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  • Articles  (395)
  • Latest Papers from Table of Contents or Articles in Press  (395)
  • Cloning, Molecular  (233)
  • Cells, Cultured  (175)
  • 1990-1994  (395)
  • 1935-1939
  • Natural Sciences in General  (395)
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  • Articles  (395)
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  • Latest Papers from Table of Contents or Articles in Press  (395)
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  • 1
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    Delocalization of Vg1 mRNA from the vegetal cortex in Xenopus oocytes after destruction of Xlsirt RNA (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-19
    Description: The Xlsirts are a family of transcribed repeat sequence genes that do not code for protein. Xlsirt RNAs become localized to the vegetal cortex of Xenopus oocytes early in oogenesis, before the localization of the messenger RNA Vg1, which encodes a transforming growth factor-beta-like molecule involved in mesoderm formation, and coincident with the localization of Xcat2 transcripts, which encode a nanos-like molecule. Destruction of the localized Xlsirts by injection of antisense oligodeoxynucleotides into stage 4 oocytes resulted in the release of Vg1 transcripts but not Xcat2 transcripts from the vegetal cortex. Xlsirt RNAs, which may be a structural component of the vegetal cortex, are a crucial part of a genetic pathway necessary for the proper localization of Vg1 that leads to subsequent normal pattern formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kloc, M -- Etkin, L D -- New York, N.Y. -- Science. 1994 Aug 19;265(5175):1101-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas, M.D. Anderson Cancer Center, Houston 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7520603" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cells, Cultured ; Glycoproteins/*genetics ; Molecular Sequence Data ; Oligonucleotides, Antisense/pharmacology ; Oogenesis ; RNA/*genetics ; RNA, Messenger/genetics/*metabolism ; RNA-Binding Proteins/genetics ; Repetitive Sequences, Nucleic Acid ; Transforming Growth Factor beta/genetics ; Xenopus ; *Xenopus Proteins ; Zinc Fingers
    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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    Functional participation of the IL-2 receptor gamma chain in IL-7 receptor complexes (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-11
    Description: The gamma chain of the interleukin-2 (IL-2) receptor is shared with the functional IL-4 receptor and is causatively related to X-linked severe combined immunodeficiency (XSCID), which is ascribed to a profound T cell defect. Studies with monoclonal antibodies specific for the IL-2 receptor gamma chain showed that the gamma chain participates in the functional high-affinity receptor complexes for IL-7 that are involved in the differentiation of T and B cells. Participation of the gamma subunit in more than one receptor may enable the elucidation of the mechanisms of XSCID development and lymphocyte differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kondo, M -- Takeshita, T -- Higuchi, M -- Nakamura, M -- Sudo, T -- Nishikawa, S -- Sugamura, K -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1453-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Tohoku University School of Medicine, Sendai, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128231" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; B-Lymphocytes/*immunology ; Cell Line ; Cells, Cultured ; Female ; Genetic Linkage ; Interleukin-7/*metabolism/pharmacology ; Mice ; Mice, Inbred C57BL ; Receptors, Interleukin/*metabolism ; Receptors, Interleukin-2/genetics/immunology/*metabolism ; Receptors, Interleukin-7 ; Severe Combined Immunodeficiency/genetics/immunology ; T-Lymphocytes/*immunology ; X Chromosome
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Circadian clock mutants of cyanobacteria (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-18
    Description: A diverse set of circadian clock mutants was isolated in a cyanobacterial strain that carries a bacterial luciferase reporter gene attached to a clock-controlled promoter. Among 150,000 clones of chemically mutagenized bioluminescent cells, 12 mutants were isolated that exhibit a broad spectrum of periods (between 16 and 60 hours), and 5 mutants were found that show a variety of unusual patterns, including arrhythmia. These mutations appear to be clock-specific. Moreover, it was demonstrated that in this cyanobacterium it is possible to clone mutant genes by complementation, which provides a means to genetically dissect the circadian mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kondo, T -- Tsinoremas, N F -- Golden, S S -- Johnson, C H -- Kutsuna, S -- Ishiura, M -- GM37040/GM/NIGMS NIH HHS/ -- MH43836/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1233-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute for Basic Biology, Okazaki, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973706" target="_blank"〉PubMed〈/a〉
    Keywords: Circadian Rhythm/*genetics ; Cloning, Molecular ; Cyanobacteria/*genetics/growth & development/physiology ; Darkness ; *Genes, Bacterial ; Genetic Complementation Test ; Light ; Luminescent Measurements ; Mutagenesis ; Mutation ; Temperature
    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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    Engineering poliovirus as a vaccine vector for the expression of diverse antigens (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-02
    Description: As a step toward developing poliovirus as a vaccine vector, poliovirus recombinants were constructed by fusing exogenous peptides (up to 400 amino acids) and an artificial cleavage site for viral protease 3Cpro to the amino terminus of the viral polyprotein. Viral replication proceeded normally. An extended polyprotein was produced in infected cells and proteolytically processed into the complete array of viral proteins plus the foreign peptide, which was excluded from mature virions. The recombinants retained exogenous sequences through successive rounds of replication in culture and in vivo. Infection of animals with recombinants elicited a humoral immune response to the foreign peptides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Andino, R -- Silvera, D -- Suggett, S D -- Achacoso, P L -- Miller, C J -- Baltimore, D -- Feinberg, M B -- AI22346/AI/NIAID NIH HHS/ -- AI35545/AI/NIAID NIH HHS/ -- RR00169/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1448-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of California, San Francisco.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073288" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Bacterial/biosynthesis ; Antibodies, Viral/biosynthesis ; Antigens, Bacterial/genetics/immunology ; Antigens, Viral/genetics/immunology ; Base Sequence ; Cloning, Molecular ; *Genetic Engineering ; Genetic Vectors ; HeLa Cells ; Humans ; Macaca fascicularis ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Poliovirus/*genetics/immunology/physiology ; Poliovirus Vaccine, Oral/*genetics ; *Protein Biosynthesis ; Proteins/metabolism ; Recombinant Proteins/biosynthesis/metabolism ; Vaccines, Synthetic/genetics/*immunology ; Virus Replication
    Print ISSN: 0036-8075
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  • 5
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    GDNF: a potent survival factor for motoneurons present in peripheral nerve and muscle (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: For survival, embryonic motoneurons in vertebrates depend on as yet undefined neurotrophic factors present in the limb bud. Members of the neurotrophin family are currently the best candidates for such neurotrophic factors, but inactivation of their receptor genes leads to only partial loss of motoneurons, which suggests that other factors are involved. Glial cell line-derived neurotrophic factor (GDNF), originally identified as a trophic factor specific for dopaminergic neurons, was found to be 75-fold more potent than the neurotrophins in supporting the survival of purified embryonic rat motoneurons in culture. GDNF messenger RNA was found in the immediate vicinity of motoneurons during the period of cell death in development. In vivo, GDNF rescues and prevents the atrophy of facial motoneurons that have been deprived of target-derived survival factors by axotomy. GDNF may therefore be a physiological trophic factor for spinal motoneurons. Its potency and specificity in vitro and in vivo also make it a good candidate for treatment of motoneuron disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Henderson, C E -- Phillips, H S -- Pollock, R A -- Davies, A M -- Lemeulle, C -- Armanini, M -- Simmons, L -- Moffet, B -- Vandlen, R A -- Simpson LC corrected to Simmons, L -- Koliatsos, V E -- Rosenthal, A -- NS 10580/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1062-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U.382, IBDM, Marseille, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973664" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor ; Cell Death ; Cell Survival/drug effects ; Cells, Cultured ; Ciliary Neurotrophic Factor ; Face/innervation ; Glial Cell Line-Derived Neurotrophic Factor ; Growth Inhibitors/pharmacology ; *Interleukin-6 ; Leukemia Inhibitory Factor ; Lymphokines/pharmacology ; Molecular Sequence Data ; Motor Neurons/*cytology/drug effects ; Muscle Fibers, Skeletal/*metabolism ; Nerve Growth Factors/analysis/biosynthesis/genetics/*pharmacology ; Nerve Tissue Proteins/*analysis/biosynthesis/genetics/*pharmacology ; Neurons, Afferent/cytology/drug effects ; Peripheral Nerves/*metabolism ; RNA, Messenger/analysis/genetics ; Rats ; Schwann Cells/metabolism
    Print ISSN: 0036-8075
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  • 6
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    Drosophila TAFII150: similarity to yeast gene TSM-1 and specific binding to core promoter DNA (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-13
    Description: In Drosophila and human cells, the TATA binding protein (TBP) of the transcription factor IID (TFIID) complex is tightly associated with multiple subunits termed TBP-associated factors (TAFs) that are essential for mediating regulation of RNA polymerase II transcription. The Drosophila TAFII150 has now been molecularly cloned and biochemically characterized. The deduced primary amino acid sequence of dTAFII150 reveals a striking similarity to the essential yeast gene, TSM-1. Furthermore, like dTAFII150, the TSM-1 protein is found associated with the TBP in vivo, thus identifying the first yeast homolog of a TAF associated with TFIID. Both the product of TSM-1 and dTAFII150 bind directly to TBP and dTAFII250, demonstrating a functional similarity between human and yeast TAFs. Surprisingly, DNA binding studies indicate that purified recombinant dTAFII150 binds specifically to DNA sequences overlapping the start site of transcription. The data demonstrate that at least one of the TAFs is a sequence-specific DNA binding protein and that dTAFII150 together with TBP are responsible for TFIID interactions with an extended region of the core promoter.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Verrijzer, C P -- Yokomori, K -- Chen, J L -- Tjian, R -- New York, N.Y. -- Science. 1994 May 13;264(5161):933-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California, Berkeley 94720-3202.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178153" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; DNA/*metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Drosophila ; *Drosophila Proteins ; Genes, Fungal ; Genes, Insect ; Histone Acetyltransferases ; Humans ; Molecular Sequence Data ; Nuclear Proteins/metabolism ; *Promoter Regions, Genetic ; RNA Polymerase II/metabolism ; Recombinant Proteins/metabolism ; Saccharomyces cerevisiae/genetics ; *Saccharomyces cerevisiae Proteins ; Sequence Alignment ; TATA Box ; *TATA-Binding Protein Associated Factors ; TATA-Box Binding Protein ; Transcription Factor TFIID ; Transcription Factors/chemistry/genetics/*metabolism
