballou, W R -- Baron, L S -- Majarian, W R -- Brey, R N -- Hockmeyer, W T -- Young, J F -- Cryz, S J -- Ou, J -- Lowell, G H -- New York, N.Y. -- Science. 1988 Apr 15;240(4850):336-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bacterial Diseases, Walter Reed Army Institute of Research, Washington, DC 20307-5100.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3281260" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Surface/*immunology ; Bacterial Vaccines/*immunology ; Female ; Liver/microbiology ; Malaria/*immunology/prevention & control ; Mice ; Mice, Inbred BALB C ; Plasmids ; Plasmodium berghei/*immunology ; *Protozoan Proteins ; Salmonella typhimurium/genetics/*immunology
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  • 29
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    Infection of the SCID-hu mouse by HIV-1 (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-12-23
    Description: SCID-hu mice with human fetal thymic or lymph node implants were inoculated with the cloned human immunodeficiency virus-1 isolate, HIV-1JR-CSF. In a time- and dose-dependent fashion, viral replication spread within the human lymphoid organs. Combination immunohistochemistry and in situ hybridization revealed only viral RNA transcripts in most infected cells, but some cells had both detectable viral transcripts and viral protein. Infected cells were always more apparent in the medulla than in the cortex of the thymus. These studies demonstrate that an acute infection of human lymphoid organs with HIV-1 can be followed in the SCID-hu mouse.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Namikawa, R -- Kaneshima, H -- Lieberman, M -- Weissman, I L -- McCune, J M -- AR5P40RR03624-029/AR/NIAMS NIH HHS/ -- CA03352/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1684-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201256" target="_blank"〉PubMed〈/a〉
    Keywords: *Acquired Immunodeficiency Syndrome ; Animals ; Chimera ; *Disease Models, Animal ; HIV/genetics/*physiology ; Humans ; Immunohistochemistry ; Lymph Nodes/microbiology/transplantation ; Mice ; Mice, Mutant Strains ; Nucleic Acid Hybridization ; RNA, Viral/genetics ; Thymus Gland/microbiology/transplantation ; Transcription, Genetic ; Viral Proteins/biosynthesis ; Virus Replication
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A gene for dihydrofolate reductase in a herpesvirus (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-03-04
    Description: The enzyme dihydrofolate reductase (DHFR) is found ubiquitously in both prokaryotes and eukaryotes. It is essential for de novo synthesis of purines and of deoxythymidine monophosphate for DNA synthesis. Among viruses, however, only the T-even and T5 bacteriophage have been found to encode their own DHFR. In this study a gene for DHFR was found in a specific subgroup of the gamma or lymphotropic class of herpesviruses. DNA sequences for DHFR were found in herpesvirus saimiri and herpesvirus ateles but not in Epstein-Barr virus, Marek's disease virus, herpes simplex virus, varicella-zoster virus, herpesvirus tamarinus, or human cytomegalovirus. The predicted sequence of herpesvirus saimiri DHFR is 186 amino acids in length, the same length as human, murine, and bovine DHFR. The human and herpesvirus saimiri DHFRs share 83 percent positional identity in amino acid sequence. The herpesvirus saimiri DHFR gene is devoid of intron sequences, suggesting that it was acquired by some process involving reverse transcription. This is to our knowledge the first example of a mammalian virus with a gene for DHFR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trimble, J J -- Murthy, S C -- Bakker, A -- Grassmann, R -- Desrosiers, R C -- 31363/PHS HHS/ -- RR00168/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 4;239(4844):1145-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉New England Regional Primate Research Center, Harvard Medical School, Southborough, MA 01772.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2830673" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cattle ; Chickens ; Cytomegalovirus/enzymology ; Herpesviridae/*enzymology ; Herpesvirus 2, Saimiriine/*enzymology ; Herpesvirus 4, Human/enzymology ; Humans ; Introns ; Mice ; Molecular Sequence Data ; Sequence Homology, Nucleic Acid ; Tetrahydrofolate Dehydrogenase/*genetics
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    cDNA expression cloning of the IL-1 receptor, a member of the immunoglobulin superfamily (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-29
    Description: Interleukin-1 alpha and -1 beta (IL-1 alpha and IL-1 beta) are cytokines that participate in the regulation of immune responses, inflammatory reactions, and hematopoiesis. A direct expression strategy was used to clone the receptor for IL-1 from mouse T cells. The product of the cloned complementary DNA binds both IL-1 alpha and IL-1 beta in a manner indistinguishable from that of the native T cell IL-1 receptor. The extracellular, IL-1 binding portion of the receptor is 319 amino acids in length and is composed of three immunoglobulin-like domains. The cytoplasmic portion of the receptor is 217 amino acids long.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sims, J E -- March, C J -- Cosman, D -- Widmer, M B -- MacDonald, H R -- McMahan, C J -- Grubin, C E -- Wignall, J M -- Jackson, J L -- Call, S M -- New York, N.Y. -- Science. 1988 Jul 29;241(4865):585-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Corporation, Seattle, WA 98101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2969618" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; DNA/genetics ; Gene Expression Regulation ; Genes, Immunoglobulin ; Interleukin-1/*physiology ; Mice ; Molecular Sequence Data ; *Multigene Family ; Receptors, Immunologic/*genetics ; Receptors, Interleukin-1
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  • 32
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    Purification and characterization of mouse hematopoietic stem cells (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-07-01
    Description: Mouse bone marrow hematopoietic stem cells were isolated with the use of a variety of phenotypic markers. These cells can proliferate and differentiate with approximately unit efficiency into myelomonocytic cells, B cells, or T cells. Thirty of these cells are sufficient to save 50 percent of lethally irradiated mice, and to reconstitute all blood cell types in the survivors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spangrude, G J -- Heimfeld, S -- Weissman, I L -- AI 09072/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 1;241(4861):58-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2898810" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigens, Surface/immunology ; Antigens, Thy-1 ; B-Lymphocytes/cytology ; *Bone Marrow Cells ; Cell Count ; Cell Differentiation ; Cell Division ; Cell Separation/*methods ; Colony-Forming Units Assay ; Erythrocytes/cytology ; Granulocytes/cytology ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*cytology/immunology ; Mice ; Mice, Inbred C57BL ; Spleen/cytology ; T-Lymphocytes/cytology ; Thymus Gland/cytology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Human T cell leukemia viruses use a receptor determined by human chromosome 17 (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-12-16
    Description: Human T cell leukemia viruses (HTLV-I and HTLV-II) can infect many cell types in vitro. HTLV-I and HTLV-II use the same cell surface receptor, as shown by interference with syncytium formation and with infection by vesicular stomatitis virus (VSV) pseudotypes bearing the HTLV envelope glycoproteins. Human-mouse somatic cell hybrids were used to determine which human chromosome was required to confer susceptibility to VSV(HTLV) infection. The only human chromosome common to all susceptible cell hybrids was chromosome 17, and the receptor gene was localized to 17cen-qter. Antibodies to surface antigens known to be determined by genes on 17q did not block the HTLV receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sommerfelt, M A -- Williams, B P -- Clapham, P R -- Solomon, E -- Goodfellow, P N -- Weiss, R A -- New York, N.Y. -- Science. 1988 Dec 16;242(4885):1557-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chester Beatty Laboratories, Institute of Cancer Research, London, U.K.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201246" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cell Line ; Chromosome Mapping ; *Chromosomes, Human, Pair 17 ; Cricetinae ; *Genes ; Human T-lymphotropic virus 1/*physiology ; Human T-lymphotropic virus 2/*physiology ; Humans ; Hybrid Cells/cytology/microbiology ; Mice ; Rats ; Receptors, Virus/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Introduction of nucleophiles and spectroscopic probes into antibody combining sites (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-11-18
    Description: A general chemical strategy has been developed whereby antibody combining sites can be selectively derivatized with natural or synthetic molecules, such as catalytic groups, drugs, metals, or reporter molecules. Cleavable affinity labels were used to selectively introduce a thiol into the combining site of the immunoglobulin A MOPC 315. This thiol acted both as a nucleophile to accelerate ester thiolysis 60,000-fold and as a handle for selectively derivatizing the antibody with additional functional groups. For example, derivatization of the antibody with a fluorophore made possible a direct spectroscopic assay of antibody-ligand complexation. This chemistry should not only extend our ability to exploit antibody specificity in chemical catalysis, diagnostics, and therapeutics, but may also prove generally applicable to the functional modification of other proteins for which detailed structural information is unavailable.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pollack, S J -- Nakayama, G R -- Schultz, P G -- AI24695-02/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 18;242(4881):1038-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3194752" target="_blank"〉PubMed〈/a〉
    Keywords: Affinity Labels ; Animals ; *Antigen-Antibody Reactions ; *Binding Sites, Antibody ; Chemical Phenomena ; Chemistry ; Dinitrobenzenes ; Immunoglobulin Fab Fragments ; Mice ; Spectrometry, Fluorescence ; Sulfhydryl Compounds
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    The SCID-hu mouse: murine model for the analysis of human hematolymphoid differentiation and function (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-23
    Description: The study of human hematopoietic cells and the human immune system is hampered by the lack of a suitable experimental model. Experimental data are presented showing that human fetal liver hematopoietic cells, human fetal thymus, and human fetal lymph node support the differentiation of mature human T cells and B cells after engraftment into mice with genetically determined severe combined immunodeficiency. The resultant SCID-hu mice are found to have a transient wave of human CD4+ and CD8+ T cells and human IgG (immunoglobulin G) in the peripheral circulation. The functional status of the human immune system within this mouse model is not yet known.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCune, J M -- Namikawa, R -- Kaneshima, H -- Shultz, L D -- Lieberman, M -- Weissman, I L -- AI09072/AI/NIAID NIH HHS/ -- CA03352/CA/NCI NIH HHS/ -- CA20408/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 23;241(4873):1632-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2971269" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/physiology ; Cell Differentiation ; *Chimera ; Hematopoietic Stem Cells/*physiology ; Humans ; Liver/cytology ; Liver Transplantation ; Lymph Nodes/transplantation ; Mice ; Mice, Mutant Strains/*immunology ; *Models, Biological ; T-Lymphocytes/physiology ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Regulatory/immunology ; Thymus Gland/anatomy & histology/physiology/transplantation ; Transplantation, Heterologous
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    Legless, a novel mutation found in PHT1-1 transgenic mice (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-08-12
    Description: In this report it is shown that the PHT1-1 line of transgenic mice exhibited a pattern of developmental abnormalities when the mice were homozygous for the transgene insertion. Hindlimbs were uniformly truncated at the distal end of the femur, resulting in a "legless" appearance. Forelimbs lacked anterior structures including digits and the radius. The brains had many defects, particularly in the anterior structures of the cerebrum, including the olfactory lobes. Craniofacial malformations in the form of facial clefts also commonly occurred. Furthermore, heterozygotes of this line, with only one copy of the DNA insertion, and other transgenic lines carrying the same DNA construct appeared normal, suggesting that in the PHT1-1 line a gene significant in mammalian development has been disrupted.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McNeish, J D -- Scott, W J Jr -- Potter, S S -- New York, N.Y. -- Science. 1988 Aug 12;241(4867):837-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Basic Science Research, Children's Hospital Research Foundation, Cincinnati, OH.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3406741" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Brain/*abnormalities ; Embryo, Mammalian ; Hindlimb/*abnormalities ; Mice ; Mice, Transgenic/*anatomy & histology ; *Mutation
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    T cell CD3-zeta eta heterodimer expression and coupling to phosphoinositide hydrolysis (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-10-28
