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  • Cloning, Molecular  (26)
  • American Association for the Advancement of Science (AAAS)  (26)
  • Annual Reviews
  • 1985-1989  (26)
  • 1975-1979
  • 1940-1944
  • 1986  (26)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (26)
  • Annual Reviews
Years
  • 1985-1989  (26)
  • 1975-1979
  • 1940-1944
Year
  • 1
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    Deletion in cysteine-rich region of LDL receptor impedes transport to cell surface in WHHL rabbit (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-06-06
    Description: The Watanabe heritable hyperlipidemic (WHHL) rabbit, an animal with familial hypercholesterolemia, produces a mutant receptor for plasma low-density lipoprotein (LDL) that is not transported to the cell surface at a normal rate. Cloning and sequencing of complementary DNA's from normal and WHHL rabbits, shows that this defect arises from an in-frame deletion of 12 nucleotides that eliminates four amino acids from the cysteine-rich ligand binding domain of the LDL receptor. A similar mutation, detected by S1 nuclease mapping of LDL receptor messenger RNA, occurred in a patient with familial hypercholesterolemia whose receptor also fails to be transported to the cell surface. These findings suggest that animal cells may have fail-safe mechanisms that prevent the surface expression of improperly folded proteins with unpaired or improperly bonded cysteine residues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4451858/" 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/PMC4451858/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamamoto, T -- Bishop, R W -- Brown, M S -- Goldstein, J L -- Russell, D W -- HL 01287/HL/NHLBI NIH HHS/ -- HL 20948/HL/NHLBI NIH HHS/ -- HL 31346/HL/NHLBI NIH HHS/ -- P01 HL020948/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Jun 6;232(4755):1230-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3010466" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Biological Transport ; *Chromosome Deletion ; Cloning, Molecular ; Cysteine/genetics ; Dna ; DNA Restriction Enzymes ; Genes ; Humans ; Hyperlipoproteinemia Type II/*genetics ; Mutation ; RNA, Messenger ; Rabbits ; Receptors, LDL/*genetics
    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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    Activation of mouse T-helper cells induces abundant preproenkephalin mRNA synthesis (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-09
    Description: Antigenic or mitogenic stimulation of T cells induces the secretion of an array of protein hormones that regulate immune responses. Molecular cloning has contributed strongly to our present understanding of the nature of this regulation. A complementary DNA (cDNA) library prepared from a cloned concanavalin A-activated mouse T-helper cell line was screened for abundant and induction-specific cDNA's. One such randomly chosen cDNA was found to encode mouse preproenkephalin messenger RNA (mRNA). Preproenkephalin mRNA represented about 0.4 percent of the mRNA in the activated cell line but was absent in resting cells of this line. Other induced T-helper cell lines have 0.1 to 0.5 percent of their mRNA as preproenkephalin mRNA. Induced T-helper cell culture supernatants have [Met]enkephalin-immunoreactive material. The production by activated T cells of a peptide neurotransmitter identifies a signal that can potentially permit T cells to modulate the nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zurawski, G -- Benedik, M -- Kamb, B J -- Abrams, J S -- Zurawski, S M -- Lee, F D -- New York, N.Y. -- Science. 1986 May 9;232(4751):772-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2938259" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cattle ; Cell Line ; Cloning, Molecular ; DNA/genetics ; Enkephalins/*biosynthesis/genetics ; Humans ; *Lymphocyte Activation ; Mice ; Protein Precursors/*biosynthesis/genetics ; RNA, Messenger/*biosynthesis ; Rats ; T-Lymphocytes, Helper-Inducer/drug effects/metabolism/*physiology
    Print ISSN: 0036-8075
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  • 3
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    T-cell recognition of Ia molecules selectively altered by a single amino acid substitution (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-01-17
    Description: T lymphocytes recognize foreign antigen together with allele-specific determinants on membrane-bound class I and class II (Ia) gene products of the major histocompatibility complex. To identify amino acids of class II molecules critical to this recognition process, the genes encoding the beta chains of the I-Ak molecule were cloned from a wild-type B-cell hybridoma and from an immunoselected variant subline showing distinct serological and T-cell stimulatory properties. Nucleotide sequencing and DNA-mediated gene transfer established that a single base transition (G----A) encoding a change from glutamic acid to lysine at position 67 in the I-Ak beta molecule accounted for all the observed phenotypic changes of the variant cells. These results confirm the importance of residues 62 to 78 in the amino terminal domain of I-A beta for class II-restricted T-cell recognition of antigen and demonstrate the ability of a single substitution in this region to alter this recognition event.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, M A -- Glimcher, L A -- Nielsen, E A -- Paul, W E -- Germain, R N -- New York, N.Y. -- Science. 1986 Jan 17;231(4735):255-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3484558" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/genetics/immunology ; Base Sequence ; Cloning, Molecular ; Histocompatibility Antigens Class II/*immunology ; Humans ; Hybridomas/immunology ; Major Histocompatibility Complex ; Mice ; Mice, Inbred BALB C ; T-Lymphocytes/*immunology
