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  • Nucleic Acid Hybridization  (13)
  • 2020-2022
  • 1985-1989  (13)
  • 1975-1979
  • 1945-1949
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Year
  • 1
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    Molecular cloning of two types of GAP complementary DNA from human placenta (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-23
    Description: The ras p21 GTPase-activating protein (GAP) was purified from human placental tissue. Internal amino acid sequence was obtained from this 120,000-dalton protein and, by means of this sequence, two types of complementary DNA clones were isolated and characterized. One type encoded GAP with a predicted molecular mass of 116,000 daltons and 96% identity with bovine GAP. The messenger RNA of this GAP was detected in human lung, brain, liver, leukocytes, and placenta. The second type appeared to be generated by a differential splicing mechanism and encoded a novel form of GAP with a predicted molecular mass of 100,400 daltons. This protein lacks the hydrophobic amino terminus characteristic of the larger species, but retains GAP activity. The messenger RNA of this type was abundantly expressed in placenta and in several human cell lines, but not in adult tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trahey, M -- Wong, G -- Halenbeck, R -- Rubinfeld, B -- Martin, G A -- Ladner, M -- Long, C M -- Crosier, W J -- Watt, K -- Koths, K -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1697-700.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Cetus Corp., Emeryville, CA 94608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201259" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Brain Chemistry ; *Cloning, Molecular ; DNA/*genetics/isolation & purification ; Female ; GTPase-Activating Proteins ; Gene Expression Regulation ; Humans ; Leukocytes/analysis ; Liver/analysis ; Lung/analysis ; Molecular Sequence Data ; Molecular Weight ; Nucleic Acid Hybridization ; Oligonucleotide Probes ; Placenta/*analysis ; Pregnancy ; Proteins/*genetics/isolation & purification ; RNA, Messenger/analysis/genetics ; Sequence Homology, Nucleic Acid ; ras GTPase-Activating Proteins
    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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    Cloning and sequencing of porcine LH-hCG receptor cDNA: variants lacking transmembrane domain (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-08-04
    Description: Complementary DNA clones, encoding the LH-hCG (luteinizing hormone-human choriogonadotropic hormone) receptor were isolated by screening a lambda gt11 library with monoclonal antibodies. The primary structure of the protein was deduced from the DNA sequence analysis; the protein contains 696 amino acids with a putative signal peptide of 27 amino acids. Hydropathy analysis suggests the existence of seven transmembrane domains that show homology with the corresponding regions of other G protein-coupled receptors. Three other types of clones corresponding to shorter proteins were observed, in which the putative transmembrane domain was absent. These probably arose through alternative splicing. RNA blot analysis showed similar patterns in testis and ovary with a major RNA of 4700 nucleotides and several minor species. The messenger RNA was expressed in COS-7 cells, yielding a protein that bound hCG with the same affinity as the testicular receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Loosfelt, H -- Misrahi, M -- Atger, M -- Salesse, R -- Vu Hai-Luu Thi, M T -- Jolivet, A -- Guiochon-Mantel, A -- Sar, S -- Jallal, B -- Garnier, J -- New York, N.Y. -- Science. 1989 Aug 4;245(4917):525-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut National de la Sante et de la Recherche Medicale Unite 135, Hopital de Bicetre, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2502844" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Membrane/*metabolism ; *Cloning, Molecular ; DNA/*genetics ; Female ; GTP-Binding Proteins/metabolism ; Male ; Molecular Sequence Data ; Mutation ; Nucleic Acid Hybridization ; Ovary/analysis ; Protein Sorting Signals/genetics ; RNA, Messenger/analysis/genetics ; Receptors, LH/*genetics/metabolism ; Sequence Homology, Nucleic Acid ; Swine ; Testis/analysis ; Tissue Distribution
    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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    A new DNA marker tightly linked to the fragile X locus (FRAXA) (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-12-08
    Description: The fragile X syndrome is the most common cause of familial mental retardation. Genetic counseling and gene isolation are hampered by a lack of DNA markers close to the disease locus. Two somatic cell hybrids that each contain a human X chromosome with a breakpoint close to the fragile X locus have been characterized. A new DNA marker (DXS296) lies between the chromosome breakpoints and is the closest marker to the fragile X locus yet reported. The Hunter syndrome gene, which causes iduronate sulfatase deficiency, is located at the X chromosome breakpoint that is distal to this new marker, thus localizing the Hunter gene distal to the fragile X locus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suthers, G K -- Callen, D F -- Hyland, V J -- Kozman, H M -- Baker, E -- Eyre, H -- Harper, P S -- Roberts, S H -- Hors-Cayla, M C -- Davies, K E -- New York, N.Y. -- Science. 1989 Dec 8;246(4935):1298-300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Histopathology, Adelaide Children's Hospital, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2573953" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Female ; Fragile X Syndrome/*genetics ; Genetic Counseling ; *Genetic Linkage ; *Genetic Markers ; Genomic Library ; Humans ; Hybrid Cells ; Likelihood Functions ; Mice ; Mucopolysaccharidosis II/genetics ; Mutation ; Nucleic Acid Hybridization ; Polymorphism, Restriction Fragment Length ; Sex Chromosome Aberrations/*genetics ; Translocation, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Identification of the cystic fibrosis gene: chromosome walking and jumping (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-09-08