    Description: The T cell antigen receptor consists of an antigen-binding heterodimer that is noncovalently associated with at least five CD3 subunits (gamma, delta, epsilon, zeta, and eta). The CD3-zeta chains are either disulfide-linked homodimers (CD3-zeta 2) or disulfide-linked heterodimers with eta (CD3-zeta eta). Variants of a murine antigen-specific T cell hybridoma that express normal amounts of CD3-zeta 2 but decreased amounts of CD3-zeta eta were isolated. When activated, the parental cell line increased both phosphatidylinositol hydrolysis and serine-specific protein kinase activity to a much greater extent than the variants. In contrast, the activation of a tyrosine-specific kinase after stimulation with a cross-linking antibody to CD3 was similar among these cells. There was a positive linear relation between the expression of CD3-zeta eta and phosphoinositide hydrolysis stimulated by the TCR, suggesting a differential coupling of the T cell alpha beta heterodimer to signal transduction mechanisms due to alpha beta association with either CD3-zeta 2 or CD3-zeta eta.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mercep, M -- Bonifacino, J S -- Garcia-Morales, P -- Samelson, L E -- Klausner, R D -- Ashwell, J D -- New York, N.Y. -- Science. 1988 Oct 28;242(4878):571-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biological Response Modifiers Program, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2845582" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; Antigens, CD3 ; Antigens, Differentiation, T-Lymphocyte/*physiology ; Cell Line ; Electrophoresis, Gel, Two-Dimensional ; Macromolecular Substances ; *Membrane Proteins ; Mice ; Phosphatidylinositols/*metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Precipitin Tests ; Protein Kinase C/physiology ; Receptors, Antigen, T-Cell/*physiology ; T-Lymphocytes/*physiology
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    Unusual immunoglobulin gene rearrangement leads to replacement of recombinational signal sequences (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-10-14
    Description: An unexpected immunoglobulin gene rearrangement, signal sequence replacement, was observed in which the recombinational signal sequences of a VH gene segment are fused intact to the 5' end of a DJH element. Nucleotides are not lost from the signal sequences, but they may be lost from the DJH coding sequence. Signal sequence replacement may result from the alternative resolution of an intermediate in VH-to-DJH recombination. This type of rearrangement provides a means to alter the targeting of immunoglobulin gene segments and suggests a mechanism for the occurrence of VH-JH junctions in vivo. Signal sequence replacement may represent an additional pathway for the generation of antibody diversity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morzycka-Wroblewska, E -- Lee, F E -- Desiderio, S V -- New York, N.Y. -- Science. 1988 Oct 14;242(4876):261-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute Laboratory of Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3140378" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; DNA, Recombinant ; *Gene Rearrangement ; *Genes, Immunoglobulin ; Immunoglobulin Heavy Chains/genetics ; Immunoglobulin Variable Region/genetics ; Mice ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Protein Sorting Signals/*genetics ; Recombination, Genetic ; Retroviridae/genetics
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  • 39
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    Poliovirus host range is determined by a short amino acid sequence in neutralization antigenic site I (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-08
    Description: The mouse-adapted strain of poliovirus type 2 (Lansing) induces fatal poliomyelitis in mice after intracerebral inoculation, whereas mice inoculated with poliovirus type 1 (Mahoney) show no signs of disease. Previous work indicated that the adaptation to mouse virulence is associated with the viral capsid proteins and that mutations in neutralization antigenic site I of poliovirus reduce neurovirulence of the Lansing strain in mice. The role of antigenic site I in mouse neurovirulence was further explored by constructing an antigenic hybrid virus. Six amino acids in antigenic site I of the Mahoney strain were replaced with a sequence specific for the Lansing strain by using a mutagenesis cartridge. The hybrid virus was neutralized by polyclonal antisera elicited by the type 1 and type 2 strains of poliovirus and by neutralizing monoclonal antibodies directed against antigenic site I of type 2 virus. The hybrid virus induced paralytic disease in mice, an observation demonstrating that a short sequence of amino acids in antigenic site I is an important determinant of poliovirus host range. Antigenic site I may be involved in attachment of poliovirus to cells of the mouse central nervous system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3908517/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3908517/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murray, M G -- Bradley, J -- Yang, X F -- Wimmer, E -- Moss, E G -- Racaniello, V R -- AI 15122/AI/NIAID NIH HHS/ -- AI 20017/AI/NIAID NIH HHS/ -- CA 28146/CA/NCI NIH HHS/ -- R01 AI015122/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 8;241(4862):213-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, School of Medicine, State University of New York, Stony Brook 11794.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2838906" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/immunology ; Antigens, Viral/*physiology ; Capsid/physiology ; DNA Mutational Analysis ; Mice ; Nervous System Diseases/microbiology ; Neutralization Tests ; Poliovirus/growth & development/immunology/*pathogenicity ; Virus Replication
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    Diabetic mouse incorrectly typed (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prochazka, M -- Leiter, E H -- Serreze, D V -- Coleman, D L -- Jackson, R A -- New York, N.Y. -- Science. 1988 Nov 11;242(4880):945.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Jackson Laboratory, Bar Harbor, ME 04609.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3187535" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crosses, Genetic ; DNA/genetics ; Diabetes Mellitus, Type 1/*genetics ; *Genes, Recessive ; Major Histocompatibility Complex ; Mice ; Recombination, Genetic
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    Wound macrophages express TGF-alpha and other growth factors in vivo: analysis by mRNA phenotyping (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-05
    Description: The presence of macrophages is required for the regeneration of many cell types during wound healing. Macrophages have been reported to express a wide range of mitogenic factors and cytokines, but none of these factors has been shown in vivo to sustain all the wound-healing processes. It has been suggested that transforming growth factor-alpha (TGF-alpha) may mediate angiogenesis, epidermal regrowth, and formation of granulation tissue in vivo. Macrophages isolated from a wound site, and not exposed to cell culture conditions, expressed messenger RNA transcripts for TGF-alpha, TGF-beta, platelet-derived growth factor A-chain, and insulin-like growth factor-1. The expression of these transcripts was determined by a novel method for RNA analysis in which low numbers of mouse macrophages were isolated from wound cylinders, their RNA was purified and reverse-transcribed, and the complementary DNA was amplified in a polymerase chain reaction primed with growth factor sequence-specific primers. This single-cell RNA phenotyping procedure is rapid and has the potential for quantification, and mRNA transcripts from a single cell or a few cells can be unambiguously demonstrated, with the simultaneous analysis of several mRNA species. Macrophages from wounds expressed TGF-alpha antigen, and wound fluids contained TGF-alpha. Elicited macrophages in culture also expressed TGF-alpha transcripts and polypeptide in a time-dependent manner after stimulation with modified low-density lipoproteins and lipopolysaccharide endotoxin, which are characteristic of the activators found in injured tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rappolee, D A -- Mark, D -- Banda, M J -- Werb, Z -- AR 32746/AR/NIAMS NIH HHS/ -- GM 27345/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 5;241(4866):708-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Radiobiology and Environmental Health, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3041594" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; DNA/genetics ; Enzyme-Linked Immunosorbent Assay ; Epidermal Growth Factor/biosynthesis/genetics ; Fibroblast Growth Factors/biosynthesis/genetics ; Fibroblasts/metabolism ; Fluorescent Antibody Technique ; Growth Substances/*biosynthesis/genetics ; Insulin-Like Growth Factor I/biosynthesis/genetics ; Macrophages/*metabolism ; Male ; Mice ; Nucleic Acid Hybridization ; *Peptide Biosynthesis ; Peptides/genetics ; Platelet-Derived Growth Factor/biosynthesis/genetics ; Protein Biosynthesis ; RNA, Messenger/*biosynthesis ; Rabbits ; Transcription, Genetic ; Transforming Growth Factors ; *Wound Healing ; Wounds and Injuries/*pathology
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    Coding of two sphingolipid activator proteins (SAP-1 and SAP-2) by same genetic locus (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-26
    Description: Several complementary DNAs (cDNAs) coding for sphingolipid activator protein-2 (SAP-2) were isolated from a lambda gt-11 human hepatoma library by means of polyclonal antibodies. The nucleotide sequence of the largest cDNA was colinear with the derived amino acid sequence of SAP-2 and with the nucleotide sequence of the cDNA coding for the 70-kilodalton precursor of SAP-1 (SAP precursor cDNA). The coding sequence for mature SAP-2 was located 3' to that coding for SAP-1 in the SAP precursor cDNA. Both SAP-1 and SAP-2 appeared to be derived by proteolytic processing from a common precursor that is coded by a genetic locus on human chromosome 10. Two other domains similar to SAP-1 and SAP-2 were also identified in SAP precursor protein. Each of the four domains was approximately 80 amino acid residues long, had nearly identical placement of cysteine residues, potential glycosylation sites, and proline residues. Each domain also contained internal amino acid sequences capable of forming amphipathic helices separated by helix breakers to give a cylindrical hydrophobic domain that is probably stabilized by disulfide bridges. Protein immunoblotting experiments indicated that SAP precursor protein (70 kilodaltons) as well as immunoreactive SAP-like proteins of intermediate sizes (65, 50, and 31 kilodaltons) are present in most human tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Brien, J S -- Kretz, K A -- Dewji, N -- Wenger, D A -- Esch, F -- Fluharty, A L -- DK 38795/DK/NIDDK NIH HHS/ -- HD 18983/HD/NICHD NIH HHS/ -- NS 08682/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Aug 26;241(4869):1098-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosciences, University of California, San Diego, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2842863" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Carcinoma, Hepatocellular/analysis ; Chromosome Mapping ; Chromosomes, Human, Pair 10 ; DNA/genetics/isolation & purification ; Glycoproteins/analysis/*genetics ; Humans ; Liver Neoplasms/analysis ; Male ; Mice ; Mice, Nude ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Protein Conformation ; Protein Precursors/analysis/genetics ; Protein Processing, Post-Translational ; Rats ; Saposins ; Sphingolipid Activator Proteins ; Tissue Distribution
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    Beta-N-methylamino-L-alanine neurotoxicity: requirement for bicarbonate as a cofactor (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-19
    Description: Ingestion of the excitotoxic cycad seed amino acid beta-N-methylamino-L-alanine may be responsible for the neuronal degeneration associated with Guam amyotrophic lateral sclerosis-parkinsonism-dementia in man. However, the basis for the central neurotoxicity of beta-N-methylamino-L-alanine has been unclear, as it lacks the omega acidic (or equivalent electronegative) moiety characteristic of other excitatory amino acids. beta-N-methylamino-L-alanine produced neurotoxic and neuroexcitatory effects in murine cortical cell cultures only when physiological concentrations of bicarbonate were available in the extracellular bathing medium. Bicarbonate may interact noncovalently with beta-N-methylamino-L-alanine to produce, in combination, a molecular configuration that activates glutamate receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weiss, J H -- Choi, D W -- NS12151/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 19;241(4868):973-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Stanford University Medical Center, Stanford 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3136549" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids, Diamino/*toxicity ; Animals ; Bicarbonates/*metabolism ; Cells, Cultured ; Cerebral Cortex/*drug effects ; Electrophysiology ; Hydrogen-Ion Concentration ; Mice ; Microelectrodes ; Neurons/*drug effects ; Oxadiazoles/toxicity ; Quisqualic Acid ; beta-Alanine/analogs & derivatives/toxicity
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  • 44
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    Molecular cloning of the zeta chain of the T cell antigen receptor (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-26