    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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    Cloned fragment of the hepatitis delta virus RNA genome: sequence and diagnostic application (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-16
    Description: Hepatitis delta virus (HDV) is a replication-defective etiological agent of hepatitis that requires hepatitis B virus (HBV) as a helper. A complementary DNA (cDNA) fragment of the RNA genome of HDV was cloned into the plasmid vector pBR322, and the primary nucleotide sequence and predicted protein products of the cDNA fragment were determined. This cloned cDNA fragment has been used as a sensitive radioactive probe for the detection of HDV RNA in the serum of patients with either acute or chronic HDV infections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Denniston, K J -- Hoyer, B H -- Smedile, A -- Wells, F V -- Nelson, J -- Gerin, J L -- N01-AI-22665/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1986 May 16;232(4752):873-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3704630" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cloning, Molecular ; Hepatitis D/*diagnosis/microbiology ; Hepatitis Delta Virus/*genetics ; Humans ; Nucleic Acid Hybridization ; Pan troglodytes ; RNA, Viral/*genetics
    Print ISSN: 0036-8075
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  • 5
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    Cloning of a cDNA for a T cell-specific serine protease from a cytotoxic T lymphocyte (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-16
    Description: A new serine protease was encoded by a clone isolated from a murine cytotoxic T-lymphocyte complementary DNA library by an RNA-hybridization competition protocol. Complementary transcripts were detected in cytotoxic T lymphocytes, spleen cells from nude mice, a rat natural killer cell leukemia, and in two of eight T-helper clones (both cytotoxic), but not in normal mouse kidney, liver, spleen, or thymus, nor in several tested T- and B-cell tumors. T-cell activation with concanavalin A plus interleukin-2 induced spleen cells to express this gene with kinetics correlating with the acquisition of cytolytic capacity. The nucleotide sequence of this gene encoded an amino acid sequence of approximately 25,700 daltons, with 25 to 35 percent identity to members of the serine protease family. The active site "charge-relay" residues (His57, Asp102, and Ser195 of the chymotrypsin numbering system) are conserved, as well as the trypsin-specific Asp (position 189 in trypsin). A Southern blot analysis indicated that this gene is conserved in humans, mouse, and chicken. This serine protease may have a role in lymphocyte lysis and a "lytic cascade."〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gershenfeld, H K -- Weissman, I L -- AI 19512/AI/NIAID NIH HHS/ -- CA09032/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 May 16;232(4752):854-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2422755" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cloning, Molecular ; Concanavalin A/pharmacology ; DNA/genetics ; Endopeptidases/*genetics ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Nude ; Nucleic Acid Hybridization ; RNA/genetics ; Serine Endopeptidases ; T-Lymphocytes, Cytotoxic/drug effects/*metabolism
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  • 6
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    Brain glutamate decarboxylase cloned in lambda gt-11: fusion protein produces gamma-aminobutyric acid (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-30
    Description: Glutamate decarboxylase (GAD; E.C. 4.1.1.15) converts glutamate to gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the vertebrate central nervous system. This report describes the isolation of a GAD complementary DNA clone by immunological screening of a lambda gt-11 brain complementary DNA expression library. The fusion protein produced by this clone catalyzes the conversion of glutamate to GABA and carbon dioxide, confirming its identity as GAD. Antibodies to beta-galactosidase remove GAD enzymatic activity from solution, showing that this activity is associated with the fusion protein. In immunoblotting experiments all three available antisera to GAD reacted with the fusion polypeptide and with two major polypeptides (molecular size, 60,000 and 66,000 daltons) in brain extracts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaufman, D L -- McGinnis, J F -- Krieger, N R -- Tobin, A J -- HD05615/HD/NICHD NIH HHS/ -- NS20356/NS/NINDS NIH HHS/ -- NS22256/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 May 30;232(4754):1138-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3518061" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*enzymology ; Cloning, Molecular ; DNA/genetics ; Escherichia coli/metabolism ; Glutamate Decarboxylase/biosynthesis/genetics/*metabolism ; Humans ; Mice ; Rats ; Recombinant Proteins/biosynthesis/metabolism ; gamma-Aminobutyric Acid/*biosynthesis
    Print ISSN: 0036-8075
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  • 7
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    Nucleotide sequence of SRV-1, a type D simian acquired immune deficiency syndrome retrovirus (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-03-28
