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  • 1
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    Propolypeptide of von Willebrand factor circulates in blood and is identical to von Willebrand antigen II (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-23
    Description: The generally mild bleeding disorder of von Willebrand disease is associated with abnormalities of two distinct plasma proteins, the large multimeric von Willebrand factor (vWF), which mediates platelet adhesion, and von Willebrand antigen II (vW AgII), which is of unknown function. The two proteins were found to have a common biosynthetic origin in endothelial cells and megakaryocytes, which explains their simultaneous absence in the severe form of this hereditary disease. Shared amino acid sequences from a 100-kilodalton plasma glycoprotein and from vW AgII are identical to amino acid sequences predicted from a complementary DNA clone encoding the 5' end of vWF. In addition, these proteins have identical molecular weights and immunologic cross reactivities. Monoclonal antibodies prepared against both proteins recognize epitopes on the pro-vWF subunit and on a 100-kilodalton protein that are not present on the mature vWF subunit in endothelial cell lysates. In contrast, polyclonal antibodies against vWF recognize both pro-vWF and vWF subunits. Thus, the 100-kilodalton plasma glycoprotein and vW AgII are identical proteins and represent an extremely large propolypeptide that is first cleaved from pro-vWF during intracellular processing and then released into plasma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fay, P J -- Kawai, Y -- Wagner, D D -- Ginsburg, D -- Bonthron, D -- Ohlsson-Wilhelm, B M -- Chavin, S I -- Abraham, G N -- Handin, R I -- Orkin, S H -- HL-30616/HL/NHLBI NIH HHS/ -- HL-34050/HL/NHLBI NIH HHS/ -- HL-34787/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 May 23;232(4753):995-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3486471" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antigens/immunology/*metabolism ; Blood Proteins/immunology/metabolism ; Endothelium/metabolism ; Humans ; Molecular Weight ; Peptide Fragments/analysis ; Protein Precursors/metabolism ; Protein Processing, Post-Translational ; von Willebrand Factor/*metabolism
    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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    Atrial natriuretic peptide elevation in congestive heart failure in the human (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-03-07
    Description: A sensitive radioimmunoassay for atrial natriuretic peptide was used to examine the relation between circulating atrial natriuretic peptide and cardiac filling pressure in normal human subjects, in patients with cardiovascular disease and normal cardiac filling pressure, and in patients with cardiovascular disease and elevated cardiac filling pressure with and without congestive heart failure. The present studies establish a normal range for atrial natriuretic peptide in normal human subjects. These studies also establish that elevated cardiac filling pressure is associated with increased circulating concentrations of atrial natriuretic peptide and that congestive heart failure is not characterized by a deficiency in atrial natriuretic peptide, but with its elevation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burnett, J C Jr -- Kao, P C -- Hu, D C -- Heser, D W -- Heublein, D -- Granger, J P -- Opgenorth, T J -- Reeder, G S -- New York, N.Y. -- Science. 1986 Mar 7;231(4742):1145-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2935937" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Atrial Natriuretic Factor/*blood ; Cardiovascular Diseases/blood ; Female ; Heart Failure/*blood ; Hemodynamics ; Humans ; Male ; Middle Aged ; Radioimmunoassay
    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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  • 3
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    Hu-ets-1 and Hu-ets-2 genes are transposed in acute leukemias with (4;11) and (8;21) translocations (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-01-24