    Description: The T cell antigen receptor is a multi-subunit receptor complex present on the surface of all mature and many developing T cells. It consists of clonotypic heterodimers noncovalently linked to five invariant chains that are encoded by four genes and referred to as the CD3 complex. The CD3 gamma, delta, and epsilon chains have been molecularly characterized. In this report the molecular cloning of a complementary DNA encoding the zeta chain of the murine T cell antigen receptor is described. The predicted protein sequence of the zeta chain suggests a structure distinct from those of any of the previously described receptor subunits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weissman, A M -- Baniyash, M -- Hou, D -- Samelson, L E -- Burgess, W H -- Klausner, R D -- New York, N.Y. -- Science. 1988 Feb 26;239(4843):1018-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3278377" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Membrane/metabolism ; Chromatography, High Pressure Liquid ; *Cloning, Molecular ; Cyanogen Bromide ; DNA/genetics ; Electrophoresis, Polyacrylamide Gel ; Immunosorbent Techniques ; Macromolecular Substances ; *Membrane Proteins ; Mice ; Molecular Sequence Data ; Molecular Weight ; Nucleic Acid Hybridization ; Peptide Fragments ; Protein Biosynthesis ; RNA, Messenger/genetics ; Receptors, Antigen, T-Cell/*genetics ; T-Lymphocytes/analysis ; Transcription, Genetic ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 45
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    Developmental expression of PDGF, TGF-alpha, and TGF-beta genes in preimplantation mouse embryos (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-30
    Description: Control of growth and differentiation during mammalian embryogenesis may be regulated by growth factors from embryonic or maternal sources. With the use of single-cell messenger RNA phenotyping, the simultaneous expression of growth factor transcripts in single or small numbers of preimplantation mouse embryos was examined. Transcripts for platelet-derived growth factor A chain (PDGF-A), transforming growth factor (TGF)-alpha, and TGF-beta 1, but not for four other growth factors, were found in whole blastocysts. TGF-alpha, TGF-beta 1, and PDGF antigens were detected in blastocysts by immunocytochemistry. Both PDGF-A and TGF-alpha were detected as maternal transcripts in the unfertilized ovulated oocyte, and again in blastocysts. TGF-beta 1 transcripts appeared only after fertilization. The expression of a subset of growth factors in mouse blastocysts suggests a role for these factors in the growth and differentiation of early mammalian embryos.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rappolee, D A -- Brenner, C A -- Schultz, R -- Mark, D -- Werb, Z -- 5T32 ES07106/ES/NIEHS NIH HHS/ -- HD22681/HD/NICHD NIH HHS/ -- HD23539/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 30;241(4874):1823-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Radiobiology and Environmental Health, University of California, San Francisco 94143-0750.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175624" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/*physiology ; Cleavage Stage, Ovum/physiology ; Embryonic Development ; Female ; Gene Expression Regulation ; Growth Substances/*genetics ; Mice ; Oocytes/physiology ; Platelet-Derived Growth Factor/*genetics ; Pregnancy ; RNA, Messenger/genetics ; Transcription, Genetic ; Transforming Growth Factors/*genetics
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  • 46
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    Induction of manganous superoxide dismutase by tumor necrosis factor: possible protective mechanism (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-11-11
    Description: Manganous superoxide dismutase (MnSOD) scavenges potentially toxic superoxide radicals produced in the mitochondria. Tumor necrosis factor-alpha (TNF-alpha) was found to induce the messenger RNA for MnSOD, but not the mRNAs for other antioxidant or mitochondrial enzymes tested. The increase in MnSOD mRNA occurred rapidly and was blocked by actinomycin D, but not by cycloheximide. Induction of MnSOD mRNA was also observed with TNF-beta, interleukin-1 alpha (IL-1 alpha), and IL-1 beta but not with other cytokines or agents tested. TNF-alpha induced MnSOD mRNA in all cell lines and normal cells examined in vitro and in various organs of mice in vivo. These effects of TNF-alpha and IL-1 on target cells may contribute to their reported protective activity against radiation as well as their ability to induce resistance to cell killing induced by the combination of TNF-alpha and cycloheximide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong, G H -- Goeddel, D V -- New York, N.Y. -- Science. 1988 Nov 11;242(4880):941-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Genentech, San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3263703" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Catalase/metabolism ; Cell Line ; Cycloheximide/pharmacology ; Dactinomycin/pharmacology ; Enzyme Induction/drug effects ; Humans ; Interleukin-1/pharmacology ; Kinetics ; Mice ; Mitochondria/enzymology ; RNA, Messenger/biosynthesis ; Rats ; Superoxide Dismutase/*biosynthesis/genetics/metabolism ; Tissue Distribution ; Tumor Necrosis Factor-alpha/*pharmacology
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    The cellular src gene product regulates junctional cell-to-cell communication (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-01-22
    Description: Overexpression of the cellular src gene in NIH 3T3 cells causes reduction of cell-to-cell transmission of molecules in the 400- to 700-dalton range. This down-regulation of gap junctional communication correlates with the activity of the gene product, the protein tyrosine kinase pp60c-src. The down-regulation was enhanced by point mutation of Tyr527 (a site that is phosphorylated in pp60c-src and that inhibits kinase activity) or by substitution of the viral-src for the cellular-src carboxyl-terminal coding region. Mutation of Tyr416 (a site phosphorylated upon Tyr527 mutation) suppresses both the down-regulation of communication by Tyr527 mutation and that by gene overexpression. The regulation of communication by src may be important in the control of embryonic development and cellular growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Azarnia, R -- Reddy, S -- Kmiecik, T E -- Shalloway, D -- Loewenstein, W R -- CA-14464/CA/NCI NIH HHS/ -- CA-32317/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 22;239(4838):398-401.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of Miami School of Medicine, FL 33136.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2447651" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Communication ; Cell Line ; Cell Membrane Permeability ; Gene Expression Regulation ; *Intercellular Junctions ; Mice ; Mutation ; Phosphorylation ; Plasmids ; Protein-Tyrosine Kinases/*genetics ; Proto-Oncogene Proteins/genetics/*physiology ; Proto-Oncogene Proteins pp60(c-src) ; Structure-Activity Relationship ; Transcription, Genetic ; Transfection ; Tyrosine/metabolism
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  • 48
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    Suppression of macrophage activation and T-lymphocyte function in hypoprolactinemic mice (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-01-22
    Description: The effects of prolactin on lactation and reproductive organs are well known. However, the other possible target organs and physiological consequences of altered levels of circulating prolactin remain poorly understood. In this study, mice were treated with bromocryptine, a dopamine receptor agonist that inhibits pituitary prolactin secretion. Bromocryptine treatment prevented T-cell-dependent induction of macrophage tumoricidal activity after the intraperitoneal injection of Listeria monocytogenes or Mycobacterium bovis. Coincident treatment with ovine prolactin reversed this effect. Of the multiple events leading to macrophage activation in vivo, the production by T-lymphocytes of gamma-interferon was the most impaired in bromocryptine-treated mice. Lymphocyte proliferation after stimulation with mitogens in vitro was also depressed in spleens of bromocryptine-treated mice, and coadministration of prolactin also reversed this effect. Bromocryptine treatment also reduced the number of deaths resulting from inoculation of mice with Listeria; exogenous prolactin significantly reversed this effect. The critical influence of pituitary prolactin release on maintenance of lymphocyte function and on lymphokine-dependent macrophage activation suggests that, in mice, lymphocytes are an important target tissue for circulating prolactin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bernton, E W -- Meltzer, M S -- Holaday, J W -- New York, N.Y. -- Science. 1988 Jan 22;239(4838):401-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Neurosciences, Walter Reed Army Institute of Research, Washington, DC 20307.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3122324" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Bromocriptine/pharmacology ; Concanavalin A/pharmacology ; Hypopituitarism/blood/*immunology ; Interferon-gamma/biosynthesis ; Lipopolysaccharides/pharmacology ; Listeriosis/immunology ; Lymphocyte Activation/drug effects ; Lymphokines/physiology ; Macrophage Activation/drug effects ; Macrophage-Activating Factors ; Macrophages/*immunology ; Male ; Mice ; Mice, Inbred C3H ; Mycobacterium bovis ; Prolactin/*blood/pharmacology ; Salmonella ; Spleen/cytology ; T-Lymphocytes/*immunology ; Tuberculosis/immunology
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    Limited immunological recognition of critical malaria vaccine candidate antigens (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-10-28
    Description: Current vaccine development strategies for malaria depend on widespread immunological responsiveness to candidate antigens such as the zygote surface antigens and the sporozoite coat protein, the circumsporozoite (CS) protein. Since immunological responsiveness is controlled mainly by genes mapping within the major histocompatibility complex (MHC), the humoral immune response to the zygote surface antigens and the cytotoxic T lymphocyte (CTL) response to the CS protein were examined in MHC-disparate congenic mouse strains. Only two of six strains responded to the 230-kilodalton zygote surface antigen and another two strains responded to the 48/45-kilodalton surface antigen. From two mouse strains, expressing between them five different class I MHC molecules, there was recognition of only a single CTL epitope from the CS protein, which was from a polymorphic segment of the molecule. The restricted CTL response to this protein parallels the restricted antibody response to this protein observed in humans and mice. These findings suggest that subunit malaria vaccines now being developed may be ineffective.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Good, M F -- Miller, L H -- Kumar, S -- Quakyi, I A -- Keister, D -- Adams, J H -- Moss, B -- Berzofsky, J A -- Carter, R -- New York, N.Y. -- Science. 1988 Oct 28;242(4878):574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2902690" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Protozoan/biosynthesis ; Antigens, Protozoan/*immunology ; Antigens, Surface/genetics/immunology ; CD4-Positive T-Lymphocytes/immunology ; Genes, MHC Class II ; Immunity, Cellular ; Lymphocyte Cooperation ; Malaria/*prevention & control ; Mice ; Plasmodium falciparum/*immunology ; *Protozoan Proteins ; T-Lymphocytes, Cytotoxic/immunology ; Transfection ; Vaccines/*immunology ; Zygote/immunology
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    One factor recognizes the liver-specific enhancers in alpha 1-antitrypsin and transthyretin genes (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-12
    Description: Four different regulatory sites required for transcriptional stimulation by the enhancers of two unrelated liver-specific genes alpha 1-antitrypsin and transthyretin appear to bind the same nuclear protein that is found mainly in the liver. Such proteins may provide a basis for a coordinated, hepatocyte-specific control of gene transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grayson, D R -- Costa, R H -- Xanthopoulos, K G -- Darnell, J E -- CA 160006-14/CA/NCI NIH HHS/ -- CA 18213-11/CA/NCI NIH HHS/ -- GM 1066-02/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Feb 12;239(4841 Pt 1):786-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3257586" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; *Genes ; Genes, Regulator ; Liver/*metabolism ; Mice ; Mutation ; Nuclear Proteins/*physiology ; Prealbumin/*genetics ; *Transcription, Genetic ; alpha 1-Antitrypsin/*genetics
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    Induction of an antibody that catalyzes the hydrolysis of an amide bond (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-09-02
    Description: Catalysis of amide bond hydrolysis is of singular importance in enzymology. An antibody was induced to an analog of a high-energy intermediate anticipated along the reaction coordinate of amide hydrolysis. This antibody is an amidase with high specificity and a large rate enhancement (250,000) relative to the uncatalyzed reaction. This reaction represents the kinetically most difficult hydrolysis reaction yet catalyzed by an antibody.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Janda, K D -- Schloeder, D -- Benkovic, S J -- Lerner, R A -- New York, N.Y. -- Science. 1988 Sep 2;241(4870):1188-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Research Institute of Scripps Clinic, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3413482" target="_blank"〉PubMed〈/a〉