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  • 7
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    Identification of herpesvirus-like DNA sequences in AIDS-associated Kaposi's sarcoma (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-16
    Description: Representational difference analysis was used to isolate unique sequences present in more than 90 percent of Kaposi's sarcoma (KS) tissues obtained from patients with acquired immunodeficiency syndrome (AIDS). These sequences were not present in tissue DNA from non-AIDS patients, but were present in 15 percent of non-KS tissue DNA samples from AIDS patients. The sequences are homologous to, but distinct from, capsid and tegument protein genes of the Gammaherpesvirinae, herpesvirus saimiri and Epstein-Barr virus. These KS-associated herpesvirus-like (KSHV) sequences appear to define a new human herpesvirus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, Y -- Cesarman, E -- Pessin, M S -- Lee, F -- Culpepper, J -- Knowles, D M -- Moore, P S -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1865-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7997879" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*complications ; Amino Acid Sequence ; Base Composition ; Base Sequence ; Blotting, Southern ; Cloning, Molecular ; DNA, Viral/*analysis/chemistry/genetics ; Female ; Herpesviridae/*genetics ; Herpesvirus 2, Saimiriine/genetics ; Herpesvirus 4, Human/genetics ; Humans ; Male ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Open Reading Frames ; Polymerase Chain Reaction ; Retrospective Studies ; Sarcoma, Kaposi/etiology/*virology ; Sequence Homology, Amino Acid
    Print ISSN: 0036-8075
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  • 8
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    A genetic linkage map for the zebrafish (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-29
    Description: To facilitate molecular genetic analysis of vertebrate development, haploid genetics was used to construct a recombination map for the zebrafish Danio (Brachydanio) rerio. The map consists of 401 random amplified polymorphic DNAs (RAPDs) and 13 simple sequence repeats spaced at an average interval of 5.8 centimorgans. Strategies that exploit the advantages of haploid genetics and RAPD markers were developed that quickly mapped lethal and visible mutations and that placed cloned genes on the map. This map is useful for the position-based cloning of mutant genes, the characterization of chromosome rearrangements, and the investigation of evolution in vertebrate genomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Postlethwait, J H -- Johnson, S L -- Midson, C N -- Talbot, W S -- Gates, M -- Ballinger, E W -- Africa, D -- Andrews, R -- Carl, T -- Eisen, J S -- 1RO1AI26734/AI/NIAID NIH HHS/ -- HD07470/HD/NICHD NIH HHS/ -- NS23915/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):699-703.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neurosciences, University of Oregon, Eugene 97403.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171321" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosome Mapping ; Cloning, Molecular ; Female ; Genetic Markers ; Genotype ; Male ; Mutation ; Phenotype ; Polymerase Chain Reaction ; Repetitive Sequences, Nucleic Acid ; Software ; Zebrafish/*genetics
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  • 9
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    Potential role of human cytomegalovirus and p53 interaction in coronary restenosis (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-15
    Description: A subset of patients who have undergone coronary angioplasty develop restenosis, a vessel renarrowing characterized by excessive proliferation of smooth muscle cells (SMCs). Of 60 human restenosis lesions examined, 23 (38 percent) were found to have accumulated high amounts of the tumor suppressor protein p53, and this correlated with the presence of human cytomegalovirus (HCMV) in the lesions. SMCs grown from the lesions expressed HCMV protein IE84 and high amounts of p53. HCMV infection of cultured SMCs enhanced p53 accumulation, which correlated temporally with IE84 expression. IE84 also bound to p53 and abolished its ability to transcriptionally activate a reporter gene. Thus, HCMV, and IE84-mediated inhibition of p53 function, may contribute to the development of restenosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Speir, E -- Modali, R -- Huang, E S -- Leon, M B -- Shawl, F -- Finkel, T -- Epstein, S E -- New York, N.Y. -- Science. 1994 Jul 15;265(5170):391-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiology Branch, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023160" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Aged, 80 and over ; *Angioplasty, Balloon ; Antigens, Viral/*metabolism ; Atherectomy, Coronary ; Base Sequence ; Cells, Cultured ; Coronary Disease/*etiology/pathology/therapy ; Coronary Vessels/cytology/metabolism/microbiology ; Cytomegalovirus/*physiology ; Genes, p53 ; Humans ; Immediate-Early Proteins/*metabolism ; Middle Aged ; Molecular Sequence Data ; Muscle, Smooth, Vascular/cytology/metabolism/microbiology ; Recurrence ; Transcriptional Activation ; Transfection ; Tumor Suppressor Protein p53/genetics/*metabolism
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  • 10
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    Genetic control of programmed cell death in Drosophila (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-29
    Description: A gene, reaper (rpr), that appears to play a central control function for the initiation of programmed cell death (apoptosis) in Drosophila was identified. Virtually all programmed cell death that normally occurs during Drosophila embryogenesis was blocked in embryos homozygous for a small deletion that includes the reaper gene. Mutant embryos contained many extra cells and failed to hatch, but many other aspects of development appeared quite normal. Deletions that include reaper also protected embryos from apoptosis caused by x-irradiation and developmental defects. However, high doses of x-rays induced some apoptosis in mutant embryos, and the resulting corpses were phagocytosed by macrophages. These data suggest that the basic cell death program is intact although it was not activated in mutant embryos. The DNA encompassed by the deletion was cloned and the reaper gene was identified on the basis of the ability of cloned DNA to restore apoptosis to cell death defective embryos in germ line transformation experiments. The reaper gene appears to encode a small peptide that shows no homology to known proteins, and reaper messenger RNA is expressed in cells destined to undergo apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉White, K -- Grether, M E -- Abrams, J M -- Young, L -- Farrell, K -- Steller, H -- 5 F32 NS08536/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):677-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Brain and Cognitive Sciences, Cambridge, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171319" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apoptosis/*genetics ; Base Sequence ; Cloning, Molecular ; DNA Primers ; Drosophila/cytology/embryology/*genetics ; *Drosophila Proteins ; Embryo, Nonmammalian/cytology ; *Genes, Insect ; Models, Genetic ; Molecular Sequence Data ; Mutation ; Nervous System/cytology ; Neurons/cytology ; Peptides/chemistry/*genetics/physiology
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  • 11
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    Expressed sequence tags (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, M M -- Emanuel, B S -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1790-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7997870" target="_blank"〉PubMed〈/a〉
    Keywords: Biological Specimen Banks ; Chromosome Mapping ; Cloning, Molecular ; *DNA, Complementary ; *Databases, Factual ; Gene Expression ; *Genome, Human ; Humans ; Sequence Analysis, DNA
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    Cell suicide: by ICE, not fire (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):754-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303290" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caenorhabditis elegans/genetics ; Caspase 1 ; Cells, Cultured ; Free Radicals/metabolism ; Metalloendopeptidases/*genetics/metabolism ; Mice ; Mice, Knockout ; Neurons/cytology ; Oxygen/metabolism ; Proto-Oncogene Proteins/genetics/physiology ; Proto-Oncogene Proteins c-bcl-2 ; Rats ; bcl-2-Associated X Protein ; bcl-X Protein
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  • 13
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    The Drosophila saxophone gene: a serine-threonine kinase receptor of the TGF-beta superfamily (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-25
    Description: The Drosophila decapentaplegic (dpp) gene encodes a transforming growth factor-beta (TGF-beta)-like protein that plays a key role in several aspects of development. Transduction of the DPP signal was investigated by cloning of serine-threonine kinase transmembrane receptors from Drosophila because this type of receptor is specific for the TGF-beta-like ligands. Here evidence is provided demonstrating that the Drosophila saxophone (sax) gene, a previously identified female sterile locus, encodes a TGF-beta-like type I receptor. Embryos from sax mothers and dpp embryos exhibit similar mutant phenotypes during early gastrulation, and these two loci exhibit genetic interactions, which suggest that they are utilized in the same pathway. These data suggest that sax encodes a receptor for dpp.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xie, T -- Finelli, A L -- Padgett, R W -- New York, N.Y. -- Science. 1994 Mar 25;263(5154):1756-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Waksman Institute, Rutgers University, Piscataway, NJ 08855-0759.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8134837" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; Drosophila/embryology/*genetics/metabolism ; *Drosophila Proteins ; Embryo, Nonmammalian/metabolism ; Female ; *Genes, Insect ; Insect Hormones/genetics/*metabolism ; Male ; Molecular Sequence Data ; Mutation ; Protein-Serine-Threonine Kinases/chemistry/*genetics/metabolism ; Receptors, Transforming Growth Factor beta/chemistry/*genetics/metabolism ; Signal Transduction ; Transforming Growth Factor beta/genetics/*metabolism