    Description: Human probes identifying the cellular homologs of the v-ets gene, Hu-ets-1 and Hu-ets-2, and two panels of rodent-human cell hybrids were used to study specific translocations occurring in acute leukemias. The human ets-1 gene was found to translocate from chromosome 11 to 4 in the t(4;11)(q21;23), a translocation characteristic of a subtype of leukemia that represents the expansion of a myeloid/lymphoid precursor cell. Similarly, the human ets-2 gene was found to translocate from chromosome 21 to chromosome 8 in the t(8;21)(q22;q22), a nonrandom translocation commonly found in patients with acute myeloid leukemia with morphology M2 (AML-M2). Both translocations are associated with expression different from the expression in normal lymphoid cells of ets genes, raising the possibility that these genes play a role in the pathogenesis of these leukemias.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sacchi, N -- Watson, D K -- Guerts van Kessel, A H -- Hagemeijer, A -- Kersey, J -- Drabkin, H D -- Patterson, D -- Papas, T S -- AG00029/AG/NIA NIH HHS/ -- HD17449/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1986 Jan 24;231(4736):379-82.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3941901" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chromosomes, Human, 21-22 and Y ; Chromosomes, Human, 6-12 and X ; Cricetinae ; Cricetulus ; Humans ; Hybrid Cells ; Leukemia/*genetics ; Nucleic Acid Hybridization ; *Oncogenes ; *Translocation, 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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  • 4
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    Studies of the human c-myb gene and its product in human acute leukemias (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-07-18
    Description: The myb gene is the transforming oncogene of the avian myeloblastosis virus (AMV); its normal cellular homolog, c-myb, is conserved across a broad span of evolution. In humans, c-myb is expressed in malignant hematopoietic cell lines and in primary hematopoietic tumors. Partial complementary DNA clones were generated from blast cells of patients with acute myelogenous leukemia. The sequences of the clones were compared to the c-myb of other species, as well as the v-myb of AMV. In addition, the carboxyl terminal region of human c-myb was placed in an expression vector to obtain protein for the generation of antiserum, which was used to identify the human c-myb gene product. Like v-myb, this protein was found within the nucleus of leukemic cells where it was associated with the nuclear matrix. These studies provide further evidence that c-myb might be involved in human leukemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slamon, D J -- Boone, T C -- Murdock, D C -- Keith, D E -- Press, M F -- Larson, R A -- Souza, L M -- CA36827/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Jul 18;233(4761):347-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3014652" target="_blank"〉PubMed〈/a〉
    Keywords: *Aspartate Carbamoyltransferase ; Avian Leukosis Virus/*genetics ; Avian Myeloblastosis Virus/*genetics ; Base Sequence ; *Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing) ; Cell Line ; Cloning, Molecular ; DNA/analysis ; DNA Restriction Enzymes/metabolism ; *Dihydroorotase ; Escherichia coli/genetics ; Hematopoietic Stem Cells/microbiology ; Humans ; Leukemia, Myeloid, Acute/*genetics ; Molecular Weight ; *Multienzyme Complexes ; *Oncogenes ; Proteins/analysis
    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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    Genetic selection of a Plasmodium-refractory strain of the malaria vector Anopheles gambiae (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-10-31
    Description: The anopheline mosquito is the target in most malaria control programs, primarily through the use of residual insecticides. A mosquito was studied that is refractory to most species of malaria through a genetically controlled mechanism. A strain of Anopheles gambiae, which was selected for complete refractoriness to the simian malaria parasite Plasmodium cynomolgi, also has varying degrees of refractoriness to most other malaria species examined, including the human parasites P. falciparum, P. ovale, and P. vivax for which this mosquito is the principal African vector. Furthermore, the refractoriness extends to other subhuman primate malarias, to rodent malaria, and to avian malaria. Refractoriness is manifested by encapsulation of the malaria ookinete after it completes its passage through the mosquito midgut, approximately 16 to 24 hours after ingestion of an infective blood meal. Fully encapsulated ookinetes show no abnormalities in parasite organelles, suggesting that refractoriness is due to an enhanced ability of the host to recognize the living parasite rather than to a passive encapsulation of a dead or dying parasite. Production of fully refractory and fully susceptible mosquito strains was achieved through a short series of selective breeding steps. This result indicates a relatively simple genetic basis for refractoriness. In addition to the value these strains may serve in general studies of insect immune mechanisms, this finding encourages consideration of genetic manipulation of natural vector populations as a malaria control strategy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Collins, F H -- Sakai, R K -- Vernick, K D -- Paskewitz, S -- Seeley, D C -- Miller, L H -- Collins, W E -- Campbell, C C -- Gwadz, R W -- New York, N.Y. -- Science. 1986 Oct 31;234(4776):607-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3532325" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anopheles/genetics/*parasitology ; Humans ; Insect Vectors/parasitology ; Malaria/parasitology/prevention & control ; Plasmodium/*physiology ; Plasmodium falciparum/physiology ; Plasmodium vivax/physiology ; *Selection, 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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  • 6