    Keywords: Amidohydrolases/metabolism ; Animals ; Antibodies, Monoclonal/biosynthesis/*physiology ; Antibody Specificity ; Antigens/immunology ; *Catalysis ; Chemical Phenomena ; Chemistry ; Hemocyanin/analogs & derivatives/immunology ; Hydrolysis ; Immunization ; Kinetics ; Mice ; Organophosphorus Compounds/immunology ; Substrate Specificity
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    Effects of cyclosporine A on T cell development and clonal deletion (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-23
    Description: Cyclosporine A (CsA) is an important immunosuppressive drug that is widely used in transplantation medicine. Many of its suppressive effects on T cells appear to be related to the inhibition of T cell receptor (TCR)-mediated activation events. Paradoxically, in certain situations CsA is responsible for the induction of a T cell-mediated autoimmunity. The effects of CsA on T cell development in the thymus were investigated to elucidate the physiologic events underlying this phenomenon. Two major effects were revealed: (i) CsA inhibits the development of mature single positive (CD4+8- or CD4-8+) TCR-alpha beta+ thymocytes without discernibly affecting CD4-8- TCR-gamma delta+ thymocytes and (ii) CsA interferes with the deletion of cells bearing self-reactive TCRs in the population of single positive thymocytes that do develop. This suggests a direct mechanism for CsA-induced autoimmunity and may have implications for the relative contribution of TCR-mediated signaling events in the development of the various T cell lineages.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jenkins, M K -- Schwartz, R H -- Pardoll, D M -- New York, N.Y. -- Science. 1988 Sep 23;241(4873):1655-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3262237" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigens, Differentiation, T-Lymphocyte/genetics ; Autoimmune Diseases/chemically induced ; Cell Differentiation/drug effects ; Cyclosporins/*pharmacology ; Mice ; Mice, Inbred Strains ; Receptors, Antigen, T-Cell/drug effects/genetics ; T-Lymphocytes/*drug effects/immunology
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    Growth factors regulate transin gene expression by c-fos-dependent and c-fos-independent pathways (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-09
    Description: The rapid induction of the proto-oncogene c-fos by growth factors and other bioactive agents, and the recent evidence that the c-fos protein (Fos) is associated with transcriptional complexes, suggests that Fos may represent an integral part of an intracellular messenger pathway that triggers changes in gene expression and ultimately phenotypic alterations. This report examines the role of c-fos in growth factor stimulation of transin, a matrix-degrading secreted metalloproteinase. Platelet-derived growth factor (PDGF) stimulation of transin RNA was blocked by a selective reduction in Fos synthesis with antisense c-fos mRNA, whereas epidermal growth factor (EGF) stimulation of transin occurred despite an equivalent inhibition of Fos levels. The stimulatory effect of both PDGF and EGF on transin transcription involved factors recognizing the sequence TGAGTCA, which is found in the transin promoter and is reported to be a binding site for the transcriptional factor Jun/AP-1 and for associated Fos and Fos-related complexes. Thus both Fos-dependent and Fos-independent pathways exist for growth factor regulation of gene expression, and both effects may be mediated through the same cis-acting transcription element.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kerr, L D -- Holt, J T -- Matrisian, L M -- New York, N.Y. -- Science. 1988 Dec 9;242(4884):1424-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Vanderbilt University, Nashville, TN 37232.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2462278" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; *Gene Expression Regulation ; Genes/*drug effects ; Growth Substances/*pharmacology ; Humans ; Matrix Metalloproteinase 3 ; Metalloendopeptidases/*genetics ; Mice ; Neoplasm Proteins/*genetics ; Proto-Oncogenes/*drug effects ; RNA/genetics ; RNA, Antisense ; RNA, Messenger/antagonists & inhibitors ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription, Genetic/*drug effects ; Transfection
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    Regulation of gene expression by interferons: control of H-2 promoter responses (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-03-11
    Description: The magnitude of the response to interferons and the requirement for individual elements in the promoter of the H-2Dd gene were shown to be cell-specific and dependent on the type of interferon used. Three DNA sequences in the promoter were found to bind murine nuclear factors. Two of these sequences are in functionally defined enhancer regions and also bind to the transcription factor AP-1. The third sequence is part of the region involved in interferon regulation and is homologous to the enhancer element of the interferon beta gene. A model for interferon regulation of H-2 promoters is discussed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korber, B -- Mermod, N -- Hood, L -- Stroynowski, I -- AI 19624/AI/NIAID NIH HHS/ -- T32GM7616/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1302-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3125612" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Enhancer Elements, Genetic ; *Gene Expression Regulation ; H-2 Antigens/*genetics ; Interferon Type I/*immunology ; Interferon-gamma/*immunology ; *Major Histocompatibility Complex ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; *Promoter Regions, Genetic
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    Role of the glutathione redox cycle in acquired and de novo multidrug resistance (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-05
    Description: Drug resistance represents a major obstacle to successful cancer chemotherapy. However, the specific biochemical mechanisms responsible for clinical drug resistance are unknown. In these studies resistance to the antitumor agent adriamycin was found to involve two mechanisms, one that decreased drug accumulation by the P170 mechanism and another that altered the glutathione redox cycle, an important pathway in the detoxification of reactive oxygen. This dual mechanism of drug resistance was demonstrated in cell lines that had acquired the multidrug-resistant phenotype and in human colorectal cancer cells with de novo resistance. These studies support a model of acquired and de novo multidrug resistance that includes alterations in both drug accumulation and the glutathione redox cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kramer, R A -- Zakher, J -- Kim, G -- New York, N.Y. -- Science. 1988 Aug 5;241(4866):694-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Joint Center for Radiation Therapy, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3399900" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carmustine/pharmacology ; Colonic Neoplasms ; Doxorubicin/*pharmacology ; *Drug Resistance ; Glutathione/*metabolism ; Glutathione Peroxidase/metabolism ; Glutathione Transferase/metabolism ; Humans ; Leukemia P388 ; Mice ; NADP/metabolism ; Oxidation-Reduction ; Phenotype ; Rectal Neoplasms ; Tumor Cells, Cultured ; Verapamil/pharmacology
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    Generation of cDNA probes directed by amino acid sequence: cloning of urate oxidase (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-03-11
    Description: Urate oxidase (E.C. 1.7.3.3) catalyzes the oxidation of uric acid to allantoin in most mammals except humans and certain primates. The amino-terminal amino acid sequence for porcine urate oxidase was determined and used in a novel procedure for generating complementary DNA (cDNA) probes to this amino acid sequence. The procedure is based on the polymerase chain reaction and utilizes mixed oligonucleotide primers complementary to the reverse translation products of an amino acid sequence. This rapid and simple cDNA cloning procedure is generally applicable and requires only a partial amino acid sequence. A cDNA probe developed by this procedure was used to isolate a full-length porcine urate oxidase cDNA and to demonstrate the presence of homologous genomic sequences in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, C C -- Wu, X W -- Gibbs, R A -- Cook, R G -- Muzny, D M -- Caskey, C T -- DK31428/DK/NIDDK NIH HHS/ -- GM34428/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1288-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Genetics, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3344434" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; *Cloning, Molecular ; DNA/*genetics ; Gene Amplification ; Liver/enzymology ; Mice ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Swine ; Urate Oxidase/*genetics
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    The primary structure and heterogeneity of tau protein from mouse brain (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-01-15
    Description: Tau protein is a family of microtubule binding proteins, heterogeneous in molecular weight, that are induced during neurite outgrowth and are found prominently in neurofibrillary tangles in Alzheimer's disease. The predicted amino acid sequences of two forms of tau protein from mouse brain were determined from complementary DNA clones. These forms are identical in their amino-terminal sequences but differ in their carboxyl-terminal domains. Both proteins contain repeated sequences that may be tubulin binding sites. The sequence suggests that tau is an elongated molecule with no extensive alpha-helical or beta-sheet domains. These complementary DNAs should enable the study of various functional domains of tau and the study of tau expression in normal and pathological states.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, G -- Cowan, N -- Kirschner, M -- GM32099/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 15;239(4837):285-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3122323" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; *Brain Chemistry ; Codon ; DNA/genetics ; DNA, Recombinant ; Mice ; Microtubule-Associated Proteins/*genetics ; Molecular Sequence Data ; Molecular Weight ; Nerve Tissue Proteins/genetics ; Protein Conformation ; RNA, Messenger/genetics ; Repetitive Sequences, Nucleic Acid ; tau Proteins
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    Concerted nonsyntenic allelic loss in human colorectal carcinoma (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-19
    Description: Familial polyposis coli (FPC) is caused by an autosomal dominant gene on chromosome 5, and it has been proposed that colorectal cancer in the general population arises from loss or inactivation of the FPC gene, analogous to recessive tumor genes in retinoblastoma and Wilms' tumor. Since allelic loss can be erroneously scored in nonhomogeneous samples, tumor cell populations were first microdissected from 24 colorectal carcinomas, an additional nine cancers were engrafted in nude mice, and nuclei were flow-sorted from an additional two. Of 31 cancers informative for chromosome 5 markers, only 6 (19%) showed loss of heterozygosity of chromosome 5 alleles, compared to 19 of 34 (56%) on chromosome 17, and 17 of 33 (52%) on chromosome 18. Therefore, it appears that (i) FPC is a true dominant for adenomatosis but not a common recessive gene for colon cancer; and (ii) simple Mendelian models involving loss of alleles at a single locus may be inappropriate for understanding common human solid tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Law, D J -- Olschwang, S -- Monpezat, J P -- Lefrancois, D -- Jagelman, D -- Petrelli, N J -- Thomas, G -- Feinberg, A P -- New York, N.Y. -- Science. 1988 Aug 19;241(4868):961-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Michigan Medical School, Ann Arbor 48109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2841761" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/genetics ; Adenoma/genetics ; Adenomatous Polyposis Coli/*genetics ; *Alleles ; Animals ; Chromosomes, Human, Pair 17 ; Chromosomes, Human, Pair 18 ; Chromosomes, Human, Pair 5 ; Colonic Neoplasms/*genetics ; DNA, Neoplasm/analysis ; Genes, Dominant ; *Genetic Linkage ; Humans ; Mice ; Precancerous Conditions/genetics ; Rectal Neoplasms/*genetics
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    Induction of gene amplification by arsenic (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-01
    Description: Arsenic is a well-established carcinogen in humans, but there is little evidence for its carcinogenicity in animals and it is inactive as an initiator or tumor promoter in two-stage models of carcinogenicity in mice. Two arsenic salts (sodium arsenite and sodium arsenate) induced a high frequency of methotrexate-resistant 3T6 cells, which were shown to have amplified copies of the dihydrofolate reductase gene. The ability of arsenic to induce gene amplification may relate to its carcinogenic effects in humans since amplification of oncogenes is observed in many human tumors. The inability of arsenic to induce gene mutations may relate to the negative results of arsenic in long-term animal studies and suggests that these experiments may not detect some environmental agents that act late in the carcinogenic process in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, T C -- Tanaka, N -- Lamb, P W -- Gilmer, T M -- Barrett, J C -- New York, N.Y. -- Science. 1988 Jul 1;241(4861):79-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3388020" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arsenates/*pharmacology ; Arsenic/*pharmacology ; *Arsenites ; Cell Line ; DNA/genetics ; Drug Resistance ; Gene Amplification/*drug effects ; Humans ; Methotrexate ; Mice ; Neoplasms, Experimental/chemically induced/genetics ; Nucleic Acid Hybridization ; Oncogenes ; *Sodium Compounds ; Tetrahydrofolate Dehydrogenase/*genetics