    Description: Simian acquired immune deficiency syndrome (SAIDS) in the macaque genus of monkeys at the California Primate Research Center is apparently caused by infection by a type D retrovirus. The complete nucleotide sequence (8173 base pairs) of a molecular clone of the prototype SAIDS virus isolate, SRV-1, reveals a typical retrovirus structure with long terminal repeats (346 base pairs) and open reading frames for the gag (663 codons), pol (867 codons), and env (605 codons) genes. SRV-1 also has a separate open reading frame of 314 codons between the gag and pol genes that defines the viral protease gene (prt) and a short open reading frame of unknown significance downstream from the env gene. The SRV-1 protease region shows a high degree of homology to its counterpart in the hamster intracisternal A-type particle genome; both these protease genes are about twice as long as the analogous region of other retroviruses. SRV-1 has no notable similarity in either genetic organization or sequence to the human AIDS retroviruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Power, M D -- Marx, P A -- Bryant, M L -- Gardner, M B -- Barr, P J -- Luciw, P A -- AI20573/AI/NIAID NIH HHS/ -- CA37467/CA/NCI NIH HHS/ -- RR00169/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1567-72.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3006247" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/microbiology/*veterinary ; Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; DNA Restriction Enzymes/metabolism ; Genes, Viral ; Macaca/*microbiology ; Peptide Hydrolases/genetics ; Retroviridae/*genetics ; Retroviridae Proteins/genetics ; Sequence Homology, Nucleic Acid
    Print ISSN: 0036-8075
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  • 8
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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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  • 9
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    Isolation and sequence of L3T4 complementary DNA clones: expression in T cells and brain (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-10-31
    Description: T lymphocytes express on their surface not only a specific receptor for antigen and major histocompatibility complex proteins, but also a number of additional glycoproteins that are thought to play accessory roles in the processes of recognition and signal transduction. L3T4 is one such T-cell surface protein that is expressed on most mouse thymocytes and on mature mouse T cells that recognize class II (Ia) major histocompatibility complex proteins. Such cells are predominantly of the helper/inducer phenotype. In this study, complementary DNA clones encoding L3T4 were isolated and sequenced. The predicted protein sequence shows that L3T4 is a member of the immunoglobulin gene superfamily. It is encoded by a single gene that does not require rearrangement prior to expression. Although the protein has not previously been demonstrated on nonhematopoietic cells, two messenger RNA species specific for L3T4 are found in brain. The minor species comigrates with the L3T4 transcript in T cells, whereas the major species is 1 kilobase smaller.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tourvieille, B -- Gorman, S D -- Field, E H -- Hunkapiller, T -- Parnes, J R -- 1 F32 CA07877-01/CA/NCI NIH HHS/ -- AI11313/AI/NIAID NIH HHS/ -- GM34991/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Oct 31;234(4776):610-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3094146" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, Differentiation, T-Lymphocyte ; Antigens, Surface/genetics/*isolation & purification ; Base Sequence ; Brain/*metabolism ; Cloning, Molecular ; DNA/genetics/isolation & purification ; Humans ; Mice ; Mice, Inbred C57BL ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Sequence Homology, Nucleic Acid ; T-Lymphocytes/*immunology/metabolism
    Print ISSN: 0036-8075
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  • 10
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    Novel serine proteases encoded by two cytotoxic T lymphocyte-specific genes (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-16
    Description: Genes that are expressed exclusively in cytotoxic T cells should encode proteins that are essential for target cell lysis in cell-mediated immune responses. The sequences of two cytotoxic T lymphocyte-specific complementary DNA's (cDNA's) suggest that the two genes encode serine proteases. A full-length cDNA corresponding to one of the genes was isolated and sequenced. The predicted protein resembles serine proteases in that it includes all the residues that form the catalytic triad of the active site of serine proteases. Moreover, it has sequence characteristics thought to occur only in rat mast cell protease type II. These results are in accord with the view that a protease cascade plays a key role in cytotoxic T-cell activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lobe, C G -- Finlay, B B -- Paranchych, W -- Paetkau, V H -- Bleackley, R C -- New York, N.Y. -- Science. 1986 May 16;232(4752):858-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3518058" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cloning, Molecular ; DNA/genetics ; Endopeptidases/*genetics ; Genes ; Mice ; Serine Endopeptidases ; T-Lymphocytes, Cytotoxic/*metabolism
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  • 11
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    Fine structure genetic analysis of a beta-globin promoter (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-02