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    Induction of macrophage tumoricidal activity by granulocyte-macrophage colony-stimulating factor (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-04-25
    Description: Monocytes are a subpopulation of peripheral blood leukocytes, which when appropriately activated by the regulatory hormones of the immune system, are capable of becoming macrophages--potent effector cells for immune response to tumors and parasites. A complementary DNA for the T lymphocyte-derived lymphokine, granulocyte-macrophage colony-stimulating factor (GM-CSF), has been cloned, and recombinant GM-CSF protein has been expressed in yeast and purified to homogeneity. This purified human recombinant GM-CSF stimulated peripheral blood monocytes in vitro to become cytotoxic for the malignant melanoma cell line A375. Another T cell-derived lymphokine, gamma-interferon (IFN-gamma), also stimulated peripheral blood monocytes to become tumoricidal against this malignant cell line. When IFN-gamma activates monocytes to become tumoricidal, additional stimulation by exogenously added lipopolysaccharide is required. No such exogenous signals were required for the activation of monocytes by GM-CSF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grabstein, K H -- Urdal, D L -- Tushinski, R J -- Mochizuki, D Y -- Price, V L -- Cantrell, M A -- Gillis, S -- Conlon, P J -- New York, N.Y. -- Science. 1986 Apr 25;232(4749):506-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3083507" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Colony-Stimulating Factors/biosynthesis/*pharmacology ; Cytotoxicity, Immunologic/*drug effects ; Humans ; Interferon-gamma/biosynthesis/pharmacology ; Macrophages/*drug effects ; Melanoma/immunology ; Monocytes/drug effects ; Neoplasms/*immunology ; Recombinant Proteins/biosynthesis/pharmacology
    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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  • 7
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    Antiserum to a synthetic peptide recognizes the HTLV-III envelope glycoprotein (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-03-28
    Description: In a study performed to determine which regions of the human T-cell lymphotrophic virus type III (HTLV-III) may represent vaccine candidates to prevent the acquired immune deficiency syndrome (AIDS), a synthetic peptide corresponding to amino acid sequence 735 to 752 of the precursor envelope glycoprotein of HTLV-III was used to immunize rabbits. The resulting rabbit antiserum to the synthetic peptide specifically recognized the precursor envelope glycoprotein (gp160) of HTLV-III. Human sera positive for antibody to HTLV-III reacted with this peptide. These findings indicate that synthetic peptides can be used to induce an immune response directed against a native envelope glycoprotein epitope of HTLV-III. The data are discussed in terms of using synthetic peptides to identify antigenic determinants involved in the induction of protective immunity and possibly as vaccine candidates against the etiologic agent of AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kennedy, R C -- Henkel, R D -- Pauletti, D -- Allan, J S -- Lee, T H -- Essex, M -- Dreesman, G R -- N0I-HL-23505/HL/NHLBI NIH HHS/ -- R23-AI-22307-01/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1556-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3006246" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/*immunology ; Antibody Specificity ; Antigens, Viral/*immunology ; Deltaretrovirus/*immunology ; Humans ; Molecular Weight ; Peptides/chemical synthesis/*immunology ; Rabbits ; Solubility ; Viral Envelope Proteins/*immunology
    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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  • 8
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    Evidence for the involvement of GM-CSF and FMS in the deletion (5q) in myeloid disorders (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-02-28