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    Development of disease and virus recovery in transgenic mice containing HIV proviral DNA (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-23
    Description: Transgenic mice containing intact copies of the human immunodeficiency virus (HIV) proviral DNA were constructed. Founder animals were not viremic for HIV and remained healthy during a 9-month observation period. After being mated with nontransgenic animals, one founder mouse (No. 13) gave rise to F1 progeny that developed a disease syndrome characterized by marked epidermal hyperplasia, lymphadenopathy, splenomegaly, pulmonary lymphoid infiltrates, growth retardation, and death by day 25 of life. Infectious HIV, indistinguishable from parental virus by immunoblot analysis, was recovered from the spleen, lymph nodes, and skin of five of five affected animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leonard, J M -- Abramczuk, J W -- Pezen, D S -- Rutledge, R -- Belcher, J H -- Hakim, F -- Shearer, G -- Lamperth, L -- Travis, W -- Fredrickson, T -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1665-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201255" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology/*microbiology/pathology ; Animals ; DNA Probes ; *DNA, Viral/analysis ; *Disease Models, Animal ; Epidermis/pathology ; HIV/*genetics/immunology/isolation & purification ; HIV Antibodies/analysis ; Lung/pathology ; Lymph Nodes/microbiology/pathology ; Mice ; Mice, Transgenic ; Nucleic Acid Hybridization ; Skin/microbiology/pathology ; Spleen/microbiology/pathology
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    A previously undetected MHC gene with an unusual periodic structure (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-04-08
    Description: The major histocompatibility complex is a chromosomal segment embodying several gene clusters among which those with immune functions are the best characterized. This region is suspected to host other as yet undetected genes whose characterization may shed light on the population genetics and evolution of the whole gene complex and thus on its unexplained character of marker locus for a number of diseases of nonimmune or unknown pathogenesis. A novel gene was identified that is transcribed in all tissues tested and is located in mouse and man between the CA and Bf genes of the H-2 and HLA complexes, respectively. From the nucleotide sequence, derived from liver complementary DNA clones, it is predicted that this novel single-copy gene encodes a 42-kilodalton polypeptide that bears no recognizable relation to the protein families known so far, but it displays striking hallmarks of natural selection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levi-Strauss, M -- Carroll, M C -- Steinmetz, M -- Meo, T -- New York, N.Y. -- Science. 1988 Apr 8;240(4849):201-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U 276, Institut Pasteur, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3353717" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; Genes ; Liver/physiology ; *Major Histocompatibility Complex ; Mice ; Molecular Sequence Data ; Periodicity ; Selection, Genetic
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    Subset-specific expression of potassium channels in developing murine T lymphocytes (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-12
    Description: Ion channels were studied in four major subsets of developing murine thymocytes by using patch-clamp recording and cell-surface staining techniques. The expression of three types of voltage-gated potassium channels in thymocytes varies consistently with the cell's developmental state and functional class as defined by cell-surface markers. One class of potassium channel (type n) predominates in immature thymocyte subsets as well as in mature-phenotype CD4+CD8- thymocytes (precursors to helper T lymphocytes), and the average surface density of this channel type correlates with the extent of cell proliferation. Two additional types of potassium channels (types n' and l) are found in the mature CD4-CD8+ thymocyte subset that contains precursors to cytotoxic and suppressor T cells. The subset-specific expression of type n' and l potassium channels suggests their use as additional cell-surface markers with which to identify precursors to the cytotoxic suppressor T cell lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewis, R S -- Cahalan, M D -- AI21808/AI/NIAID NIH HHS/ -- NS08021/NS/NINDS NIH HHS/ -- NS14609/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 12;239(4841 Pt 1):771-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, California College of Medicine, University of California, Irvine 92717.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2448877" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigens, Surface/analysis ; Electric Conductivity ; Ion Channels/*physiology ; Membrane Potentials ; Mice ; Phenotype ; T-Lymphocytes/classification/immunology/*physiology
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    Microtubule-associated protein MAP2 shares a microtubule binding motif with tau protein (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-11-11
    Description: The microtubule-associated protein MAP2 is a prominent large-sized component of purified brain microtubules that, like the 36- to 38-kilodalton tau proteins, bears antigenic determinants found in association with the neurofibrillary tangles of Alzheimer's disease. The complete sequence of mouse brain MAP2 was determined from a series of overlapping cloned complementary DNAs. The sequence of the carboxyl-terminal 185 amino acids is very similar (67 percent) to a corresponding region of tau protein, and includes a series of three imperfect repeats, each 18 amino acids long and separated by 13 or 14 amino acids. A subcloned fragment spanning the first two of the 18-amino acid repeats was expressed as a polypeptide by translation in vitro. This polypeptide copurified with microtubules through two successive cycles of polymerization and depolymerization, whereas a control polypeptide derived from the amino-terminal region of MAP2 completely failed to copurify. These data imply that the carboxyl-terminal domain containing the 18-amino acid repeats constitutes the microtubule binding site in MAP2. The occurrence of these repeats in tau protein suggests that these may be a general feature of microtubule binding proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewis, S A -- Wang, D H -- Cowan, N J -- New York, N.Y. -- Science. 1988 Nov 11;242(4880):936-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, New York University Medical Center, NY 10016.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3142041" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; DNA/genetics ; Mice ; Microtubule-Associated Proteins/genetics/*metabolism ; Microtubules/*metabolism ; Molecular Sequence Data ; Molecular Weight ; Nerve Tissue Proteins ; Protein Biosynthesis ; Repetitive Sequences, Nucleic Acid ; Sequence Homology, Nucleic Acid ; Tubulin/metabolism ; tau Proteins
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    Distinct cloned class II MHC DNA binding proteins recognize the X box transcription element (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-10-07
    Description: The class II (Ia) major histocompatibility complex (MHC) antigens are a family of integral membrane proteins whose expression is limited to certain cell types. A pair of consensus sequences, X and Y, is found upstream of all class II genes, and deletion of each of these sequences eliminates expression of transfected genes. Furthermore, the absence of a specific X box binding protein in patients with severe combined immunodeficiency disease whose cells lack class II suggests an important role for these proteins in class II regulation. Here, the cloning of two lambda gt11 complementary DNAs encoding DNA binding proteins (murine X box binding proteins lambda mXBP and lambda mXBP-2) is reported. Both phage-encoded fusion proteins bind specifically to the X box of the A alpha, but not to E alpha or E beta class II genes. These two independent isolates do not cross-hybridize. The lambda mXBP complementary DNA hybridizes to two RNA species, 6.2 and 3.0 kilobases in mouse, that are expressed in both Ia positive and Ia negative cells. By means of DNA blot analysis with the lambda mXBP complementary DNA insert and probes generated from each end of this complementary DNA insert, lambda mXBP was found to arise from a multigene family. These data illustrate the high degree of complexity in the transcriptional control of this coordinately regulated gene family.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liou, H C -- Boothby, M R -- Glimcher, L H -- New York, N.Y. -- Science. 1988 Oct 7;242(4875):69-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Harvard School of Public Health, Boston, Massachusetts 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3140376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Cloning, Molecular ; DNA-Binding Proteins/*genetics ; Gene Expression Regulation ; *Genes ; *Genes, MHC Class II ; Humans ; Mice ; Molecular Sequence Data ; *Transcription, Genetic ; Transfection
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    Proteosome-lipopeptide vaccines: enhancement of immunogenicity for malaria CS peptides (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-05-06
    Description: Proteosomes are hydrophobic, membranous, multimolecular preparations of meningococcal outer membrane proteins that are also B cell mitogens. These characteristics suggested that proteosomes may serve as carrier proteins and adjuvants to enhance peptide immunogenicity. Although high titers of malaria circumsporozoite (CS) antibodies protect against malaria, vaccines thus far tested in humans have been insufficiently immunogenic to be clinically useful. Here it is shown that synthetic CS peptides hydrophobically complexed to proteosomes by way of lauroyl-cysteine become highly immunogenic in mice without other adjuvants. The high titers of antibodies produced and the safety of proteosomes in humans suggest that this novel system is widely applicable for the development of peptide vaccines to protect against many diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lowell, G H -- Ballou, W R -- Smith, L F -- Wirtz, R A -- Zollinger, W D -- Hockmeyer, W T -- New York, N.Y. -- Science. 1988 May 6;240(4853):800-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bacterial Diseases, Walter Reed Army Institute of Research, Washington, DC 20307-5100.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2452484" target="_blank"〉PubMed〈/a〉
    Keywords: Adjuvants, Immunologic ; Animals ; Antibody Specificity ; Antigens/*immunology ; Antigens, Protozoan/immunology ; Antigens, Surface/*immunology ; Apicomplexa/immunology ; Bacterial Outer Membrane Proteins/*immunology ; Epitopes/immunology ; Immunization ; Immunoglobulin G/analysis/biosynthesis ; Liposomes/immunology ; Mice ; *Neisseria meningitidis ; Plasmodium falciparum/immunology ; Plasmodium vivax/immunology ; *Protozoan Proteins ; Vaccines, Synthetic/*immunology
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    Radioimmunotherapy with alpha-particle-emitting immunoconjugates (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-05-20
    Description: Alpha particles are energetic short-range ions whose higher linear energy transfer produces extreme cytotoxicity. An alpha-particle-emitting radioimmunoconjugate consisting of a bismuth-212-labeled monoclonal immunoglobulin M specific for the murine T cell/neuroectodermal surface antigen Thy 1.2 was prepared. Analysis in vitro showed that the radioimmunoconjugate was selectively cytotoxic to a Thy 1.2+ EL-4 murine tumor cell line. Approximately three bismuth-212-labeled immunoconjugates per target cell reduced the uptake of [3H]thymidine by the EL-4 target cells to background levels. Mice inoculated intraperitoneally with EL-4 cells were cured of their ascites after intraperitoneal injection of 150 microcuries of the antigen-specific radioimmunoconjugate, suggesting a possible role for such conjugates in intracavitary cancer therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Macklis, R M -- Kinsey, B M -- Kassis, A I -- Ferrara, J L -- Atcher, R W -- Hines, J J -- Coleman, C N -- Adelstein, S J -- Burakoff, S J -- 5 PO1-CA39542-03/CA/NCI NIH HHS/ -- 5T32 CA 09536-01/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 May 20;240(4855):1024-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Joint Center for Radiation Therapy, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2897133" target="_blank"〉PubMed〈/a〉
    Keywords: *Alpha Particles ; Animals ; *Antigens, Surface ; Antigens, Thy-1 ; Bismuth/therapeutic use ; *Immunoglobulin M ; Immunotherapy ; Lymphoma/*radiotherapy ; Mice ; Mice, Inbred C57BL ; Radioisotopes/therapeutic use
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    Selective activation of transcription by a novel CCAAT binding factor (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-29