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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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    Arabidopsis ABA response gene ABI1: features of a calcium-modulated protein phosphatase (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-03
    Description: The Arabidopsis ABI1 locus is essential for a wide spectrum of abscisic acid (ABA) responses throughout plant development. Here, ABI1 was shown to regulate stomatal aperture in leaves and mitotic activity in root meristems. The ABI1 gene was cloned and predicted to encode a signaling protein. Although its carboxyl-terminal domain is related to serine-threonine phosphatase 2C, the ABI1 protein has a unique amino-terminal extension containing an EF hand calcium-binding site. These results suggest that the ABI1 protein is a Ca(2+)-modulated phosphatase and functions to integrate ABA and Ca2+ signals with phosphorylation-dependent response pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leung, J -- Bouvier-Durand, M -- Morris, P C -- Guerrier, D -- Chefdor, F -- Giraudat, J -- New York, N.Y. -- Science. 1994 Jun 3;264(5164):1448-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut des Sciences Vegetales, Centre National de la Recherche Scientifique UPR 40, Gif-sur-Yvette, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7910981" target="_blank"〉PubMed〈/a〉
    Keywords: Abscisic Acid/*pharmacology ; Amino Acid Sequence ; Arabidopsis/chemistry/cytology/*genetics/physiology ; *Arabidopsis Proteins ; Calcium/*metabolism ; Cloning, Molecular ; *Genes, Plant ; Mitosis ; Molecular Sequence Data ; Mutation ; Phenotype ; Phosphoprotein Phosphatases/chemistry/*genetics/*metabolism ; Phosphorylation ; Plants, Genetically Modified ; Polymorphism, Restriction Fragment Length ; Signal Transduction ; Transformation, Genetic
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  • 15
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    Coding of hemolysins within the ribosomal RNA repeat on a plasmid in Entamoeba histolytica (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-11
    Description: The pathogenesis of amoebic dysentery is a result of cytolysis of the colonic mucosa by the parasitic protozoan Entamoeba histolytica. The cytolysis results in extensive local ulceration and allows the amoeba to penetrate and metastasize to distant sites. Factors involved in this process were defined with three clones that express hemolytic activities in Escherichia coli. These potential amoebic virulence determinants were also toxic to human colonic epithelial cells, the primary cellular targets in amoebal invasion of the large intestine. The coding sequences for the hemolysins were close to each other on a 2.6-kilobase segment of a 25-kilobase extrachromosomal DNA element. The structural genes for the hemolysins were within inverted repeats that encode ribosomal RNAs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jansson, A -- Gillin, F -- Kagardt, U -- Hagblom, P -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1440-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Uppsala University, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128227" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Survival/drug effects ; Cloning, Molecular ; Entamoeba histolytica/*genetics/pathogenicity ; Escherichia coli/genetics ; *Genes, Protozoan ; Hemolysin Proteins/*genetics/toxicity ; Molecular Sequence Data ; Open Reading Frames ; *Plasmids ; RNA, Protozoan/genetics ; RNA, Ribosomal/*genetics ; Repetitive Sequences, Nucleic Acid ; Tumor Cells, Cultured ; Virulence
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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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    Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin's lymphoma (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-04
    Description: The 2;5 chromosomal translocation occurs in most anaplastic large-cell non-Hodgkin's lymphomas arising from activated T lymphocytes. This rearrangement was shown to fuse the NPM nucleolar phosphoprotein gene on chromosome 5q35 to a previously unidentified protein tyrosine kinase gene, ALK, on chromosome 2p23. In the predicted hybrid protein, the amino terminus of nucleophosmin (NPM) is linked to the catalytic domain of anaplastic lymphoma kinase (ALK). Expressed in the small intestine, testis, and brain but not in normal lymphoid cells, ALK shows greatest sequence similarity to the insulin receptor subfamily of kinases. Unscheduled expression of the truncated ALK may contribute to malignant transformation in these lymphomas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morris, S W -- Kirstein, M N -- Valentine, M B -- Dittmer, K G -- Shapiro, D N -- Saltman, D L -- Look, A T -- CA 21765/CA/NCI NIH HHS/ -- KO8 CA 01702/CA/NCI NIH HHS/ -- P01 CA 20180/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 4;263(5151):1281-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Oncology, St. Jude Children's Research Hospital, Memphis, TN 38105.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8122112" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Brain/enzymology ; Cell Transformation, Neoplastic ; Chromosome Walking ; Chromosomes, Human, Pair 2 ; Chromosomes, Human, Pair 5 ; Cloning, Molecular ; Gene Expression Regulation, Neoplastic ; Humans ; Intestine, Small/enzymology ; Lymphoma, Large-Cell, Anaplastic/chemistry/enzymology/*genetics ; Male ; Molecular Sequence Data ; Nuclear Proteins/chemistry/*genetics ; Phosphoproteins/chemistry/*genetics ; Promoter Regions, Genetic ; Protein-Tyrosine Kinases/chemistry/*genetics ; RNA, Messenger/genetics/metabolism ; Receptor Protein-Tyrosine Kinases ; Sequence Alignment ; Signal Transduction ; Testis/enzymology ; *Translocation, Genetic ; Tumor Cells, Cultured
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  • 17
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    A molecular determinant for submillisecond desensitization in glutamate receptors (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: The decay of excitatory postsynaptic currents in central neurons mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) receptors is likely to be shaped either by receptor desensitization or by offset after removal of glutamate from the synaptic cleft. Native AMPA receptors show desensitization time constants of 1 to about 10 milliseconds, but the underlying molecular determinants of these large differences are unknown. Cloned AMPA receptors carrying the "flop" splice variants of glutamate receptor subtype C (GluR-C) and GluR-D are shown to have desensitization time constants of around 1 millisecond, whereas those with the "flip" variants are about four times slower. Cerebellar granule cells switch their expression of GluR-D splice variants from mostly flip forms in early stages to predominantly flop forms in the adult rat brain. These findings suggest that rapid desensitization of AMPA receptors can be regulated by the expression and alternative splicing of GluR-D gene transcripts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mosbacher, J -- Schoepfer, R -- Monyer, H -- Burnashev, N -- Seeburg, P H -- Ruppersberg, J P -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1059-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur medizinische Forschung, Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973663" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; Cells, Cultured ; Cerebellum/cytology/metabolism ; Cloning, Molecular ; Glutamic Acid/*pharmacology ; In Situ Hybridization ; Oocytes ; Patch-Clamp Techniques ; Rats ; Receptors, AMPA/drug effects/genetics/*physiology ; Recombinant Proteins ; Synaptic Transmission ; Xenopus laevis
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  • 18
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    Nitric oxide activation of poly(ADP-ribose) synthetase in neurotoxicity (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-04
    Description: Poly(adenosine 5'-diphosphoribose) synthetase (PARS) is a nuclear enzyme which, when activated by DNA strand breaks, adds up to 100 adenosine 5'-diphosphoribose (ADP-ribose) units to nuclear proteins such as histones and PARS itself. This activation can lead to cell death through depletion of beta-nicotinamide adenine dinucleotide (the source of ADP-ribose) and adenosine triphosphate. Nitric oxide (NO) stimulated ADP-ribosylation of PARS in rat brain. Benzamide and other derivatives, which inhibit PARS, blocked N-methyl-D-aspartate- and NO-mediated neurotoxicity with relative potencies paralleling their ability to inhibit PARS. Thus, NO appeared to elicit neurotoxicity by activating PARS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, J -- Dawson, V L -- Dawson, T M -- Snyder, S H -- DA-00074/DA/NIDA NIH HHS/ -- DA-00266/DA/NIDA NIH HHS/ -- DA-271-90-7408/DA/NIDA NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):687-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, 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/8080500" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzamides/pharmacology ; Brain/cytology/drug effects/enzymology ; Cell Death/drug effects ; Cell Line ; Cells, Cultured ; Cerebral Cortex/cytology/drug effects/enzymology ; DNA Damage ; Enzyme Activation ; Humans ; N-Methylaspartate/*toxicity ; Neurons/cytology/*drug effects/enzymology ; Nitric Oxide/*toxicity ; Poly(ADP-ribose) Polymerase Inhibitors ; Poly(ADP-ribose) Polymerases/*metabolism ; Rats ; Rats, Sprague-Dawley
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  • 19
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    Visualization of quantal synaptic transmission by dendritic calcium imaging (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-28
    Description: As changes in synaptic strength are thought to be critical for learning and memory, it would be useful to monitor the activity of individual identified synapses on mammalian central neurons. Calcium imaging of cortical neurons grown in primary culture was used to visualize the activation of individual postsynaptic elements by miniature excitatory synaptic currents elicited by spontaneous quantal release. This approach revealed that the probability of spontaneous activity differed among synapses on the same dendrite. Furthermore, synapses that undergo changes in activity induced by glutamate or phorbol ester treatment were identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, T H -- Baraban, J M -- Wier, W G -- Blatter, L A -- New York, N.Y. -- Science. 1994 Jan 28;263(5146):529-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, 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/7904774" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Cells, Cultured ; Cerebral Cortex ; Dendrites/*metabolism ; Glutamates/pharmacology ; Glutamic Acid ; Kinetics ; Microelectrodes ; Neuronal Plasticity ; Neurons/*physiology ; Phorbol Esters/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/physiology ; Synapses/*physiology ; *Synaptic Transmission ; Tetrodotoxin/pharmacology
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  • 20
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    Requirement for the yeast gene LON in intramitochondrial proteolysis and maintenance of respiration (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-08