    Description: An understanding of the basic defect in the inherited disorder cystic fibrosis requires cloning of the cystic fibrosis gene and definition of its protein product. In the absence of direct functional information, chromosomal map position is a guide for locating the gene. Chromosome walking and jumping and complementary DNA hybridization were used to isolate DNA sequences, encompassing more than 500,000 base pairs, from the cystic fibrosis region on the long arm of human chromosome 7. Several transcribed sequences and conserved segments were identified in this cloned region. One of these corresponds to the cystic fibrosis gene and spans approximately 250,000 base pairs of genomic DNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rommens, J M -- Iannuzzi, M C -- Kerem, B -- Drumm, M L -- Melmer, G -- Dean, M -- Rozmahel, R -- Cole, J L -- Kennedy, D -- Hidaka, N -- DK34944/DK/NIDDK NIH HHS/ -- DK39690/DK/NIDDK NIH HHS/ -- N01-CO-74102/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1989 Sep 8;245(4922):1059-65.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Hospital for Sick Children, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2772657" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cattle ; Chickens ; *Chromosome Mapping ; *Chromosomes, Human, Pair 7 ; Cloning, Molecular/methods ; Cricetinae ; Cystic Fibrosis/*genetics ; DNA Probes ; Genes, Overlapping ; *Genes, Recessive ; Genetic Markers ; Humans ; Mice ; Nucleic Acid Hybridization ; Restriction Mapping/methods
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 5
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    Molecular genetics of human blue cone monochromacy (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-08-25
    Description: Blue cone monochromacy is a rare X-linked disorder of color vision characterized by the absence of both red and green cone sensitivities. In 12 of 12 families carrying this trait, alterations are observed in the red and green visual pigment gene cluster. The alterations fall into two classes. One class arose from the wild type by a two-step pathway consisting of unequal homologous recombination and point mutation. The second class arose by nonhomologous deletion of genomic DNA adjacent to the red and green pigment gene cluster. These deletions define a 579-base pair region that is located 4 kilobases upstream of the red pigment gene and 43 kilobases upstream of the nearest green pigment gene; this 579-base pair region is essential for the activity of both pigment genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nathans, J -- Davenport, C M -- Maumenee, I H -- Lewis, R A -- Hejtmancik, J F -- Litt, M -- Lovrien, E -- Weleber, R -- Bachynski, B -- Zwas, F -- New York, N.Y. -- Science. 1989 Aug 25;245(4920):831-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Wilmer Ophthalmologic Institute, 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/2788922" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Base Sequence ; Child ; Child, Preschool ; Chromosome Deletion ; Color Vision Defects/*genetics ; DNA/analysis ; Female ; Humans ; Male ; Molecular Sequence Data ; Mutation ; Nucleic Acid Hybridization ; Retinal Pigments/genetics ; Thalassemia/genetics ; X Chromosome
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 6
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    Studies of the HER-2/neu proto-oncogene in human breast and ovarian cancer (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-05-12
    Description: Carcinoma of the breast and ovary account for one-third of all cancers occurring in women and together are responsible for approximately one-quarter of cancer-related deaths in females. The HER-2/neu proto-oncogene is amplified in 25 to 30 percent of human primary breast cancers and this alteration is associated with disease behavior. In this report, several similarities were found in the biology of HER-2/neu in breast and ovarian cancer, including a similar incidence of amplification, a direct correlation between amplification and over-expression, evidence of tumors in which overexpression occurs without amplification, and the association between gene alteration and clinical outcome. A comprehensive study of the gene and its products (RNA and protein) was simultaneously performed on a large number of both tumor types. This analysis identified several potential shortcomings of the various methods used to evaluate HER-2/neu in these diseases (Southern, Northern, and Western blots, and immunohistochemistry) and provided information regarding considerations that should be addressed when studying a gene or gene product in human tissue. The data presented further support the concept that the HER-2/neu gene may be involved in the pathogenesis of some human cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slamon, D J -- Godolphin, W -- Jones, L A -- Holt, J A -- Wong, S G -- Keith, D E -- Levin, W J -- Stuart, S G -- Udove, J -- Ullrich, A -- CA 36827/CA/NCI NIH HHS/ -- CA 48780/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1989 May 12;244(4905):707-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, U.C.L.A. School of Medicine 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2470152" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers, Tumor ; Breast Neoplasms/*genetics ; Cloning, Molecular ; DNA/analysis ; Female ; Gene Amplification ; Gene Expression Regulation ; Humans ; Immunohistochemistry ; Nucleic Acid Hybridization ; Ovarian Neoplasms/*genetics ; Prognosis ; Protein Kinases ; Proto-Oncogene Proteins/*genetics ; *Proto-Oncogenes ; RNA/analysis ; Receptor, ErbB-2
    Print ISSN: 0036-8075
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  • 7
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    Germline transmission of exogenous genes in the chicken (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-01-27