    Description: A novel CCAAT binding factor (CBF) composed of two different subunits has been extensively purified from rat liver. Both subunits are needed for specific binding to DNA. Addition of this purified protein to nuclear extracts of NIH 3T3 fibroblasts stimulates transcription from several promoters including the alpha 2(I) collagen, the alpha 1(I) collagen, the Rous sarcoma virus long terminal repeat (RSV-LTR), and the adenovirus major late promoter. Point mutations in the CCAAT motif that show either no binding or a decreased binding of CBF likewise abolish or reduce activation of transcription by CBF. Activation of transcription requires, therefore, the specific binding of CBF to its recognition sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maity, S N -- Golumbek, P T -- Karsenty, G -- de Crombrugghe, B -- New York, N.Y. -- Science. 1988 Jul 29;241(4865):582-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, Univesity of Texas, M.D. Anderson Cancer Center, Houston 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3399893" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Nucleus/physiology ; Collagen/genetics ; DNA-Binding Proteins/*physiology ; In Vitro Techniques ; Macromolecular Substances ; Mice ; Nuclear Proteins/physiology ; *Promoter Regions, Genetic ; Rats ; *Regulatory Sequences, Nucleic Acid ; Transcription Factors/*physiology ; *Transcription, Genetic
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    Animals of invention (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Booth, W -- New York, N.Y. -- Science. 1988 May 6;240(4853):718.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3163178" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Experimentation ; Animals ; *Animals, Laboratory ; Federal Government ; *Genetic Engineering ; *Government Regulation ; Mice ; Neoplasms, Experimental/genetics ; Patents as Topic/*legislation & jurisprudence
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    Of mice, oncogenes, and Rifkin (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-01-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Booth, W -- New York, N.Y. -- Science. 1988 Jan 22;239(4838):341-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3257302" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Experimentation ; Animals ; Antigens, Differentiation, T-Lymphocyte/genetics ; Biomedical Research ; *Containment of Biohazards ; DNA, Recombinant ; Environmental Exposure ; Federal Government ; *Genes, Viral ; Genetic Engineering ; Government Regulation ; HIV/*genetics ; HeLa Cells ; Humans ; Legislation, Medical ; Mice ; Mice, Transgenic/*genetics ; *Oncogenes ; Recombination, Genetic ; *Risk Assessment ; Risk Factors
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Autologous peptides constitutively occupy the antigen binding site on Ia (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-11-18
    Description: Low molecular weight material associated with affinity-purified class II major histocompatibility complex (MHC) molecules of mouse (Ia) had the expected properties of peptides bound to the antigen binding site of Ia. Thus, the low molecular weight material derived from the I-Ad isotype was efficient in inhibiting the binding of 125I-labeled I-Ad-specific peptide to I-Ad, but did not significantly inhibit the binding of an I-Ed-specific peptide to I-Ed; the reciprocal isotype-specific inhibition was demonstrated with low molecular weight material derived from I-Ed. The inhibitory material was predominantly peptide in nature, as shown by its susceptibility to protease digestion. It was heterogeneous as measured by gel filtration (mean molecular weight approximately 3000), and when characterized by high-performance liquid chromatography, it eluted over a wide concentration of solvent. Such self peptide-MHC complexes may have broad significance in the biology of T cell responses, including generation of the T cell repertoire, the specificity of mixed lymphocyte responses, and the immune surveillance of self and nonself antigens in peripheral lymphoid tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buus, S -- Sette, A -- Colon, S M -- Grey, H M -- AI09758/AI/NIAID NIH HHS/ -- AI18634/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 18;242(4881):1045-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3194755" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoantigens/immunology ; Binding Sites ; Chromatography, High Pressure Liquid ; Histocompatibility Antigens Class II/isolation & purification/*metabolism ; Mice ; Molecular Weight ; Ovalbumin/metabolism ; Peptides/*metabolism
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    Iron-responsive elements: regulatory RNA sequences that control mRNA levels and translation (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-05-13
    Description: The biosynthetic rates for both the transferrin receptor (TfR) and ferritin are regulated by iron. An iron-responsive element (IRE) in the 5' untranslated portion of the ferritin messenger RNA (mRNA) mediates iron-dependent control of its translation. In this report the 3' untranslated region of the mRNA for the human TfR was shown to be necessary and sufficient for iron-dependent control of mRNA levels. Deletion studies identified a 678-nucleotide fragment of the TfR complementary DNA that is critical for this iron regulation. Five potential stem-loops that resemble the ferritin IRE are contained within the region critical for TfR regulation. Each of two of the five TfR elements was independently inserted into the 5' untranslated region of an indicator gene transcript. In this location they conferred iron regulation of translation. Thus, an mRNA element has been implicated in the mediation of distinct regulatory phenomena dependent on the context of the element within the transcript.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Casey, J L -- Hentze, M W -- Koeller, D M -- Caughman, S W -- Rouault, T A -- Klausner, R D -- Harford, J B -- New York, N.Y. -- Science. 1988 May 13;240(4854):924-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2452485" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; DNA/genetics ; DNA, Recombinant ; Ferritins/biosynthesis/*genetics ; Growth Hormone/genetics ; Humans ; Iron/*pharmacology ; Mice ; Plasmids ; Protein Biosynthesis/*drug effects ; RNA/*genetics ; RNA, Messenger/*genetics ; Receptors, Transferrin/biosynthesis/*genetics ; *Regulatory Sequences, Nucleic Acid ; Transcription, Genetic ; Transfection ; Transformation, Genetic
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    Expression of the murine Duchenne muscular dystrophy gene in muscle and brain (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-03-18
    Description: Complementary DNA clones were isolated that represent the 5' terminal 2.5 kilobases of the murine Duchenne muscular dystrophy (Dmd) messenger RNA (mRNA). Mouse Dmd mRNA was detectable in skeletal and cardiac muscle and at a level approximately 90 percent lower in brain. Dmd mRNA is also present, but at much lower than normal levels, in both the muscle and brain of three different strains of dystrophic mdx mice. The identification of Dmd mRNA in brain raises the possibility of a relation between human Duchenne muscular dystrophy (DMD) gene expression and the mental retardation found in some DMD males. These results also provide evidence that the mdx mutations are allelic variants of mouse Dmd gene mutations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chamberlain, J S -- Pearlman, J A -- Muzny, D M -- Gibbs, R A -- Ranier, J E -- Caskey, C T -- Reeves, A A -- New York, N.Y. -- Science. 1988 Mar 18;239(4846):1416-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Genetics, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3347839" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; DNA/genetics ; DNA, Recombinant ; *Gene Expression Regulation ; Intellectual Disability/genetics ; Mice ; Mice, Inbred ICR ; Mice, Mutant Strains ; Muscles/*metabolism ; Muscular Dystrophy, Animal/*genetics ; Mutation ; Nucleic Acid Hybridization ; RNA, Messenger/metabolism ; Ribonuclease, Pancreatic/metabolism
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    Comparison of biological properties and transforming potential of human PDGF-A and PDGF-B chains (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-09
    Description: Human platelet-derived growth factor (PDGF) consists of two distinct but related polypeptide chains designated PDGF-A and PDGF-B. The gene encoding PDGF-B has given rise to the v-sis oncogene. In the present study the transforming activities of PDGF-A and PDGF-B genes are compared. The PDGF-A chain gene is markedly less efficient in inducing transformation than the PDGF-B gene under the influence of the same promoter. There are significant differences in the secretory and growth stimulating properties of the two chains. These properties appear to account for the much more potent transforming ability of the PDGF-B gene. These findings provide insights into biologic properties of a growth factor responsible for potent autocrine stimulation of abnormal cell proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beckmann, M P -- Betsholtz, C -- Heldin, C H -- Westermark, B -- Di Marco, E -- Di Fiore, P P -- Robbins, K C -- Aaronson, S A -- New York, N.Y. -- Science. 1988 Sep 9;241(4871):1346-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2842868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Compartmentation ; Cell Line ; *Cell Transformation, Neoplastic ; Gene Expression Regulation ; Immunologic Techniques ; Mice ; Molecular Weight ; Platelet-Derived Growth Factor/*physiology ; Proto-Oncogene Proteins/*physiology ; Receptors, Cell Surface/*physiology ; Receptors, Platelet-Derived Growth Factor ; Solubility
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    Demethylated CD8 gene in CD4+ T cells suggests that CD4+ cells develop from CD8+ precursors (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-11-25
    Description: Mature T cells and medullary thymocytes bear either the CD4 or CD8 differentiation antigen. Precursor cells in the thymus express neither CD4 nor CD8 (CD4-8-), but most cortical thymocytes are CD4+8+. Whether CD4+ and CD8+ mature T cells arise directly from CD4-8- precursors or from a CD4+8+ intermediate remains unresolved. In this study, methylation of the CD8 gene in murine T cells and thymocytes was examined. There was progressive demethylation of the CD8 gene in the thymus during the transition from CD4-8- to CD4+8+. A similar pattern of demethylation of the CD8 gene was seen in CD4+ mature T cells, suggesting previous expression of CD8 in the CD4+ lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carbone, A M -- Marrack, P -- Kappler, J W -- New York, N.Y. -- Science. 1988 Nov 25;242(4882):1174-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2460926" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Differentiation, T-Lymphocyte/*genetics ; DNA/*metabolism ; Deoxyribonuclease BamHI/metabolism ; Deoxyribonuclease HpaII ; Deoxyribonucleases, Type II Site-Specific/metabolism ; Exons ; Hematopoietic Stem Cells/*immunology ; Hybridomas/immunology ; Introns ; Methylation ; Mice ; Mice, Inbred AKR ; T-Lymphocytes/*immunology
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    Neonatal hepatitis induced by alpha 1-antitrypsin: a transgenic mouse model (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-09
    Description: Transgenic mouse lineages were established that carry the normal (M) or mutant (Z) alleles of the human alpha 1-antitrypsin (alpha 1-Pi) gene. All of the alpha 1-Pi transgenic mice expressed the human protein in the liver, cartilage, gut, kidneys, lymphoid macrophages, and thymus. The human M-allele protein was secreted normally into the serum. However, the human Z-allele protein accumulated in several cell types, but particularly in hepatocytes, and was found in serum in tenfold lower concentrations than the M-allele protein. Mice in one lineage carrying the mutant Z allele expressed high levels of human alpha 1-Pi RNA and displayed significant runting (50% of normal weight) in the neonatal period. This lineage was found to have alpha 1-Pi-induced liver pathology in the neonatal period, concomitant with the accumulation of human Z protein in diastase-resistant cytoplasmic globules that could be revealed in the Periodic acid-Schiff reaction (PAS). The phenotype of mice in the strain expressing high levels of the Z allele is remarkably similar to human neonatal hepatitis, and this strain may prove to be a useful animal model for studying this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dycaico, M J -- Grant, S G -- Felts, K -- Nichols, W S -- Geller, S A -- Hager, J H -- Pollard, A J -- Kohler, S W -- Short, H P -- Jirik, F R -- N01-HR-56024/HR/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Dec 9;242(4884):1409-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, Cedars Sinai Medical Center, Los Angeles, CA 90048.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3264419" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Animals, Newborn ; Disease Models, Animal ; *Genes ; Hepatitis/congenital/*genetics/pathology ; Humans ; Liver/pathology ; Mice ; Mice, Inbred Strains ; Mice, Transgenic ; *Mutation ; alpha 1-Antitrypsin/*genetics
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    In vivo administration of anti-CD3 prevents malignant progressor tumor growth (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-10-28