    Description: A novel procedure for saturation mutagenesis of cloned DNA was used to obtain more than 100 single base substitutions within the promoter of the mouse beta-major globin gene. The effects of these promoter substitutions on transcription were determined by transfecting the cloned mutant genes into HeLa cells on plasmids containing an SV40 transcription enhancer, and measuring the levels of correctly initiated beta-globin transcripts after 2 days. Mutations in three regions of the promoter resulted in a significant decrease in the level of transcription: (i) the CACCC box, located between -87 and -95, (ii) the CCAAT box, located between -72 and -77, and (iii) the TATA box, located between -26 and -30 relative to the start site of transcription. In contrast, two different mutations in nucleotides immediately upstream from the CCAAT box resulted in a 3- to 3.5-fold increase in transcription. With two minor exceptions, single base substitutions in all other regions of the promoter had no effect on transcription. These results precisely delineate the cis-acting sequences required for accurate and efficient initiation of beta-globin transcription, and they establish a general approach for the fine structure genetic analysis of eukaryotic regulatory sequences.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myers, R M -- Tilly, K -- Maniatis, T -- New York, N.Y. -- Science. 1986 May 2;232(4750):613-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3457470" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cloning, Molecular ; DNA/genetics ; Genes ; Genetic Engineering ; Globins/biosynthesis/*genetics ; HeLa Cells ; Humans ; Mice ; Mutation ; *Promoter Regions, Genetic ; Transcription, Genetic
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  • 12
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    Expression cloning of a lymphocyte homing receptor cDNA: ubiquitin is the reactive species (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-02-21
    Description: The lymphocyte cell surface receptor for the high endothelial venules (HEV's) of peripheral lymph nodes is specifically recognized by the monoclonal antibody MEL-14. Three independent complementary DNA (cDNA) clones, each of which encodes the protein ubiquitin, were detected by virtue of the expression of the MEL-14 antigenic determinant on cDNA-beta-galactosidase bacterial fusion proteins. The antigenic determinant defined by MEL-14 resides in the carboxyl terminal 13-amino-acid proteolytic peptide of ubiquitin, but is undetected in intact undenatured ubiquitin and other cellular ubiquitinated proteins. Antisera and monoclonal antibodies to ubiquitin determinants bind to the surface of both HEV-receptor positive and negative cell lines. The MEL-14-identified cDNA clones hydridize to RNA transcripts that encode tandemly repeated ubiquitins. Sequence analysis of these polyubiquitin cDNA's does not identify a leader sequence for export to the cell surface. The expression of the MEL-14 epitope of ubiquitin depends upon its local environment. The steady-state levels of expression of the ubiquitin messenger RNA's do not correlate with either the tissue derivation of the RNA or the expression of the lymphocyte HEV receptor. Regulation of the expression of the HEV receptor is not likely to reflect the transcriptional control of ubiquitin genes, but rather to reflect control of the expression of the HEV core polypeptide or its level or form of ubiquitination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉St John, T -- Gallatin, W M -- Siegelman, M -- Smith, H T -- Fried, V A -- Weissman, I L -- AI19512/AI/NIAID NIH HHS/ -- CA 09151/CA/NCI NIH HHS/ -- GM 31461/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Feb 21;231(4740):845-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3003914" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/*immunology ; Antibody Specificity ; Base Sequence ; Cloning, Molecular ; Endothelium/metabolism ; Gene Expression Regulation ; High Mobility Group Proteins/*genetics ; Lymphatic System/metabolism ; Lymphocytes/*physiology ; Mice ; Receptors, Cell Surface/*genetics/immunology/metabolism ; Ubiquitins/*genetics/immunology/metabolism
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  • 13
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    The structure, function, and expression of interleukin-2 receptors on normal and malignant lymphocytes (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-09
    Description: Antigen or mitogen-induced activation of resting T cells induces the synthesis of interleukin-2 (IL-2) as well as the expression of specific cell surface receptors for this lymphokine. Failure of the production of either IL-2 or its receptor results in a failure of the T-cell immune response. The receptor is composed of a 33,000-dalton (251-amino acid) peptide precursor that is post-translationally glycosylated into the mature 55,000-dalton form. In contrast to resting T cells, human T-cell lymphotrophic virus I (HTLV-I)-associated adult T-cell leukemia cells constitutively express large numbers of IL-2 receptors. Because IL-2 receptors are present on the malignant T cells but not on normal resting cells, clinical trials have been initiated in which patients with adult T-cell leukemia are treated with a monoclonal antibody that binds to the IL-2 receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waldmann, T A -- New York, N.Y. -- Science. 1986 May 9;232(4751):727-32.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3008337" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology ; Animals ; Antibodies, Monoclonal/therapeutic use ; B-Lymphocytes/physiology ; Clinical Trials as Topic ; Cloning, Molecular ; DNA/genetics ; Deltaretrovirus/physiology ; Gene Expression Regulation ; Humans ; Interleukin-2/physiology ; Leukemia/*immunology/therapy ; Lymphocytes/microbiology/*physiology ; Mice/immunology ; Receptors, Immunologic/genetics/isolation & purification/*physiology ; Receptors, Interleukin-2 ; T-Lymphocytes/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    Amplification and expression of genes associated with multidrug resistance in mammalian cells (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-09