    Description: The role of protein degradation in mitochondrial homeostasis was explored by cloning of a gene from Saccharomyces cerevisiae that encodes a protein resembling the adenosine triphosphate (ATP)-dependent bacterial protease Lon. The predicted yeast protein has a typical mitochondrial matrix-targeting sequence at its amino terminus. Yeast cells lacking a functional LON gene contained a nonfunctional mitochondrial genome, were respiratory-deficient, and lacked an ATP-dependent proteolytic activity present in the mitochondria of Lon+ cells. Lon- cells were also impaired in their ability to catalyze the energy-dependent degradation of several mitochondrial matrix proteins and they accumulated electron-dense inclusions in their mitochondrial matrix.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzuki, C K -- Suda, K -- Wang, N -- Schatz, G -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):273-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biozentrum der Universitat Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146662" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Dependent Proteases ; Adenosine Triphosphatases/genetics/metabolism ; Amino Acid Sequence ; Base Sequence ; Cloning, Molecular ; Fungal Proteins/metabolism ; *Genes, Fungal ; Heat-Shock Proteins/*genetics/metabolism ; Microscopy, Electron ; Mitochondria/*metabolism/ultrastructure ; Molecular Sequence Data ; *Oxygen Consumption ; Saccharomyces cerevisiae/*genetics/metabolism ; Serine Endopeptidases/*genetics/metabolism
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  • 21
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    Direct signaling from astrocytes to neurons in cultures of mammalian brain cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-25
    Description: Although astrocytes have been considered to be supportive, rather than transmissive, in the adult nervous system, recent studies have challenged this assumption by demonstrating that astrocytes possess functional neurotransmitter receptors. Astrocytes are now shown to directly modulate the free cytosolic calcium, and hence transmission characteristics, of neighboring neurons. When a focal electric field potential was applied to single astrocytes in mixed cultures of rat forebrain astrocytes and neurons, a prompt elevation of calcium occurred in the target cell. This in turn triggered a wave of calcium increase, which propagated from astrocyte to astrocyte. Neurons resting on these astrocytes responded with large increases in their concentration of cytosolic calcium. The gap junction blocker octanol attenuated the neuronal response, which suggests that the astrocytic-neuronal signaling is mediated through intercellular connections rather than synaptically. This neuronal response to local astrocytic stimulation may mediate local intercellular communication within the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nedergaard, M -- New York, N.Y. -- Science. 1994 Mar 25;263(5154):1768-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Cornell University Medical College, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8134839" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/drug effects/*metabolism ; Calcium/*metabolism ; Cell Communication ; Cells, Cultured ; Electric Stimulation ; Excitatory Amino Acid Antagonists ; Gap Junctions/physiology ; Kynurenic Acid/pharmacology ; Neurons/drug effects/*metabolism ; Nifedipine/pharmacology ; Octanols/pharmacology ; Prosencephalon/*cytology/embryology ; Rats ; *Signal Transduction ; Synapses/metabolism ; Tetrodotoxin/pharmacology
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  • 22
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    Association of intestinal peptide transport with a protein related to the cadherin superfamily (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-15
    Description: The first step in oral absorption of many medically important peptide-based drugs is mediated by an intestinal proton-dependent peptide transporter. This transporter facilitates the oral absorption of beta-lactam antibiotics and angiotensin-converting enzyme inhibitors from the intestine into enterocytes lining the luminal wall. A monoclonal antibody that blocked uptake of cephalexin was used to identify and clone a gene that encodes an approximately 92-kilodalton membrane protein that was associated with the acquisition of peptide transport activity by transport-deficient cells. The amino acid sequence deduced from the complementary DNA sequence of the cloned gene indicated that this transport-associated protein shares several conserved structural elements with the cadherin superfamily of calcium-dependent, cell-cell adhesion proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dantzig, A H -- Hoskins, J A -- Tabas, L B -- Bright, S -- Shepard, R L -- Jenkins, I L -- Duckworth, D C -- Sportsman, J R -- Mackensen, D -- Rosteck, P R Jr -- New York, N.Y. -- Science. 1994 Apr 15;264(5157):430-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN 46285.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8153632" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Transport ; CHO Cells ; Cadherins/*chemistry ; Carrier Proteins/*chemistry/genetics/isolation & purification/metabolism ; Cephalexin/*metabolism ; Cloning, Molecular ; Cricetinae ; Glycosylation ; Humans ; Hydrogen-Ion Concentration ; Intestinal Mucosa/*metabolism ; Leucine/analogs & derivatives/metabolism ; *Membrane Transport Proteins ; Mice ; Mice, Inbred A ; Molecular Sequence Data ; Open Reading Frames ; Sequence Homology, Amino Acid ; Transfection ; Tumor Cells, Cultured
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  • 23
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    Fas and perforin pathways as major mechanisms of T cell-mediated cytotoxicity (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-07-22
    Description: Two molecular mechanisms of T cell-mediated cytotoxicity, one perforin-based, the other Fas-based, have been demonstrated. To determine the extent of their contribution to T cell-mediated cytotoxicity, a range of effector cells from normal control or perforin-deficient mice were tested against a panel of target cells with various levels of Fas expression. All cytotoxicity observed was due to either of these mechanisms, and no third mechanism was detected. Thus, the perforin- and Fas-based mechanisms may account for all T cell-mediated cytotoxicity in short-term in vitro assays.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kagi, D -- Vignaux, F -- Ledermann, B -- Burki, K -- Depraetere, V -- Nagata, S -- Hengartner, H -- Golstein, P -- New York, N.Y. -- Science. 1994 Jul 22;265(5171):528-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7518614" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD95 ; Antigens, Surface/*immunology ; Cells, Cultured ; Concanavalin A/pharmacology ; *Cytotoxicity, Immunologic ; Ionomycin/pharmacology ; Leukemia L1210 ; Lymphocyte Culture Test, Mixed ; Lymphocytic choriomeningitis virus/immunology ; Membrane Glycoproteins/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Molecular Sequence Data ; Perforin ; Pore Forming Cytotoxic Proteins ; T-Lymphocytes, Cytotoxic/*immunology ; Tetradecanoylphorbol Acetate/pharmacology ; Tumor Cells, Cultured
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  • 24
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    Crystal structure of rat DNA polymerase beta: evidence for a common polymerase mechanism (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-06-24
    Description: Structures of the 31-kilodalton catalytic domain of rat DNA polymerase beta (pol beta) and the whole 39-kilodalton enzyme were determined at 2.3 and 3.6 angstrom resolution, respectively. The 31-kilodalton domain is composed of fingers, palm, and thumb subdomains arranged to form a DNA binding channel reminiscent of the polymerase domains of the Klenow fragment of Escherichia coli DNA polymerase I, HIV-1 reverse transcriptase, and bacteriophage T7 RNA polymerase. The amino-terminal 8-kilodalton domain is attached to the fingers subdomain by a flexible hinge. The two invariant aspartates found in all polymerase sequences and implicated in catalytic activity have the same geometric arrangement within structurally similar but topologically distinct palms, indicating that the polymerases have maintained, or possibly re-evolved, a common nucleotidyl transfer mechanism. The location of Mn2+ and deoxyadenosine triphosphate in pol beta confirms the role of the invariant aspartates in metal ion and deoxynucleoside triphosphate binding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sawaya, M R -- Pelletier, H -- Kumar, A -- Wilson, S H -- Kraut, J -- CA17374/CA/NCI NIH HHS/ -- ES06839/ES/NIEHS NIH HHS/ -- GM10928/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1930-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of California, San Diego 92093-0317.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7516581" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cloning, Molecular ; Crystallization ; Crystallography, X-Ray ; DNA/metabolism ; DNA Polymerase I/*chemistry/metabolism ; DNA-Directed RNA Polymerases/chemistry/metabolism ; Deoxyadenine Nucleotides/chemistry/metabolism ; Deoxycytosine Nucleotides/chemistry/metabolism ; Dideoxynucleotides ; HIV Reverse Transcriptase ; Protein Folding ; Protein Structure, Secondary ; RNA-Directed DNA Polymerase/chemistry/metabolism ; Rats ; Recombinant Proteins/chemistry ; Viral Proteins
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  • 25
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    Modulation of epithelial cell growth by intraepithelial gamma delta T cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-18
    Description: The role played in immune surveillance by gamma delta T cells residing in various epithelia has not been clear. It is shown here that activated gamma delta T cells obtained from skin and intestine express the epithelial cell mitogen keratinocyte growth factor (KGF). In contrast, intraepithelial alpha beta T cells, as well as all lymphoid alpha beta and gamma delta T cell populations tested, did not produce KGF or promote the growth of cultured epithelial cells. These results suggest that intraepithelial gamma delta T cells function in surveillance and in repair of damaged epithelial tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boismenu, R -- Havran, W L -- AI32751/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1253-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973709" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Division ; Cell Line ; Cells, Cultured ; Cloning, Molecular ; Dendritic Cells/*physiology ; Epithelial Cells ; Fibroblast Growth Factor 10 ; Fibroblast Growth Factor 7 ; *Fibroblast Growth Factors ; Growth Substances/*biosynthesis/genetics ; Keratinocytes/*cytology ; Lymphocyte Activation ; Mice ; Molecular Sequence Data ; *Receptors, Antigen, T-Cell, gamma-delta ; T-Lymphocyte Subsets/immunology/metabolism/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Regulation of melanin biosynthesis in the human epidermis by tetrahydrobiopterin (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-11