    Description: By in situ chromosomal hybridization, the GM-CSF and FMS genes were localized to human chromosome 5 at bands q23 to q31, and at band 5q33, respectively. These genes encode proteins involved in the regulation of hematopoiesis, and are located within a chromosome region frequently deleted in patients with neoplastic myeloid disorders. Both genes were deleted in the 5q-chromosome from bone marrow cells of two patients with refractory anemia and a del(5)(q15q33.3). The GM-CSF gene alone was deleted in a third patient with acute nonlymphocytic leukemia (ANLL) who has a smaller deletion, del(5)(q22q33.1). Leukemia cells from a fourth patient who has ANLL and does not have a del(5q), but who has a rearranged chromosome 5 that is missing bands q31.3 to q33.1 [ins(21;5)(q22;q31.3q33.1)] were used to sublocalize these genes; both genes were present on the rearranged chromosome 5. Thus, the deletion of one or both of these genes may be important in the pathogenesis of myelodysplastic syndromes or of ANLL.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Le Beau, M M -- Westbrook, C A -- Diaz, M O -- Larson, R A -- Rowley, J D -- Gasson, J C -- Golde, D W -- Sherr, C J -- CA 16910/CA/NCI NIH HHS/ -- CA 23954/CA/NCI NIH HHS/ -- CA 30388/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Feb 28;231(4741):984-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3484837" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Refractory/genetics ; Bone Marrow Diseases/*genetics ; *Chromosome Deletion ; Chromosome Mapping ; *Chromosomes, Human, 4-5 ; Colony-Stimulating Factors/*genetics ; Humans ; Leukemia/genetics ; *Proto-Oncogenes
    Print ISSN: 0036-8075
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  • 9
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    HTLV-III/LAV-neutralizing antibodies to an E. coli-produced fragment of the virus envelope (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-12-12
    Description: Immunization with either an Escherichia coli recombinant segment of the human T-cell lymphotropic virus (HTLV-III/LAV) envelope protein (gp 120) or with deglycosylated gp 120 envelope protein produced antibodies that neutralize HTLV-III/LAV infection in vitro. Virus neutralization titers of these antisera were equivalent to those obtained with purified native gp120 as immunogen. This localizes at least one class of neutralizing epitopes to the carboxyl-terminal half of the molecule. In addition, native gp120 prevented HTLV-III/LAV--mediated cell fusion, whereas the recombinant gp120 fragment did not. This shows that although glycosylation is not required for induction of neutralizing antibodies, it may be important for interaction with CD4, the virus receptor. A segment of the HTLV-III/LAV envelope produced in E. coli may be an important ingredient of a vaccine for acquired immune deficiency syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Putney, S D -- Matthews, T J -- Robey, W G -- Lynn, D L -- Robert-Guroff, M -- Mueller, W T -- Langlois, A J -- Ghrayeb, J -- Petteway, S R Jr -- Weinhold, K J -- 1PO1-CA43447-01/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Dec 12;234(4782):1392-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2431482" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Viral/*immunology ; Electrophoresis, Polyacrylamide Gel ; Enzyme-Linked Immunosorbent Assay ; Epitopes/analysis ; Escherichia coli/*genetics ; HIV Antibodies ; Humans ; Immunization ; Molecular Weight ; Receptors, Virus/metabolism ; Recombinant Proteins/immunology ; Viral Envelope Proteins/genetics/*immunology
    Print ISSN: 0036-8075
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  • 10
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    Molecular genetics of human color vision: the genes encoding blue, green, and red pigments (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-04-11
    Description: Human color vision is based on three light-sensitive pigments. The isolation and sequencing of genomic and complementary DNA clones that encode the apoproteins of these three pigments are described. The deduced amino acid sequences show 41 +/- 1 percent identity with rhodopsin. The red and green pigments show 96 percent mutual identity but only 43 percent identity with the blue pigment. Green pigment genes vary in number among color-normal individuals and, together with a single red pigment gene, are proposed to reside in a head-to-tail tandem array within the X chromosome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nathans, J -- Thomas, D -- Hogness, D S -- New York, N.Y. -- Science. 1986 Apr 11;232(4747):193-202.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2937147" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Biological Evolution ; Cattle ; Cebidae ; Cercopithecidae ; Color ; Color Perception/*physiology ; DNA/metabolism ; Drosophila melanogaster ; Eye Proteins/genetics/physiology ; *Genes ; Humans ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Photoreceptor Cells/physiology ; RNA, Messenger/genetics ; Retinal Pigments/*genetics ; Retinaldehyde/physiology ; Rhodopsin/genetics ; Rod Opsins ; X Chromosome
    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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