    Description: In multidrug resistance, which is observed clinically and in tissue culture, cells that are challenged with certain cytotoxic drugs develop resistance not only to the selective agent but also to other, seemingly unrelated, agents. The multidrug-resistant phenotype is associated with DNA sequence amplification and with the overproduction of a number of cytosolic and membrane glycoproteins. The differential amplification and altered expression of at least two related genes, termed multidrug-resistant associated genes has been shown in multidrug-resistant Chinese hamster cells. In multidrug-resistant mouse and human cells, genes homologous to those in Chinese hamster cells are also amplified. The level of expression of these genes varied and did not correlate with their copy number. Furthermore, in Chinese hamster cells, the development of resistance to a single drug and multidrug resistance were closely related, but uncoupled, events. The overexpression of the multidrug-resistant genes was better correlated with the degree of resistance to the selective agent than it was with the extent of multidrug resistance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scotto, K W -- Biedler, J L -- Melera, P W -- CA-08748/CA/NCI NIH HHS/ -- CA-09207/CA/NCI NIH HHS/ -- CA-28595/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 May 9;232(4751):751-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2421411" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cloning, Molecular ; Colchicine/pharmacology ; Cricetinae ; Cricetulus ; DNA/genetics ; Dactinomycin/pharmacology ; Daunorubicin/pharmacology ; *Drug Resistance ; Gene Amplification/*drug effects ; Gene Expression Regulation/*drug effects ; Humans ; Lung/cytology/drug effects ; Mice ; Nucleic Acid Hybridization ; RNA/genetics ; Vincristine/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Specific DNA probe for the diagnosis of Plasmodium falciparum malaria (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-03-21
    Description: Malaria can be diagnosed either by direct microscopic examination of blood smears, which is time consuming and requires expertise, or by immunological techniques, which are effective but do not distinguish between past and present infections. In this study, a simple procedure was developed for spotting lysed blood from infected patients directly onto nitrocellulose paper and identifying the malaria species on the basis of hybridization of parasite DNA with a species-specific probe. A genomic DNA library of Plasmodium falciparum was screened to detect clones containing DNA sequences that are highly repeated within the parasite genome. Several such clones were further analyzed to identify those that hybridize specifically with P. falciparum DNA but not with DNA from humans, P. vivax, or P. cynomolgi. This technique appears to be sensitive enough to detect 10 picograms of purified P. falciparum DNA (equivalent to 100 parasites) and in field studies is able to detect approximately 40 parasites per microliter of blood.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barker, R H Jr -- Suebsaeng, L -- Rooney, W -- Alecrim, G C -- Dourado, H V -- Wirth, D F -- 2 PO1 AI 16305-06/AI/NIAID NIH HHS/ -- T32 AI 07167/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1986 Mar 21;231(4744):1434-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3513309" target="_blank"〉PubMed〈/a〉
    Keywords: Cloning, Molecular ; Collodion ; DNA/genetics/*isolation & purification ; Humans ; Malaria/*diagnosis/genetics ; Nucleic Acid Hybridization ; Plasmodium/genetics ; Plasmodium falciparum/*genetics ; Plasmodium vivax/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    Human DNA repository (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-01-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Felix, J S -- Badman, W S -- New York, N.Y. -- Science. 1986 Jan 17;231(4735):203.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3941895" target="_blank"〉PubMed〈/a〉
    Keywords: Cloning, Molecular ; *Dna ; Humans ; National Institutes of Health (U.S.) ; United States
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  • 17
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    Infectious mutants of HTLV-III with changes in the 3' region and markedly reduced cytopathic effects (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-08-08
    Description: A variant of human T-lymphotropic virus type III (HTLV-III) is described that replicates but does not kill normal human T cells in vitro. This variant, designated X10-1, was derived from the genome of a cytopathic HTLV-III clone (pHXB2D) by excision of a 200-base pair segment in the 3' region of the virus, spanning the env and 3'-orf genes. Comparable variants with 55 to 109 base pairs deleted exclusively in 3'-orf produced, in contrast, virus that was extremely cytopathic. On the basis of these findings it is concluded that the 3'-orf gene is not required for cytopathogenicity or replication of HTLV-III. In addition, the results suggest that virus replication and cytotoxicity are not intrinsically coupled. Furthermore, since clone X10-1 retains the ability to trans-activate genes linked to the viral long terminal repeats, trans-activation per se is not responsible for T-cell killing by HTLV-III. These results also raise the possibility that the carboxyl terminus of the envelope gene of HTLV-III has a direct role in T-cell killing by this virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fisher, A G -- Ratner, L -- Mitsuya, H -- Marselle, L M -- Harper, M E -- Broder, S -- Gallo, R C -- Wong-Staal, F -- New York, N.Y. -- Science. 1986 Aug 8;233(4764):655-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3014663" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Cloning, Molecular ; Deltaretrovirus/*genetics/pathogenicity ; Humans ; Mutation ; Nucleic Acid Hybridization ; RNA, Viral/genetics ; T-Lymphocytes/microbiology