    Description: The participation of (6R) 5,6,7,8-tetrahydrobiopterin (6-BH4) in regulating the tyrosine supply for melanin biosynthesis was investigated by the examination of human keratinocytes, melanocytes, and epidermal suction blisters from normal human skin and from patients with the depigmentation disorder vitiligo. Cells, as well as total epidermis, contained high phenylalanine hydroxylase activities and also displayed the capacity to synthesize and recycle 6-BH4, the essential cofactor for this enzyme. In vitiligo, 4a-hydroxy-BH4 dehydratase activity was extremely low or absent, yielding an accumulation of the nonenzymatic by-product 7-tetrahydrobiopterin (7-BH4) at concentrations up to 8 x 10(-6) M in the epidermis. This by-product is a potent competitive inhibitor in the phenylalanine hydroxylase reaction with an inhibition constant of 10(-6) M. Thus, 6-BH4 seems to control melanin biosynthesis in the human epidermis, whereas 7-BH4 may initiate depigmentation in patients with vitiligo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schallreuter, K U -- Wood, J M -- Pittelkow, M R -- Gutlich, M -- Lemke, K R -- Rodl, W -- Swanson, N N -- Hitzemann, K -- Ziegler, I -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1444-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, University of Hamburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128228" target="_blank"〉PubMed〈/a〉
    Keywords: Biopterin/*analogs & derivatives/biosynthesis/metabolism/pharmacology ; Cell Differentiation ; Cells, Cultured ; Epidermis/*metabolism ; GTP Cyclohydrolase/metabolism ; Humans ; Keratinocytes/metabolism ; Melanins/*biosynthesis ; Melanocytes/metabolism ; Phenylalanine Hydroxylase/antagonists & inhibitors/metabolism ; Tyrosine/biosynthesis ; Vitiligo/*metabolism
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    Padlock probes: circularizing oligonucleotides for localized DNA detection (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-30
    Description: Nucleotide sequence information derived from DNA segments of the human and other genomes is accumulating rapidly. However, it frequently proves difficult to use such short DNA segments to identify clones in genomic libraries or fragments in blots of the whole genome or for in situ analysis of chromosomes. Oligonucleotide probes, consisting of two target-complementary segments, connected by a linker sequence, were designed. Upon recognition of the specific nucleic acid molecule the ends of the probes were joined through the action of a ligase, creating circular DNA molecules catenated to the target sequence. These probes thus provide highly specific detection with minimal background.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nilsson, M -- Malmgren, H -- Samiotaki, M -- Kwiatkowski, M -- Chowdhary, B P -- Landegren, U -- New York, N.Y. -- Science. 1994 Sep 30;265(5181):2085-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beijer Laboratory, Department of Medical Genetics, Biomedical Center, Uppsala, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7522346" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cells, Cultured ; Chromosomes, Human, Pair 12 ; Cystic Fibrosis Transmembrane Conductance Regulator ; DNA/*analysis ; DNA, Circular/*analysis ; Genetic Vectors ; Humans ; In Situ Hybridization ; Lymphocytes ; Membrane Proteins/genetics ; Models, Molecular ; Molecular Sequence Data ; Nucleic Acid Conformation ; *Oligonucleotide Probes/chemistry ; Repetitive Sequences, Nucleic Acid ; Templates, Genetic
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    Requirement of human renal water channel aquaporin-2 for vasopressin-dependent concentration of urine (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-01
    Description: Concentration of urine in mammals is regulated by the antidiuretic hormone vasopressin. Binding of vasopressin to its V2 receptor leads to the insertion of water channels in apical membranes of principal cells in collecting ducts. In nephrogenic diabetes insipidus (NDI), the kidney fails to concentrate urine in response to vasopressin. A male patient with an autosomal recessive form of NDI was found to be a compound heterozygote for two mutations in the gene encoding aquaporin-2, a water channel. Functional expression studies in Xenopus oocytes revealed that each mutation resulted in nonfunctional water channel proteins. Thus, aquaporin-2 is essential for vasopressin-dependent concentration of urine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deen, P M -- Verdijk, M A -- Knoers, N V -- Wieringa, B -- Monnens, L A -- van Os, C H -- van Oost, B A -- New York, N.Y. -- Science. 1994 Apr 1;264(5155):92-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Physiology, University of Nijmegen, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8140421" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Aquaporin 2 ; Aquaporin 6 ; *Aquaporins ; Base Sequence ; Cloning, Molecular ; Deamino Arginine Vasopressin/*pharmacology ; Diabetes Insipidus/*genetics/physiopathology ; Female ; Genes, Recessive ; Heterozygote ; Humans ; Kidney/metabolism/*physiology ; *Kidney Concentrating Ability ; Male ; Membrane Proteins/chemistry/genetics/*physiology ; Molecular Sequence Data ; Oocytes ; Pedigree ; Point Mutation ; Protein Structure, Secondary ; RNA, Complementary/genetics ; Water/metabolism ; Xenopus laevis
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    Cloning of a T cell growth factor that interacts with the beta chain of the interleukin-2 receptor (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-13
    Description: A cytokine was identified that stimulated the proliferation of T lymphocytes, and a complementary DNA clone encoding this new T cell growth factor was isolated. The cytokine, designated interleukin-15 (IL-15), is produced by a wide variety of cells and tissues and shares many biological properties with IL-2. Monoclonal antibodies to the beta chain of the IL-2 receptor inhibited the biological activity of IL-15, and IL-15 competed for binding with IL-2, indicating that IL-15 uses components of the IL-2 receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grabstein, K H -- Eisenman, J -- Shanebeck, K -- Rauch, C -- Srinivasan, S -- Fung, V -- Beers, C -- Richardson, J -- Schoenborn, M A -- Ahdieh, M -- New York, N.Y. -- Science. 1994 May 13;264(5161):965-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Research and Development Corporation, Seattle, WA 98101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178155" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; *Cloning, Molecular ; Haplorhini ; Humans ; Interleukin-15 ; Interleukin-2/immunology/metabolism/pharmacology ; Interleukins/chemistry/*genetics/metabolism/pharmacology ; Killer Cells, Lymphokine-Activated/immunology ; Leukocytes, Mononuclear/immunology/metabolism ; Lymphocyte Activation ; Lymphocyte Culture Test, Mixed ; Molecular Sequence Data ; Protein Structure, Secondary ; Receptors, Interleukin-2/immunology/*metabolism ; T-Lymphocytes/*immunology ; T-Lymphocytes, Cytotoxic/immunology
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    T cells and suppression in vitro (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scott, B -- Kaye, J -- Lo, D -- New York, N.Y. -- Science. 1994 Oct 21;266(5184):464-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939690" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; *Clonal Anergy ; *Lymphocyte Activation ; Mice ; Mice, Transgenic ; T-Lymphocytes, Regulatory/*immunology
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    Noradrenergic regulation of cholinergic differentiation (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: When the sympathetic nerves that innervate rat sweat glands reach their targets, they are induced to switch from using norepinephrine as their neurotransmitter to acetylcholine. Catecholamines (such as norepinephrine) released by nerves growing to the sweat gland induce this phenotypic conversion by stimulating production of a cholinergic differentiation factor [sweat gland factor (SGF)] by gland cells. Here, culture of gland cells with sympathetic, but not sensory, neurons induced SGF production. Blockage of alpha 1- or beta-adrenergic receptors prevented acquisition of the cholinergic phenotype in sympathetic neurons co-cultured with sweat glands, and sweat glands from sympathectomized animals lacked SGF. Thus, reciprocal instructive interactions, mediated in part by small molecule neurotransmitters, direct the development of this synapse.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Habecker, B A -- Landis, S C -- NS-023678/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1602-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106-4975.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202714" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Base Sequence ; Cell Differentiation ; Cells, Cultured ; Culture Media, Conditioned ; Glycoproteins/*biosynthesis ; Molecular Sequence Data ; Neuregulins ; Neurons/cytology/physiology ; Neurons, Afferent/cytology/physiology ; Parasympathetic Nervous System/cytology/*physiology ; Phenotype ; Rats ; Receptors, Adrenergic/*physiology ; Sweat Glands/cytology/*innervation/metabolism ; Sympathectomy ; Sympathetic Nervous System/cytology/*physiology
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    Glia: the brain's other cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Travis, J -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):970-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973679" target="_blank"〉PubMed〈/a〉
    Keywords: Astrocytes/physiology ; Brain/*cytology/physiology ; Calcium/metabolism ; Cell Communication ; Cells, Cultured ; Humans ; Nerve Growth Factors/biosynthesis ; Neuroglia/*physiology ; Neurons/physiology ; Neurotransmitter Agents/metabolism ; Synapses/metabolism
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    Human severe combined immunodeficiency due to a defect in ZAP-70, a T cell tyrosine kinase (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: A homozygous mutation in the kinase domain of ZAP-70, a T cell receptor-associated protein tyrosine kinase, produced a distinctive form of human severe combined immunodeficiency. Manifestations of this disorder included profound immunodeficiency, absence of peripheral CD8+ T cells, and abundant peripheral CD4+ T cells that were refractory to T cell receptor-mediated activation. These findings demonstrate that ZAP-70 is essential for human T cell function and suggest that CD4+ and CD8+ T cells depend on different intracellular signaling pathways to support their development or survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elder, M E -- Lin, D -- Clever, J -- Chan, A C -- Hope, T J -- Weiss, A -- Parslow, T G -- AI29313/AI/NIAID NIH HHS/ -- GM43574/GM/NIGMS NIH HHS/ -- RR01271/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1596-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of California, San Francisco 94143-0110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202712" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Cloning, Molecular ; Female ; Frameshift Mutation ; Gene Deletion ; Homozygote ; Humans ; Infant ; Male ; Molecular Sequence Data ; Polymerase Chain Reaction ; Protein-Tyrosine Kinases/*genetics/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Severe Combined Immunodeficiency/*genetics/immunology ; Signal Transduction ; T-Lymphocyte Subsets/*immunology ; Transfection ; Tumor Cells, Cultured ; ZAP-70 Protein-Tyrosine Kinase