    Description: Malignant progressor tumors are only weakly immunogenic and can evade host recognition and rejection. One approach to therapy involves activation of the host antitumor cellular effector mechanisms. Since monoclonal antibodies to CD3 (anti-CD3) can activate T cells in vitro, an attempt was made to determine if tumor immunity could be achieved by the administration of anti-CD3 in vivo. T lymphocytes from mice injected with anti-CD3 showed increased interleukin-2 receptor (IL-2R) expression, increased proliferation to recombinant IL-2 (rIL-2), and enhanced reactivity in both an allogeneic mixed lymphocyte reaction and a mixed lymphocyte tumor culture. Malignant tumor growth in treated mice was also examined. The anti-CD3 treatment prevented tumor outgrowth that would have killed untreated animals and also stimulated an in vivo response against a malignant progressor tumor providing lasting tumor immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ellenhorn, J D -- Hirsch, R -- Schreiber, H -- Bluestone, J A -- New York, N.Y. -- Science. 1988 Oct 28;242(4878):569-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2902689" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD3 ; Antigens, Differentiation, T-Lymphocyte/analysis/*physiology ; Antigens, Surface/analysis ; Antigens, Thy-1 ; Dose-Response Relationship, Immunologic ; Immunosuppression ; Immunotherapy ; Lymph Nodes/immunology ; *Lymphocyte Activation ; Mice ; Neoplasm Transplantation ; Neoplasms, Experimental/*therapy ; Receptors, Antigen, T-Cell/*physiology ; Receptors, Interleukin-2/metabolism ; T-Lymphocytes/*immunology
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    Voltage-sensitive calcium channels in normal and transformed 3T3 fibroblasts (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-26
    Description: Patch clamp recordings of whole-cell and single channel currents revealed the presence of two voltage-sensitive calcium channel types in the membrane of 3T3 fibroblasts. The two calcium channel types were identified by their unitary properties and pharmacological sensitivities. Both calcium channel types were present in all control 3T3 cells, but one type was selectively suppressed in 3T3 cells that had been transformed by activated c-H-ras, EJ-ras, v-fms, or polyoma middle T oncogenes. The presence of voltage-sensitive calcium channels in these nonexcitable cells and the control of their functional expression by transforming oncogenes raises questions about their role in the control of calcium-sensitive processes such as cell motility, cytoskeletal organization, and cell growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, C F -- Corbley, M J -- Roberts, T M -- Hess, P -- CA21082/CA/NCI NIH HHS/ -- HL37124/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 26;239(4843):1024-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2449730" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channel Agonists ; Cell Division ; Cell Line ; Cell Line, Transformed ; *Cell Transformation, Neoplastic ; Electric Conductivity ; Fibroblasts/*physiology ; Ion Channels/drug effects/*physiology ; Kinetics ; Membrane Potentials ; Mice ; Nicotinic Acids/pharmacology ; Oncogenes ; *Oxadiazoles
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    Isotypic exclusion of gamma delta T cell receptors in transgenic mice bearing a rearranged beta-chain gene (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-26
    Description: The rearrangement of T cell antigen receptor beta- and gamma-chain gene segments was studied in transgenic mice that bear a functional beta-chain gene. Virtually all CD3-positive T cells derived from transgenic mice express beta chains containing the transgene-encoded V beta 8.2 variable region on their surfaces and do not express endogenous beta-chain variable regions. Expression of endogenous V beta genes is inhibited at the level of somatic recombination during thymic ontogeny. Furthermore, rearrangements of the TCR gamma-chain genes are also markedly inhibited in these transgenic animals. Hence expression of the TCR beta transgene has led to allelic exclusion of alpha beta receptors and isotypic exclusion of gamma delta T cell receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fenton, R G -- Marrack, P -- Kappler, J W -- Kanagawa, O -- Seidman, J G -- New York, N.Y. -- Science. 1988 Aug 26;241(4869):1089-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2970670" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Antibodies, Monoclonal ; Bacteriophage lambda/genetics ; Cloning, Molecular ; DNA, Recombinant ; Enhancer Elements, Genetic ; Gene Expression Regulation ; Genes, Immunoglobulin ; Immunoassay ; Immunoglobulin Heavy Chains/genetics ; Liver/analysis ; Mice ; Mice, Transgenic ; Ovalbumin/immunology ; Receptors, Antigen, T-Cell/*genetics ; Recombination, Genetic ; T-Lymphocytes/metabolism ; Thymus Gland/analysis
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    Long lives for homozygous trembler mutant mice despite virtual absence of peripheral nerve myelin (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-15
    Description: Nervous system functions are dependent on point-to-point communication of signals along neuronal axons, and axonal insulation by myelin is thought to speed such conduction. Loss of previously formed myelin or lack of myelin formation can have serious, even fatal, consequences. Mice homozygous for the trembler mutation make virtually no peripheral nervous system myelin, yet have long and functional lives. This result calls into question the view that peripheral nervous system myelin plays a vital role, at least in this species.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Henry, E W -- Sidman, R L -- NS20820/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 15;241(4863):344-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuropathology, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3388045" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Demyelinating Diseases/genetics/pathology/physiopathology ; Longevity ; Mice ; Mice, Neurologic Mutants/*physiology ; Myelin Sheath/*physiology ; Neural Conduction ; Peripheral Nerves/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 80
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    Overexpression of low density lipoprotein (LDL) receptor eliminates LDL from plasma in transgenic mice (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-03-11
    Description: A complementary DNA encoding the human low density lipoprotein (LDL) receptor under control of the mouse metallothionein-I promoter was injected into fertilized mouse eggs, and a strain of mice expressing high levels of LDL receptors was established. After administration of cadmium, these mice cleared intravenously injected 125I-labeled LDL from blood eight to ten times more rapidly than did normal mice. The plasma concentrations of apoproteins B-100 and E, the two ligands for the LDL receptor, declined by more than 90 percent after cadmium treatment, but the concentration of another apoprotein, A-I, was unaffected. Therefore, overexpression of an endocytotic receptor can dramatically lower the ambient concentration of its ligand in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hofmann, S L -- Russell, D W -- Brown, M S -- Goldstein, J L -- Hammer, R E -- HL 01287/HL/NHLBI NIH HHS/ -- HL 20948/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1277-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3344433" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; DNA/genetics ; Female ; *Genes ; Humans ; Kinetics ; Lipoproteins, LDL/*blood ; Mice ; Mice, Transgenic ; Plasmids ; Receptors, LDL/*genetics/metabolism ; Reference Values ; Transcription, Genetic
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  • 81
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    Inhibition of cellular proliferation by antisense oligodeoxynucleotides to PCNA cyclin (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-06-10
    Description: The proliferating cell nuclear antigen (PCNA or cyclin) is a nuclear protein recently identified as a cofactor of DNA polymerase delta. When exponentially growing Balb/c3T3 cells are exposed to antisense oligodeoxynucleotides to PCNA, both DNA synthesis and mitosis are completely suppressed. A corresponding sense oligodeoxynucleotide has no inhibitory effects. These experiments indicate that PCNA (cyclin) is important in cellular DNA synthesis and in cell cycle progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jaskulski, D -- deRiel, J K -- Mercer, W E -- Calabretta, B -- Baserga, R -- CA 42866/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 10;240(4858):1544-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Temple University Medical School, Philadelphia, PA 19140.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2897717" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoantigens/*genetics ; Base Sequence ; Cell Division/drug effects ; Cells, Cultured ; Codon ; DNA Replication/*drug effects ; Kinetics ; Mice ; Mice, Inbred BALB C ; Mitosis/*drug effects ; Molecular Sequence Data ; Nuclear Proteins/*genetics ; Oligodeoxyribonucleotides/*pharmacology ; Proliferating Cell Nuclear Antigen
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 82
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    Overexpression of metallothionein confers resistance to anticancer drugs (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-30
    Description: Resistance to antineoplastic agents is the major obstacle to curative therapy of cancer. Tumor cell lines with acquired resistance to the antineoplastic agent cis-diamminedichloroplatinum(II) overexpressed metallothionein and demonstrated cross-resistance to alkylating agents such as chlorambucil and melphalan. Human carcinoma cells that maintained high levels of metallothionein because of chronic exposure to heavy metals were resistant to cis-diamminedichloroplatinum(II), melphalan, and chlorambucil. Furthermore, cells transfected with bovine papilloma virus expression vectors containing DNA encoding human metallothionein-IIA were resistant to cis-diamminedichloroplatinum(II), melphalan, and chlorambucil but not to 5-fluorouracil or vincristine. Thus, overexpression of metallothionein represents one mechanism of resistance to a subset of clinically important anticancer drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kelley, S L -- Basu, A -- Teicher, B A -- Hacker, M P -- Hamer, D H -- Lazo, J S -- CA-01012/CA/NCI NIH HHS/ -- CA-38497/CA/NCI NIH HHS/ -- CA-43917/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Sep 30;241(4874):1813-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pharmaceutical Research and Development Division, Bristol Myers Co., Wallingford, CT 06492.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175622" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antineoplastic Agents ; Blotting, Northern ; Cells, Cultured ; *Drug Resistance ; In Vitro Techniques ; Metallothionein/*physiology ; Mice
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  • 83
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    ADP-ribosyltransferase activity of pertussis toxin and immunomodulation by Bordetella pertussis (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-04-29
    Description: Pertussis toxin is produced by the causative agent of whooping cough, Bordetella pertussis, and is an adenosine diphosphate (ADP)-ribosyltransferase capable of covalently modifying and thereby inactivating many eukaryotic G proteins involved in cellular metabolism. The toxin is a principal determinant of virulence in whooping cough and is a primary candidate for an acellular pertussis vaccine, yet it is unclear whether the ADP-ribosyltransferase activity is required for both pathogenic and immunoprotective activities. A B. pertussis strain that produced an assembled pertussis holotoxin with only 1 percent of the ADP-ribosyltransferase activity of the native toxin was constructed and was found to be deficient in pathogenic activities associated with B. pertussis including induction of leukocytosis, potentiation of anaphylaxis, and stimulation of histamine sensitivity. Moreover, this mutant strain failed to function as an adjuvant and was less effective in protecting mice from intracerebral challenge infection. These data suggest that the ADP-ribosyltransferase activity is necessary for both pathogenicity and optimum immunoprotection. These findings bear directly on the design of a nontoxic pertussis vaccine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Black, W J -- Munoz, J J -- Peacock, M G -- Schad, P A -- Cowell, J L -- Burchall, J J -- Lim, M -- Kent, A -- Steinman, L -- Falkow, S -- AI-22462/AI/NIAID NIH HHS/ -- AI-23945/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 29;240(4852):656-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2896387" target="_blank"〉PubMed〈/a〉
    Keywords: ADP Ribose Transferases ; Adjuvants, Immunologic ; Anaphylaxis/etiology ; Animals ; Antigens/immunology ; Bordetella pertussis/enzymology/genetics/*immunology ; Codon ; Drug Tolerance ; Histamine/pharmacology ; Immunization ; Leukocytosis/etiology ; Macromolecular Substances ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mutation ; Ovalbumin/immunology ; Pentosyltransferases/*metabolism ; *Pertussis Toxin ; Virulence Factors, Bordetella/genetics/immunology/*metabolism
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  • 84
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    Escherichia coli secretion of an active chimeric antibody fragment (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-05-20
    Description: A chimeric mouse-human Fab protein that binds specifically to the human carcinoma cell line C3347 has been expressed and secreted from Escherichia coli. This molecule, which contains functionally assembled kappa and Fd proteins, binds as effectively to sites on the surface of C3347 cells as Fab fragments prepared proteolytically from whole chimeric or mouse antibody. The production in Escherichia coli of foreign heterodimeric protein reagents, such as Fab, should prove useful in the management of human disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Better, M -- Chang, C P -- Robinson, R R -- Horwitz, A H -- New York, N.Y. -- Science. 1988 May 20;240(4855):1041-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉International Genetic Engineering Inc. (INGENE), Santa Monica, CA 90404.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3285471" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigen-Antibody Complex/immunology ; Antigens, Surface/immunology ; Base Sequence ; Cell Line ; *Chimera ; Escherichia coli/*genetics ; Genes, Immunoglobulin ; Humans ; Immunoglobulin Fab Fragments/*genetics/immunology ; Mice ; Molecular Sequence Data ; Transcription, Genetic