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  • 18
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    Nucleotide sequence of a bovine clone encoding the angiogenic protein, basic fibroblast growth factor (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-08-01
    Description: Basic and acidic fibroblast growth factors (FGF's) are potent mitogens for capillary endothelial cells in vitro, stimulate angiogenesis in vivo, and may participate in tissue repair. An oligonucleotide probe for bovine basic FGF was designed from the nucleotide sequence of the amino-terminal exon of bovine acidic FGF, taking into account the 55 percent amino acid sequence homology between the two factors. With this oligonucleotide probe, a full length complementary DNA for basic FGF was isolated from bovine pituitary. Basic FGF in bovine hypothalamus was shown to be encoded by a single 5.0-kilobase messenger RNA; in a human hepatoma cell line, both 4.6- and 2.2-kilobase basic FGF messenger RNA's were present. Both growth factors seem to be synthesized with short amino-terminal extensions that are not found on the isolated forms for which the amino acid sequences have been determined. Neither basic nor acidic FGF has a classic signal peptide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abraham, J A -- Mergia, A -- Whang, J L -- Tumolo, A -- Friedman, J -- Hjerrild, K A -- Gospodarowicz, D -- Fiddes, J C -- New York, N.Y. -- Science. 1986 Aug 1;233(4763):545-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2425435" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inducing Agents/*genetics ; Animals ; Base Sequence ; Cattle ; Cloning, Molecular ; Fibroblast Growth Factors/*genetics/pharmacology ; Growth Substances/*genetics ; Neovascularization, Pathologic
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  • 19
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    Uroporphyrinogen decarboxylase structural mutant (Gly281----Glu) in a case of porphyria (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-11-07
    Description: Uroporphyrinogen decarboxylase deficiency in man is responsible for familial porphyria cutanea tarda and hepatoerythropoietic porphyria. A recent study of a family with hepatoerythropoietic porphyria showed that the enzyme defect resulted from rapid degradation of the protein in vivo. Cloning and sequencing of a complementary DNA for the mutated gene revealed that the mutation was due to the replacement of a glycine residue by a glutamic acid residue at position 281. This base change leads to a protein that is very rapidly degraded in the presence of cell lysate. Characterization of the mutation will allow comparison of this defect in a homozygous patient with defects in other patients with familial porphyria cutanea tarda.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Verneuil, H -- Grandchamp, B -- Beaumont, C -- Picat, C -- Nordmann, Y -- New York, N.Y. -- Science. 1986 Nov 7;234(4777):732-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3775362" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Carboxy-Lyases/*genetics ; Cloning, Molecular ; DNA/genetics ; Humans ; Liver Diseases/genetics ; Mutation ; Porphyrias/*genetics ; Skin Diseases/genetics ; Structure-Activity Relationship ; Uroporphyrinogen Decarboxylase/deficiency/*genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
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    Sequence and expression of human estrogen receptor complementary DNA (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-03-07
    Description: The mechanism by which the estrogen receptor and other steroid hormone receptors regulate gene expression in eukaryotic cells is not well understood. In this study, a complementary DNA clone containing the entire translated portion of the messenger RNA for the estrogen receptor from MCF-7 human breast cancer cells was sequenced and then expressed in Chinese hamster ovary (CHO-K1) cells to give a functional protein. An open reading frame of 1785 nucleotides in the complementary DNA corresponded to a polypeptide of 595 amino acids and a molecular weight of 66,200, which is in good agreement with published molecular weight values of 65,000 to 70,000 for the estrogen receptor. Homogenates of transformed Chinese hamster ovary cells containing a protein that bound [3H]estradiol and sedimented as a 4S complex in salt-containing sucrose gradients and as an 8 to 9S complex in the absence of salt. Interaction of this receptor-[3H]estradiol complex with a monoclonal antibody that is specific for primate ER confirms the identity of the expressed complementary DNA as human estrogen receptor. Amino acid sequence comparisons revealed significant regional homology among the human estrogen receptor, the human glucocorticoid receptor, and the putative v-erbA oncogene product. This suggests that steroid receptor genes and the avian erythroblastosis viral oncogene are derived from a common primordial gene. The homologous region, which is rich in cysteine, lysine, and arginine, may represent the DNA-binding domain of these proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greene, G L -- Gilna, P -- Waterfield, M -- Baker, A -- Hort, Y -- Shine, J -- CA-02897/CA/NCI NIH HHS/ -- HD17103/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1986 Mar 7;231(4742):1150-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3753802" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acids/analysis ; Antibodies, Monoclonal ; Base Sequence ; Cells, Cultured ; Cloning, Molecular ; DNA/*metabolism ; Female ; Humans ; Molecular Weight ; Receptors, Estrogen/*genetics ; Transformation, Genetic