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    Genetic engineering. Safety concerns halt U.K. study (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kingman, S -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):748.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303287" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Advisory Committees ; Cells, Cultured ; *Containment of Biohazards ; *Genetic Engineering ; *Government Regulation ; Great Britain ; Humans ; *Oncogenes ; Simian virus 40/*genetics
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    Activity-dependent changes in the intrinsic properties of cultured neurons (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-13
    Description: Learning and memory arise through activity-dependent modifications of neural circuits. Although the activity dependence of synaptic efficacy has been studied extensively, less is known about how activity shapes the intrinsic electrical properties of neurons. Lobster stomatogastric ganglion neurons fire in bursts when receiving synaptic and modulatory input but fire tonically when pharmacologically isolated. Long-term isolation in culture changed their intrinsic activity from tonic firing to burst firing. Rhythmic stimulation reversed this transition through a mechanism that was mediated by a rise in intracellular calcium concentration. These data suggest that neurons regulate their conductances to maintain stable activity patterns and that the intrinsic properties of a neuron depend on its recent history of activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turrigiano, G -- Abbott, L F -- Marder, E -- MH46742/MH/NIMH NIH HHS/ -- NS17813/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 May 13;264(5161):974-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Brandeis University, Waltham, MA 02254.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178157" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/physiology ; Cells, Cultured ; Egtazic Acid/analogs & derivatives/pharmacology ; Electric Stimulation ; Electrophysiology ; Ganglia, Invertebrate/cytology ; Membrane Potentials ; Nephropidae ; Neurites/physiology ; Neurons/cytology/*physiology ; Synapses/physiology
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    A protein phosphatase 2C involved in ABA signal transduction in Arabidopsis thaliana (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-03
    Description: The plant hormone abscisic acid (ABA) mediates various responses such as stomatal closure, the maintenance of seed dormancy, and the inhibition of plant growth. All three responses are affected in the ABA-insensitive mutant abi1 of Arabidopsis thaliana, suggesting that an early step in the signaling of ABA is controlled by the ABI1 locus. The ABI1 gene was cloned by chromosome walking, and a missense mutation was identified in the structural gene of the abi1 mutant. The ABI1 gene encodes a protein with high similarity to protein serine or threonine phosphatases of type 2C with the novel feature of a putative Ca2+ binding site. Thus, the control of the phosphorylation state of cell signaling components by the ABI1 product could mediate pleiotropic hormone responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer, K -- Leube, M P -- Grill, E -- New York, N.Y. -- Science. 1994 Jun 3;264(5164):1452-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Plant Sciences, Swiss Federal Institute of Technology, Zurich.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8197457" target="_blank"〉PubMed〈/a〉
    Keywords: Abscisic Acid/*pharmacology ; Amino Acid Sequence ; Arabidopsis/enzymology/genetics/*metabolism ; *Arabidopsis Proteins ; Binding Sites ; Calcium/metabolism ; Chromosome Walking ; Cloning, Molecular ; Genes, Plant ; Genetic Markers ; Molecular Sequence Data ; Mutation ; Phosphoprotein Phosphatases/chemistry/genetics/*metabolism ; Plants, Genetically Modified ; *Signal Transduction
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    An interleukin-4-induced transcription factor: IL-4 Stat (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-16
    Description: Interleukin-4 (IL-4) is an immunomodulatory cytokine secreted by activated T lymphocytes, basophils, and mast cells. It plays an important role in modulating the balance of T helper (Th) cell subsets, favoring expansion of the Th2 lineage relative to Th1. Imbalance of these T lymphocyte subsets has been implicated in immunological diseases including allergy, inflammation, and autoimmune disease. IL-4 may mediate its biological effects, at least in part, by activating a tyrosine-phosphorylated DNA binding protein. This protein has now been purified and its encoding gene cloned. Examination of the primary amino acid sequence of this protein indicates that it is a member of the signal transducers and activators of transcription (Stat) family of DNA binding proteins, hereby designated IL-4 Stat. Study of the inhibitory activities of phosphotyrosine-containing peptides derived from the intracellular domain of the IL-4 receptor provided evidence for direct coupling of receptor and transcription factor during the IL-4 Stat activation cycle. Such observations indicate that IL-4 Stat has the same functional domain for both receptor coupling and dimerization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hou, J -- Schindler, U -- Henzel, W J -- Ho, T C -- Brasseur, M -- McKnight, S L -- New York, N.Y. -- Science. 1994 Sep 16;265(5179):1701-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tularik, Inc., South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8085155" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Cloning, Molecular ; Cross-Linking Reagents ; DNA/metabolism ; DNA-Binding Proteins/chemistry/genetics/isolation & purification/*metabolism ; Humans ; Interleukin-4/*pharmacology ; Interleukin-4 Receptor alpha Subunit ; Models, Biological ; Molecular Sequence Data ; Monocytes/metabolism ; Phosphopeptides/metabolism/pharmacology ; Phosphorylation ; Polymers ; Receptors, Cell Surface ; Receptors, Interleukin-4 ; Receptors, Mitogen/*metabolism ; STAT6 Transcription Factor ; Trans-Activators/chemistry/genetics/isolation & purification/*metabolism ; Transcription Factors/chemistry/genetics/*metabolism
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    Prevention of vertebrate neuronal death by the crmA gene (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-11
    Description: Interleukin-1 beta converting enzyme (ICE) is a mammalian homolog of CED-3, a protein required for programmed cell death in the nematode Caenorhabditis elegans. The activity of ICE can be specifically inhibited by the product of crmA, a cytokine response modifier gene encoded by cowpox virus. Microinjection of the crmA gene into chicken dorsal root ganglion neurons was found to prevent cell death induced by deprivation of nerve growth factor. Thus, ICE is likely to participate in neuronal death in vertebrates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gagliardini, V -- Fernandez, P A -- Lee, R K -- Drexler, H C -- Rotello, R J -- Fishman, M C -- Yuan, J -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):826-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research Center, Massachusetts General Hospital, Charlestown 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303301" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caspase 1 ; Cells, Cultured ; Chickens ; Ganglia, Spinal ; Gene Expression ; Metalloendopeptidases/*genetics/physiology ; Microinjections ; Nerve Growth Factors/pharmacology ; Neurons, Afferent/*cytology/metabolism ; Proto-Oncogene Proteins/genetics/physiology ; Proto-Oncogene Proteins c-bcl-2 ; Serpins/*genetics/physiology ; *Viral Proteins
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  • 39
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    Reconstitution of transcription factor SL1: exclusive binding of TBP by SL1 or TFIID subunits (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-23
    Description: RNA polymerase I and II transcription factors SL1 and TFIID, respectively, are composed of the TATA-binding protein (TBP) and a set of TBP-associated factors (TAFs) responsible for promoter recognition. How the universal transcription factor TBP becomes committed to a TFIID or SL1 complex has not been known. Complementary DNAs encoding each of the three TAFIs that are integral components of SL1 have not been isolated. Analysis of subunit interactions indicated that the three TAFIs can bind individually and specifically to TBP. In addition, these TAFIs interact with each other to form a stable TBP-TAF complex. When TBP was bound first by either TAFI110, 63, or 48, subunits of TFIID such as TAFII250 and 150 did not bind TBP. Conversely, if TBP first formed a complex with TAFII250 or 150, the subunits of SL1 did not bind TBP. These results suggest that a mutually exclusive binding specificity for TBP intrinsic to SL1 and TFIID subunits directs the formation of promoter- and RNA polymerase-selective TBP-TAF complexes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Comai, L -- Zomerdijk, J C -- Beckmann, H -- Zhou, S -- Admon, A -- Tjian, R -- New York, N.Y. -- Science. 1994 Dec 23;266(5193):1966-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular and Cell Biology, University of California at Berkeley 94720-3204.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7801123" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Binding, Competitive ; Cloning, Molecular ; DNA, Complementary/genetics ; DNA-Binding Proteins/chemistry/genetics/isolation & purification/*metabolism ; HeLa Cells ; Humans ; Molecular Sequence Data ; *Pol1 Transcription Initiation Complex Proteins ; Promoter Regions, Genetic ; Protein Binding ; RNA Polymerase I/metabolism ; TATA Box ; *TATA-Binding Protein Associated Factors ; TATA-Box Binding Protein ; Transcription Factor TFIID ; Transcription Factors/chemistry/genetics/isolation & purification/*metabolism ; Transcription, Genetic
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    Stimulation of human gamma delta T cells by nonpeptidic mycobacterial ligands (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-08
    Description: Most human peripheral blood gamma delta T lymphocytes respond to hitherto unidentified mycobacterial antigens. Four ligands from Mycobacterium tuberculosis strain H37Rv that stimulated proliferation of a major human gamma delta T cell subset were isolated and partially characterized. One of these ligands, TUBag4, is a 5' triphosphorylated thymidine-containing compound, to which the three other stimulatory molecules are structurally related. These findings support the hypothesis that some gamma delta T cells recognize nonpeptidic ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Constant, P -- Davodeau, F -- Peyrat, M A -- Poquet, Y -- Puzo, G -- Bonneville, M -- Fournie, J J -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):267-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department III, Laboratoire de Pharmacologie et de Toxicologie Fondamentales du CNRS, Toulouse, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146660" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Bacterial/chemistry/*immunology/isolation & purification ; Cells, Cultured ; Chromatography, Ion Exchange ; Humans ; Ligands ; *Lymphocyte Activation ; Magnetic Resonance Spectroscopy ; Mycobacterium tuberculosis/*immunology ; Receptors, Antigen, T-Cell, gamma-delta/*immunology ; T-Lymphocyte Subsets/*immunology ; Thymine Nucleotides/analysis/chemistry/*immunology/isolation & purification