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  • 85
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    Tumor formation dependent on proteoglycan biosynthesis (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-26
    Description: The role proteoglycans play in tumor formation was examined by measuring the tumorigenicity of proteoglycan-deficient Chinese hamster ovary cell mutants in nude mice. When 10(7) cells were injected subcutaneously, mutants with less than about 15% of the wild-type level of proteoglycan synthesis did not produce tumors. Mutants defective in the synthesis of heparan sulfate proteoglycans also did not form tumors, whereas mutants with altered chondroitin sulfate proteoglycans were tumorigenic. Tumors arose from mixtures of wild-type and nontumorigenic mutant cells and contained both cell types, suggesting that wild-type cell proteoglycans enabled mutant cells to survive. The failure of heparan sulfate-deficient mutants to form tumors depended on the ability of the host to mount a B cell-mediated immune reaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Esko, J D -- Rostand, K S -- Weinke, J L -- GM33063/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 26;241(4869):1092-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, School of Medicine, University of Alabama, Birmingham 35294.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3137658" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Cell Line ; Chondroitin Sulfate Proteoglycans/genetics/physiology ; Chondroitin Sulfates/genetics/physiology ; Cricetinae ; Heparan Sulfate Proteoglycans ; Heparitin Sulfate/genetics/physiology ; Immunologic Deficiency Syndromes/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Mutation ; Neoplasm Transplantation ; Neoplasms, Experimental/*etiology ; Pentosyltransferases/genetics/metabolism ; Proteoglycans/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 86
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    A common PDGF receptor is activated by homodimeric A and B forms of PDGF (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-06-10
    Description: The human platelet-derived growth factor (PDGF) receptor complementary DNA was cloned and expressed by transfection of Chinese hamster ovary (CHO) fibroblasts. The ability of CHO cells expressing the human receptor complementary DNA (CHO-HR5) to interact with different recombinant forms of PDGF (AA and BB homodimers) was tested. Both forms of PDGF bind to the transfected receptor, stimulate the receptor tyrosine kinase activity, and elicit a mitogenic response in a manner that was indistinguishable from the responses of Balb/c 3T3 cells to AA and BB forms of PDGF can be attributed to a single type of receptor and show that the AA form, like the BB form, is a true mitogen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Escobedo, J A -- Navankasatussas, S -- Cousens, L S -- Coughlin, S R -- Bell, G I -- Williams, L T -- HL-32898/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 10;240(4858):1532-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2836953" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division/drug effects ; Cell Line ; Cells, Cultured ; DNA Replication/drug effects ; Enzyme Activation ; Humans ; Kinetics ; Macromolecular Substances ; Mice ; Phosphorylation ; Platelet-Derived Growth Factor/genetics/*metabolism/pharmacology ; Protein-Tyrosine Kinases/*metabolism ; Receptors, Cell Surface/genetics/*metabolism ; Receptors, Platelet-Derived Growth Factor ; Recombinant Proteins/pharmacology ; Transfection
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  • 87
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    Atrial natriuretic factor-SV40 T antigen transgenes produce tumors and cardiac arrhythmias in mice (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-26
    Description: Transgenic mice that carry fusions between the transcriptional regulatory sequences of atrial natriuretic factor (a hormone intimately involved in the regulation of blood pressure) and those encoding SV40 T antigen (an oncoprotein) were generated. Although both atria express the fusion gene, the pathological response to T antigen is asymmetrical. The right atrium undergoes a several hundredfold increase in mass while the left atrium remains relatively normal in size. Hyperplasia is accompanied by a progressive increase in both the frequency and severity of abnormalities in the atrial conduction system, which ultimately result in death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Field, L J -- HL 38605/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 26;239(4843):1029-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, NY 11724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2964082" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Polyomavirus Transforming/*genetics ; Arrhythmias, Cardiac/*genetics/physiopathology ; Atrial Natriuretic Factor/*genetics ; DNA, Recombinant ; Electrocardiography ; Electrophysiology ; Genes, Regulator ; Heart Atria/pathology/physiopathology ; Heart Conduction System/physiopathology ; Heart Neoplasms/*genetics/physiopathology ; Hyperplasia ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Transgenic ; Oncogenes ; Promoter Regions, Genetic
    Print ISSN: 0036-8075
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  • 88
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    The CD14 monocyte differentiation antigen maps to a region encoding growth factors and receptors (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-01-29
    Description: CD14 is a myelomonocytic differentiation antigen expressed by monocytes, macrophages, and activated granulocytes and is detectable with the monoclonal antibodies MO2, MY4, and LeuM3. Analyses of complementary DNA and genomic clones of CD14 show that it has a novel structure and that it maps to chromosome 5 within a region containing other genes encoding growth factors and receptors; it may therefore represent a new receptor important for myeloid differentiation. In addition, the CD14 gene is included in the "critical" region that is frequently deleted in certain myeloid leukemias.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goyert, S M -- Ferrero, E -- Rettig, W J -- Yenamandra, A K -- Obata, F -- Le Beau, M M -- R01-AI23859/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 29;239(4839):497-500.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Rheumatic Diseases, Hospital for Joint Diseases Orthopaedic Institute, New York, NY 10003.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2448876" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigens, CD14 ; Antigens, Differentiation/*genetics/immunology ; Cell Differentiation ; Chromosome Mapping ; Chromosomes, Human, Pair 5 ; DNA/genetics ; Electrophoresis, Polyacrylamide Gel ; Granulocytes/immunology ; Growth Substances/*genetics ; Humans ; Immunosorbent Techniques ; Leukemia/genetics ; Macrophages/immunology ; Mice ; Monocytes/*immunology ; Myelodysplastic Syndromes/genetics ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Receptors, Cell Surface/*genetics
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  • 89
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    Donor-derived cells in the central nervous system of twitcher mice after bone marrow transplantation (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-26
    Description: The twitcher mouse is an animal model of galactosylceramidase deficiency, comparable to Krabbe's disease, a lysosomal storage disease in humans. As in most lysosomal storage diseases, neurological deterioration is a prominent feature of the disease in these mice. Transplantation of enzymatically normal congenic bone marrow was earlier found to result in prolonged survival and increased levels of galactosylceramidase in the visceral organs of twitcher mice. It is now reported that bone marrow transplantation results in increased galactosylceramidase levels in the central nervous system (CNS). Concomitantly, the levels of psychosine, a highly toxic lipid that progressively accumulates in the CNS of untreated twitcher mice, stabilized at much lower levels in the CNS of treated twitcher mice. Histologically, a gradual disappearance of globoid cells, the histological hallmark of Krabbe's disease, and the appearance of foamy macrophages capable of metabolizing the storage product were seen in the CNS. By immunohistochemical labeling it was demonstrated that these foamy macrophages were of donor origin. The infiltration of enzymatically competent, donor-derived macrophages was accompanied by extensive remyelination in the CNS. It is concluded that after bone marrow transplantation, donor-derived macrophages infiltrate the affected brain tissue and are capable of inducing a partial reversal of the enzyme deficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoogerbrugge, P M -- Suzuki, K -- Poorthuis, B J -- Kobayashi, T -- Wagemaker, G -- van Bekkum, D W -- HD 03110/HD/NICHD NIH HHS/ -- NS 24453/NS/NINDS NIH HHS/ -- NS 24928/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 26;239(4843):1035-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University Hospital, Leiden, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3278379" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow/enzymology/immunology ; *Bone Marrow Transplantation ; Brain/*enzymology/pathology ; Cerebellum/pathology ; Galactosidases/*deficiency ; Galactosylceramidase/*deficiency/metabolism ; H-2 Antigens/analysis ; Immunohistochemistry ; Leukodystrophy, Globoid Cell/enzymology/pathology/therapy ; Macrophages/enzymology/*transplantation ; Mice ; Mice, Inbred C57BL ; Mice, Neurologic Mutants ; Microscopy, Electron ; Myelin Sheath/pathology ; Psychosine/metabolism ; Spinal Cord/*enzymology/pathology
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  • 90
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    Engraftment of immune-deficient mice with human hematopoietic stem cells (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-23
    Description: A system in which immune-deficient mice are repopulated with cells from the human myeloid lineage, and that provides an in vivo stem cell assay for human hematopoietic cells is described. Generation of the chimeric human/immune-deficient (HID) mice was dependent on the use of immune-deficient bg/nu/xid mice. Infusion of these mice with human bone marrow gave rise to increases in human macrophage progenitors during more than 5 weeks of in vivo growth, indicating the seeding, proliferation, and differentiation of human stem cells. The human identity of the progenitors was confirmed by sequence analysis and their dependence on human growth factors. The creation of HID mice lays the foundation for establishing animal models for a wide variety of human hemopathies, from leukemia to infectious disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kamel-Reid, S -- Dick, J E -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1706-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Hospital for Sick Children, Toronto, Ontario.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2904703" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Transplantation ; Cell Differentiation ; Cell Division ; Colony-Forming Units Assay ; Colony-Stimulating Factors/pharmacology ; Disease Models, Animal ; Granulocyte-Macrophage Colony-Stimulating Factor ; Growth Substances/pharmacology ; Hematologic Diseases ; *Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/pathology ; Humans ; *Immunologic Deficiency Syndromes/immunology/pathology ; Interleukin-3/pharmacology ; Killer Cells, Natural/immunology ; Macrophages/pathology ; Mice ; Mice, Inbred CBA ; Mice, Mutant Strains ; Mice, Nude ; Transplantation, Heterologous
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  • 91
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    Conversion of normal behavior to shiverer by myelin basic protein antisense cDNA in transgenic mice (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-29
    Description: Myelin basic proteins (MBPs) are coded by the single gene necessary for myelin formation in the central nervous system of the mouse. An antisense MBP mini-gene was constructed and used to determine the function of antisense DNA in transgenic mice. Several transgenic offspring of a founder transgenic mouse, AS100, were converted from the normal to mutant shiverer phenotype. Antisense MBP messenger RNA was expressed in these mice, and the endogenous MBP messenger RNA, the MBP, and the myelination in the central nervous system were reduced.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Katsuki, M -- Sato, M -- Kimura, M -- Yokoyama, M -- Kobayashi, K -- Nomura, T -- New York, N.Y. -- Science. 1988 Jul 29;241(4865):593-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of DNA Biology, School of Medicine, Tokai University, Isehara, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2456614" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Brain/physiology ; DNA/genetics ; Gene Expression Regulation ; Mice ; Mice, Neurologic Mutants/*physiology ; Mice, Transgenic ; Molecular Sequence Data ; Myelin Basic Protein/genetics/*physiology ; Myelin Sheath/physiology ; Phenotype ; RNA/*genetics ; RNA, Antisense
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