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  • 21
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    Molecular cloning and expression of neuroleukin, a neurotrophic factor for spinal and sensory neurons (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-10-31
    Description: A novel 56,000-dalton growth factor found in mouse salivary gland was purified, molecularly cloned, and expressed in monkey COS cells. The protein is a neurotrophic factor and also, surprisingly, a lymphokine product of lectin-stimulated T cells. The factor was therefore named neuroleukin. Neuroleukin promotes the survival in culture of a subpopulation of embryonic spinal neurons that probably includes skeletal motor neurons. Neuroleukin also supports the survival of cultured sensory neurons that are insensitive to nerve growth factor, but has no effect on sympathetic or parasympathetic neurons. The amino acid sequence of neuroleukin is partly homologous to a highly conserved region of the external envelope protein of HTLV-III/LAV, the retrovirus that causes acquired immune deficiency syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gurney, M E -- Heinrich, S P -- Lee, M R -- Yin, H S -- 5PO1 NS-21442/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Oct 31;234(4776):566-74.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3764429" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Chick Embryo ; Cloning, Molecular ; DNA/genetics ; Glucose-6-Phosphate Isomerase ; Growth Substances/genetics/*physiology ; Lymphokines/genetics/*physiology ; Male ; Mice ; Mice, Inbred BALB C ; Motor Neurons/drug effects ; Muscles/innervation ; Nerve Growth Factors/genetics/isolation & purification/*physiology ; Neurons/drug effects ; Neurons, Afferent/drug effects ; Salivary Glands/metabolism ; Spinal Cord/cytology
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  • 22
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    A novel human gene closely related to the abl proto-oncogene (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-12-19
    Description: A DNA sequence related to the abl proto-oncogene was identified in human placenta. Molecular cloning and nucleotide sequence analysis revealed two putative exons whose predicted amino acid sequence was most homologous to the corresponding sequences of c-abl and v-abl but was related to other tyrosine kinase genes as well. The new sequence was localized by in situ hybridization and somatic cell genetic analysis to human chromosome 1q24-25, which differs from the location of any previously identified tyrosine kinase gene. The detection of a novel 12-kb transcript by this gene in human normal and tumor cells establishes it as a new member of the tyrosine kinase family that is closely related to but distinct from c-abl.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kruh, G D -- King, C R -- Kraus, M H -- Popescu, N C -- Amsbaugh, S C -- McBride, W O -- Aaronson, S A -- New York, N.Y. -- Science. 1986 Dec 19;234(4783):1545-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3787260" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Chromosome Mapping ; Chromosomes, Human, Pair 1 ; Cloning, Molecular ; DNA/*genetics ; Exons ; Humans ; Nucleic Acid Hybridization ; *Oncogenes ; Placenta/analysis ; Protein-Tyrosine Kinases/*genetics
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  • 23
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    Human endothelial cell growth factor: cloning, nucleotide sequence, and chromosome localization (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-08-01
    Description: Several of the endothelial cell polypeptide mitogens that have been described probably play a role in blood vessel homeostasis. Two overlapping complementary DNA clones encoding human endothelial cell growth factor (ECGF) were isolated from a human brain stem complementary DNA library. Southern blot analysis suggested that there is a single copy of the ECGF gene and that it maps to human chromosome 5 at bands 5q31.3 to 33.2 A 4.8-kilobase messenger RNA was present in human brain stem messenger RNA. The complete amino acid sequence of human ECGF was deduced from the nucleic acid sequence of these clones; it encompasses all the well-characterized acidic endothelial cell polypeptide mitogens described by several laboratories. The ECGF-encoding open reading frame is flanked by translation stop codons and provides no signal peptide or internal hydrophobic domain for the secretion of ECGF. This property is shared by human interleukin-1, which is approximately 30 percent homologous to ECGF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jaye, M -- Howk, R -- Burgess, W -- Ricca, G A -- Chiu, I M -- Ravera, M W -- O'Brien, S J -- Modi, W S -- Maciag, T -- Drohan, W N -- AG04807/AG/NIA NIH HHS/ -- HL23348/HL/NHLBI NIH HHS/ -- HL35627/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 1;233(4763):541-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3523756" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Brain Stem/metabolism ; *Chromosome Mapping ; Cloning, Molecular ; DNA/genetics ; Endothelial Growth Factors ; Growth Substances/*genetics ; Humans ; Interleukin-1/genetics ; Liver/metabolism ; Nucleic Acid Hybridization ; RNA, Messenger/genetics