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    DNA repair rates mapped along the human PGK1 gene at nucleotide resolution (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-11
    Description: The repair of cyclobutane pyrimidine dimers (CPDs), DNA lesions induced by ultraviolet light, was studied at nucleotide resolution. Human fibroblasts were irradiated with ultraviolet light and allowed to repair. The DNA was enzymatically cleaved at the CPDs, and the induced breaks along the promoter and exon 1 of the PGK1 gene were mapped by ligation-mediated polymerase chain reaction. Repair rates within the nontranscribed strand varied as much as 15-fold, depending on nucleotide position. Preferential repair of the transcribed strand began just downstream of the transcription start site but was most pronounced beginning at nucleotide +140 in exon 1. The promoter contained two slowly repaired regions that coincided with two transcription factor binding sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gao, S -- Drouin, R -- Holmquist, G P -- CA54773/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1438-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beckman Research Institute of the City of Hope, Department of Biology, Duarte, CA 91010.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128226" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cells, Cultured ; *DNA Repair ; Exons ; *Genes ; HeLa Cells ; Humans ; Kinetics ; Phosphoglycerate Kinase/*genetics ; Promoter Regions, Genetic ; Pyrimidine Dimers/*metabolism ; Skin/metabolism/*radiation effects ; Transcription Factors/metabolism ; Transcription, Genetic ; Ultraviolet Rays
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  • 42
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    RPS2 of Arabidopsis thaliana: a leucine-rich repeat class of plant disease resistance genes (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-23
    Description: Plant disease resistance genes function is highly specific pathogen recognition pathways. PRS2 is a resistance gene of Arabidopsis thaliana that confers resistance against Pseudomonas syringae bacteria that express avirulence gene avrRpt2. RPS2 was isolated by the use of a positional cloning strategy. The derived amino acid sequence of RPS2 contains leucine-rich repeat, membrane-spanning, leucine zipper, and P loop domains. The function of the RPS2 gene product in defense signal transduction is postulated to involve nucleotide triphosphate binding and protein-protein interactions and may also involve the reception of an elicitor produced by the avirulent pathogen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bent, A F -- Kunkel, B N -- Dahlbeck, D -- Brown, K L -- Schmidt, R -- Giraudat, J -- Leung, J -- Staskawicz, B J -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1856-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091210" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Arabidopsis/*genetics/microbiology ; *Arabidopsis Proteins ; Chromosome Mapping ; Cloning, Molecular ; Cosmids ; DNA, Complementary/genetics ; Genes, Bacterial ; *Genes, Plant ; Leucine Zippers ; Molecular Sequence Data ; Phenotype ; Plant Diseases/*genetics ; Plant Proteins/chemistry/*genetics ; Pseudomonas/genetics/pathogenicity ; Signal Transduction ; Virulence
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    T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-25
    Description: Encounters with antigen can stimulate T cells to become activated and proliferate, become nonresponsive to antigen, or to die. T cell death was shown to be a physiological response to interleukin-2-stimulated cell cycling and T cell receptor reengagement at high antigen doses. This feedback regulatory mechanism attenuates the immune response by deleting a portion of newly dividing, antigen-reactive T cells. This mechanism deleted autoreactive T cells and abrogated the clinical and pathological signs of autoimmune encephalomyelitis in mice after repetitive administration of myelin basic protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Critchfield, J M -- Racke, M K -- Zuniga-Pflucker, J C -- Cannella, B -- Raine, C S -- Goverman, J -- Lenardo, M J -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1139-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7509084" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*immunology ; Apoptosis ; CD4-Positive T-Lymphocytes/*immunology ; Cell Division ; Cells, Cultured ; Cytochrome c Group/immunology ; Dose-Response Relationship, Immunologic ; Encephalomyelitis, Autoimmune, Experimental/*immunology/pathology/therapy ; *Immune Tolerance ; Immunotherapy ; Interleukin-2/immunology/pharmacology ; Lymphocyte Activation ; Mice ; Mice, Transgenic ; Myelin Basic Protein/immunology ; Myelin Sheath/immunology/pathology ; Spinal Cord/pathology ; T-Lymphocytes/*immunology
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    Requirement for BDNF in activity-dependent survival of cortical neurons (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-03-18
    Description: Cultured embryonic cortical neurons from rats were used to explore mechanisms of activity-dependent neuronal survival. Cell survival was increased by the activation of voltage-sensitive calcium channels (VSCCs) but not by activation of N-methyl-D-aspartate receptors. These effects correlated with the expression of brain-derived neurotrophic factor (BDNF) induced by these two classes of calcium channels. Antibodies to BDNF (which block intracellular signaling by BDNF, but not by nerve growth factor, NT3, or NT4/5) reduced the survival of cortical neurons and reversed the VSCC-mediated increase in survival. Thus, endogenous BDNF is a trophic factor for cortical neurons whose expression is VSCC-regulated and that functions in the VSCC-dependent survival of these neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ghosh, A -- Carnahan, J -- Greenberg, M E -- NS28829/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 18;263(5153):1618-23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7907431" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Brain-Derived Neurotrophic Factor ; Calcium Channels/*physiology ; Cell Division/drug effects ; Cell Survival/drug effects ; Cells, Cultured ; Cerebral Cortex/*cytology ; Cyclic AMP Response Element-Binding Protein/metabolism ; Embryo, Mammalian ; Glutamates/pharmacology ; Glutamic Acid ; N-Methylaspartate/pharmacology ; Nerve Growth Factors/biosynthesis/genetics/immunology/*physiology ; Nerve Tissue Proteins/biosynthesis/genetics/immunology/*physiology ; Neurons/*cytology ; Phosphorylation ; Potassium Chloride/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/physiology ; Signal Transduction
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    Suppression of hyphal formation in Candida albicans by mutation of a STE12 homolog (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-09
    Description: A Candida albicans gene (CPH1) was cloned that encodes a protein homologous to Saccharomyces cerevisiae Ste12p, a transcription factor that is the target of the pheromone response mitogen-activated protein kinase cascade. CPH1 complements both the mating defect of ste12 haploids and the filamentous growth defect of ste12/ste12 diploids. Candida albicans strains without a functional CPH1 gene (cph1/cph1) show suppressed hyphal formation on solid medium. However, cph1/cph1 strains can still form hyphae in liquid culture and in response to serum. Thus, filamentous growth may be activated in C. albicans by the same signaling kinase cascade that activates Ste12p in S. cerevisiae; however, alternative pathways may exist in C. albicans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, H -- Kohler, J -- Fink, G R -- GM402661/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1723-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7992058" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Candida albicans/cytology/genetics/*growth & development ; Cloning, Molecular ; Culture Media ; Fungal Proteins/chemistry/*genetics/physiology ; *Genes, Fungal ; Genetic Complementation Test ; Molecular Sequence Data ; Mutation ; Saccharomyces cerevisiae/cytology/genetics/growth & development ; *Saccharomyces cerevisiae Proteins ; Transcription Factors/chemistry/*genetics/physiology
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    The TATA-binding protein: a general transcription factor in eukaryotes and archaebacteria (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-05-27
    Description: The TATA-binding protein TBP appears to be essential for all transcription in eukaryotic cell nuclei, which suggests that its function was established early in evolution. Archaebacteria constitute a kingdom of organisms distinct from eukaryotes and eubacteria. Archaebacterial gene regulatory sequences often map to TATA box-like motifs. Here it is shown that the archaebacterium Pyrococcus woesei expresses a protein with structural and functional similarity to eukaryotic TBP molecules. This suggests that TBP's role in transcription was established before the archaebacterial and eukaryotic lineages diverged and that the transcription systems of archaebacteria and eukaryotes are fundamentally homologous.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rowlands, T -- Baumann, P -- Jackson, S P -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1994 May 27;264(5163):1326-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome/CRC Institute, Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8191287" target="_blank"〉PubMed〈/a〉
    Keywords: Adenovirus E1A Proteins/genetics ; Amino Acid Sequence ; Arabidopsis/genetics ; Archaea/chemistry/*genetics/metabolism ; Base Sequence ; *Biological Evolution ; Cloning, Molecular ; DNA-Binding Proteins/chemistry/*genetics/metabolism ; Eukaryotic Cells/*metabolism ; Genes, Bacterial ; Molecular Sequence Data ; Polymerase Chain Reaction ; Recombinant Fusion Proteins ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae Proteins ; *TATA Box ; TATA-Box Binding Protein ; Transcription Factor TFIIB ; *Transcription Factor TFIIIB ; Transcription Factors/chemistry/*genetics/metabolism ; Transcription, Genetic ; Tumor Suppressor Protein p53/genetics
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    Specification of pore properties by the carboxyl terminus of inwardly rectifying K+ channels (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-06