    Description: Difficulties associated with in vitro manipulation and culture of the early chicken embryo have restricted generation of transgenic chickens to approaches that use replication-competent retroviruses. The need to produce transgenic chickens in the absence of replicating virus prompted development of a new method of gene transfer into the chicken. Microinjection of the replication-defective reticuloendotheliosis virus (REV) vector ME111 beneath unincubated chicken embryo blastoderms results in infection of germline stem cells. This vector contains genetic information exogenous to the chicken genome, including both the herpes simplex virus type 1 thymidine kinase gene and the Tn5 neomycin phosphotransferase gene. About 8 percent of male birds hatched from injected embryos contained vector DNA in their semen. All four positive males tested passed vector sequences onto their progeny. Analysis of G1 offspring showed that gonads of G0 male birds were mosaic with respect to insertion of vector provirus. Thus, primordial germ cells present in the unincubated chicken embryo blastoderm are susceptible to infection by defective REV vectors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bosselman, R A -- Hsu, R Y -- Boggs, T -- Hu, S -- Bruszewski, J -- Ou, S -- Kozar, L -- Martin, F -- Green, C -- Jacobsen, F -- New York, N.Y. -- Science. 1989 Jan 27;243(4890):533-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Amgen Inc., Thousand Oaks, CA 91320.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2536194" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; *Blastoderm ; Blotting, Southern ; Chick Embryo ; Chickens ; DNA Probes ; DNA, Viral/analysis ; *Germ Cells ; Kanamycin Kinase ; Male ; Microinjections ; Nucleic Acid Hybridization ; Phosphotransferases/genetics ; Retroviridae/genetics ; Semen/analysis ; Simplexvirus/enzymology/genetics ; Stem Cells ; Thymidine Kinase/genetics ; *Transfection
    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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  • 8
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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
    Print ISSN: 0036-8075
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  • 9
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    Characterization of the supernumerary chromosome in cat eye syndrome (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-02
    Description: Most individuals with cat eye syndrome (CES) have a supernumerary bisatellited chromosome which, on the basis of cytogenetic evidence, has been reported to originate from either chromosome 13 or 22. To resolve this question, a single-copy DNA probe, D22S9, was isolated and localized to 22q11 by in situ hybridization to metaphase chromosomes. The number of copies of this sequence was determined in CES patients by means of Southern blots and densitometry analysis of autoradiographs. In patients with the supernumerary chromosome, four copies were found, whereas in one patient with a duplication of part of chromosome 22, there were three copies. Therefore, the syndrome results from the presence of either three or four copies of DNA sequences from 22q11; there is no evidence that sequences from other chromosomes are involved. This work demonstrates how DNA sequence dosage analysis can be used to study genetic disorders that are not readily amenable to standard cytogenetic analysis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDermid, H E -- Duncan, A M -- Brasch, K R -- Holden, J J -- Magenis, E -- Sheehy, R -- Burn, J -- Kardon, N -- Noel, B -- Schinzel, A -- CA06927/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 May 2;232(4750):646-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3961499" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Multiple/*genetics ; Chromosome Aberrations/*genetics ; Chromosome Disorders ; Chromosomes, Human, 13-15 ; Chromosomes, Human, 21-22 and Y ; Coloboma/*genetics ; DNA/genetics ; Humans ; Nucleic Acid Hybridization ; Syndrome
    Print ISSN: 0036-8075
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  • 10
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    Apolipoprotein B-48 is the product of a messenger RNA with an organ-specific in-frame stop codon (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-16
    Description: The primary structure of human apolipoprotein (apo) B-48 has been deduced and shown by a combination of DNA excess hybridization, sequencing of tryptic peptides, cloned complementary DNAs, and intestinal messenger RNAs (mRNAs) to be the product of an intestinal mRNA with an in-frame UAA stop codon resulting from a C to U change in the codon CAA encoding Gln2153 in apoB-100 mRNA. The carboxyl-terminal Ile2152 of apoB-48 purified from chylous ascites fluid has apparently been cleaved from the initial translation product, leaving Met2151 as the new carboxyl-terminus. These data indicate that approximately 85% of the intestinal mRNAs terminate within approximately 0.1 to 1.0 kilobase downstream from the stop codon. The other approximately 15% have lengths similar to hepatic apoB-100 mRNA even though they have the same in-frame stop codon. The organ-specific introduction of a stop codon to a mRNA appears unprecedented and might have implications for cryptic polyadenylation signal recognition and RNA processing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, S H -- Habib, G -- Yang, C Y -- Gu, Z W -- Lee, B R -- Weng, S A -- Silberman, S R -- Cai, S J -- Deslypere, J P -- Rosseneu, M -- GM-30998/GM/NIGMS NIH HHS/ -- HL-27341/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 16;238(4825):363-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3659919" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Apolipoprotein B-48 ; Apolipoproteins B/*genetics/metabolism ; Base Sequence ; Chylous Ascites/metabolism ; *Codon ; DNA/genetics ; Humans ; Intestine, Small/analysis ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Peptide Fragments ; *RNA, Messenger/analysis/*genetics ; Trypsin/metabolism
    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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