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  • 24
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    Synchronized rearrangement of T-cell gamma and beta chain genes in fetal thymocyte development (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-10-24
    Description: Kinetics of mouse T-cell gamma gene rearrangements in ontogeny were determined as an approach to understanding the possible role of these genes in the development of fetal thymocytes. Two of these genes (C gamma 1 and C gamma 2) rearranged rapidly during days 14 to 17 of the gestational period in BALB/c mice. Moreover, these rearrangements seemed to be tightly synchronized with rearrangements of T-cell receptor beta chain genes in the same cells. It is suggested that the early transcriptional activity of gamma genes, which precedes that of beta chain genes, may not reflect the functional activation of these genes. Nevertheless, productive and therefore potentially functional gamma gene rearrangements precede surface expression of T-cell receptors in the thymus by 2 to 3 days, which is compatible with a role for gamma gene products in thymocyte development prior to antigen-specific stages.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Born, W -- Rathbun, G -- Tucker, P -- Marrack, P -- Kappler, J -- AI 18016/AI/NIAID NIH HHS/ -- AI 18785/AI/NIAID NIH HHS/ -- AI17134/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1986 Oct 24;234(4775):479-82.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3020688" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Animals ; Cell Differentiation ; Cloning, Molecular ; DNA Restriction Enzymes ; Hybridomas/physiology ; Mice ; Receptors, Antigen, T-Cell/*genetics ; Recombination, Genetic ; T-Lymphocytes/cytology/*physiology ; Thymus Gland/*embryology/physiology
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  • 25
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    Identification of HTLV-III/LAV sor gene product and detection of antibodies in human sera (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-03-28
    Description: The nucleotide sequence of the genome of HTLV-III, the infectious agent etiologically associated with the acquired immune deficiency syndrome, predicts a small open reading frame, termed sor, located between the pol and env genes. A DNA segment containing 82 percent of the sor region was inserted into a prokaryotic expression vector, pJL6, to determine whether sor encodes a viral protein and to gain some insight into its possible function. The bacterially synthesized sor protein reacted with sera from individuals infected with HTLV-III, indicating that sor is expressed as a protein product or products that are immunogenic in vivo. Antibodies to the purified, bacterially synthesized sor protein were found to react specifically with the same protein and also with a protein of molecular weight 23,000 (23K) in HTLV-III-infected H9 cell extracts. The 23K protein comigrated with a protein immunoprecipitated by the serum of a hemophiliac patient with antibodies to HTLV-III, suggesting that this protein is probably the sor gene product.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kan, N C -- Franchini, G -- Wong-Staal, F -- DuBois, G C -- Robey, W G -- Lautenberger, J A -- Papas, T S -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1553-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3006245" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*immunology ; Antibodies, Viral/immunology ; Antigens, Viral/*genetics ; Chromosome Mapping ; Cloning, Molecular ; Deltaretrovirus/*genetics/immunology ; *Genes, Viral ; Humans ; Retroviridae Proteins/*genetics/immunology
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  • 26
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    AIDS retrovirus (ARV-2) clone replicates in transfected human and animal fibroblasts (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-23
    Description: A molecular clone of the AIDS-associated retrovirus (ARV-2) was transfected into human T lymphocyte and monocyte cell lines as well as mouse, mink, monkey, and human fibroblast lines. A replicating virus with cytopathic and biologic properties of ARV-2 was recovered from all the cell lines. The animal and human fibroblast cells are resistant to direct infection by ARV, and in these experiments virus production in the fibroblast lines, especially mouse, was reduced compared to human lymphocytes. However, human fibroblasts were more permissive to virus expression than mouse cells. These results show that, whereas the primary block to ARV infection in certain cells may occur at the cell surface, intracellular mechanisms can also participate in controlling virus replication. The results have relevance to vaccine development and encourage further work with modified molecular clones to examine regions of the ARV genome necessary for cytopathology and replication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levy, J A -- Cheng-Mayer, C -- Dina, D -- Luciw, P A -- CA34980/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 May 23;232(4753):998-1001.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3010461" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Animals ; Cloning, Molecular ; Cytopathogenic Effect, Viral ; Deltaretrovirus/*growth & development ; Fibroblasts/microbiology ; Humans ; Species Specificity ; Transfection ; Virus Replication
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