    Description: Inwardly rectifying potassium (K+) channels (IRKs) maintain the resting membrane potential of cells and permit prolonged depolarization, such as during the cardiac action potential. Inward rectification may result from block of the ion conduction pore by intracellular magnesium (Mgi2+). Two members of this family, IRK1 and ROMK1, which share 40 percent amino acid identity, differ markedly in single-channel K+ conductance and sensitivity to block by Mgi2+. The conserved H5 regions were hypothesized to determine these pore properties because they have this function in voltage-dependent K+ channels and in cyclic nucleotide-gated channels. However, exchange of the H5 region between IRK1 and ROMK1 had no effect on rectification and little or no effect on K+ conductance. By contrast, exchange of the amino- and carboxyl-terminal regions together transferred Mg2+ blockade and K+ conductance of IRK1 to ROMK1. Exchange of the carboxyl but not the amino terminus had a similar effect. Therefore, the carboxyl terminus appears to have a major role in specifying the pore properties of IRKs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taglialatela, M -- Wible, B A -- Caporaso, R -- Brown, A M -- HL36930/HL/NHLBI NIH HHS/ -- HL37044/HL/NHLBI NIH HHS/ -- NS23877/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 May 6;264(5160):844-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171340" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Cloning, Molecular ; Electric Conductivity ; Ion Channel Gating ; Magnesium/*metabolism/pharmacology ; Membrane Potentials ; Molecular Sequence Data ; Oocytes ; Potassium/*metabolism ; Potassium Channels/chemistry/*metabolism/*physiology ; *Potassium Channels, Inwardly Rectifying ; Recombinant Fusion Proteins/chemistry/metabolism ; Sequence Alignment ; Xenopus
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  • 48
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    Splicing of the rolA transcript of Agrobacterium rhizogenes in Arabidopsis (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-23
    Description: The rolA gene encoded on the Ri plasmid A4 of Agrobacterium rhizogenes is one of the transferred (TL-DNA) genes involved in the pathogenesis of hairy-root disease in plants. The function of the 100-amino acid protein product of rolA is unknown, although its expression causes physiological and developmental alterations in transgenic plants. The rolA gene of A. rhizogenes contains an intron in its untranslated leader region that has features typical of plant pre-messenger RNA introns. Transcription and splicing of the rolA pre-messenger RNA occur in the plant cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Magrelli, A -- Langenkemper, K -- Dehio, C -- Schell, J -- Spena, A -- New York, N.Y. -- Science. 1994 Dec 23;266(5193):1986-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Plank-Institut fur Zuchtungsforschung, Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7528444" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*genetics/microbiology ; Base Sequence ; Cloning, Molecular ; DNA, Bacterial/genetics ; Genes, Bacterial ; Introns ; Molecular Sequence Data ; Mutation ; Plants, Genetically Modified ; *Plasmids ; RNA Precursors/*genetics ; *RNA Splicing ; RNA, Bacterial/*genetics ; Rhizobium/*genetics ; Transcription, Genetic
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    cDNA cloning and interferon gamma down-regulation of proteasomal subunits X and Y (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-08-26
    Description: Proteasomes are the proteolytic complex responsible for major histocompatibility complex (MHC) class I-restricted antigen presentation. Interferon gamma treatment increases expression MHC-encoded LMP2 and LMP7 subunits of the proteasome and decreases expression of two proteasome subunits, named X and Y, which alters the proteolytic specificity of proteasomes. Molecular cloning of complementary DNAs encoding X and Y showed that their proteins are proteasomal subunits with high amino acid similarity to LMP7 and LMP2, respectively. Thus, interferon gamma may induce subunit replacements of X and Y by LMP7 and LMP2, respectively, producing proteasomes perhaps more appropriate for the immunological processing of endogenous antigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akiyama, K -- Yokota, K -- Kagawa, S -- Shimbara, N -- Tamura, T -- Akioka, H -- Nothwang, H G -- Noda, C -- Tanaka, K -- Ichihara, A -- New York, N.Y. -- Science. 1994 Aug 26;265(5176):1231-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Urology, School of Medicine, University of Tokushima, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8066462" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cloning, Molecular ; *Cysteine Endopeptidases ; DNA, Complementary/genetics ; *Down-Regulation ; Endopeptidases/chemistry/genetics ; Humans ; Interferon-gamma/*pharmacology ; Major Histocompatibility Complex ; Molecular Sequence Data ; *Multienzyme Complexes ; *Proteasome Endopeptidase Complex ; Proteins/chemistry/*genetics/metabolism ; Sequence Homology, Amino Acid ; Tumor Cells, Cultured
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    Cloning of a Grb2 isoform with apoptotic properties (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-13
    Description: Growth factor receptor-bound protein 2 (Grb2) links tyrosine-phosphorylated proteins to a guanine nucleotide releasing factor of the son of sevenless (Sos) class by attaching to the former by its Src homology 2 (SH2) moiety and to the latter by its SH3 domains. An isoform of grb2 complementary DNA (cDNA) was cloned that has a deletion in the SH2 domain. The protein encoded by this cDNA, Grb3-3, did not bind to phosphorylated epidermal growth factor receptor (EGFR) but retained functional SH3 domains and inhibited EGF-induced transactivation of a Ras-responsive element. The messenger RNA encoding Grb3-3 was expressed in high amounts in the thymus of rats at an age when massive negative selection of thymocytes occurs. Microinjection of Grb3-3 into Swiss 3T3 fibroblasts induced apoptosis. These findings indicate that Grb3-3, by acting as a dominant negative protein over Grb2 and by suppressing proliferative signals, may trigger active programmed cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fath, I -- Schweighoffer, F -- Rey, I -- Multon, M C -- Boiziau, J -- Duchesne, M -- Tocque, B -- New York, N.Y. -- Science. 1994 May 13;264(5161):971-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rhone-Poulenc Rorer, Centre de Recherche de Vitry-Alfortville, Vitry sur Seine, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178156" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; *Apoptosis ; Base Sequence ; Cloning, Molecular ; Epidermal Growth Factor/pharmacology ; GRB2 Adaptor Protein ; Humans ; Mice ; Molecular Sequence Data ; Proteins/*genetics/metabolism ; RNA, Messenger/genetics/metabolism ; Rats ; Receptor, Epidermal Growth Factor/*metabolism ; T-Lymphocytes/cytology ; Thymus Gland/metabolism ; Transcriptional Activation/drug effects ; Transfection
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    Obesity gene discovery may help solve weighty problem (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-12-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1477-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985012" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism ; Agouti Signaling Protein ; Animals ; Body Weight ; Cloning, Molecular ; *Genes ; Hormones/genetics/metabolism ; Humans ; *Intercellular Signaling Peptides and Proteins ; Mice ; Mice, Obese/*genetics ; *Mutation ; Obesity/*genetics/therapy ; Proteins/genetics
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    Involvement of the IRF-1 transcription factor in antiviral responses to interferons (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-24
    Description: The mechanisms underlying interferon (IFN)-induced antiviral states are not well understood. Interferon regulatory factor-1 (IRF-1) is an IFN-inducible transcriptional activator, whereas IRF-2 suppresses IRF-1 action. The inhibition of encephalomyocarditis virus (EMCV) replication by IFN-alpha and especially by IFN-gamma was impaired in cells from mice with a null mutation in the IRF-1 gene (IRF-1-/- mice). The IRF-1-/- mice were less resistant than normal mice to EMCV infection, as revealed by accelerated mortality and a larger virus titer in target organs. The absence of IRF-1 did not clearly affect replication of two other types of viruses. Thus, IRF-1 is necessary for the antiviral action of IFNs against some viruses, but IFNs activate multiple activation pathways through diverse target genes to induce the antiviral state.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kimura, T -- Nakayama, K -- Penninger, J -- Kitagawa, M -- Harada, H -- Matsuyama, T -- Tanaka, N -- Kamijo, R -- Vilcek, J -- Mak, T W -- R35CA49731/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1921-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular and Cellular Biology, Osaka University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009222" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiovirus Infections/*immunology/microbiology ; Cells, Cultured ; DNA-Binding Proteins/genetics/*physiology ; Encephalomyocarditis virus/physiology ; Gene Expression Regulation ; Interferon Regulatory Factor-1 ; Interferon-alpha/*pharmacology ; Interferon-gamma/*pharmacology ; Mice ; Mutation ; Phosphoproteins/genetics/*physiology ; Simplexvirus/physiology ; Transcription Factors/genetics/*physiology ; Vesicular stomatitis Indiana virus/physiology ; *Virus Replication
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Attractive axon guidance molecules (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baier, H -- Bonhoeffer, F -- New York, N.Y. -- Science. 1994 Sep 9;265(5178):1541-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Entwicklungsbiologie, Tubingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8079167" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Caenorhabditis elegans ; *Caenorhabditis elegans Proteins ; Cell Movement ; Chick Embryo ; Cloning, Molecular ; Helminth Proteins/genetics/metabolism ; Nerve Growth Factors/chemistry/genetics/*physiology ; *Nerve Tissue Proteins ; Rats ; Tumor Suppressor Proteins
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    Genetic dissection of complex traits (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-30
    Description: Medical genetics was revolutionized during the 1980s by the application of genetic mapping to locate the genes responsible for simple Mendelian diseases. Most diseases and traits, however, do not follow simple inheritance patterns. Genetics have thus begun taking up the even greater challenge of the genetic dissection of complex traits. Four major approaches have been developed: linkage analysis, allele-sharing methods, association studies, and polygenic analysis of experimental crosses. This article synthesizes the current state of the genetic dissection of complex traits--describing the methods, limitations, and recent applications to biological problems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lander, E S -- Schork, N J -- HG00098/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 30;265(5181):2037-48.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091226" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; *Chromosome Mapping ; Cloning, Molecular ; Crosses, Genetic ; Female ; Genetic Linkage ; Genetic Markers ; *Genetic Predisposition to Disease ; Genetics, Medical/*methods ; Genotype ; Humans ; Male ; Pedigree ; Phenotype ; Research Design
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    inhA, a gene encoding a target for isoniazid and ethionamide in Mycobacterium tuberculosis (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-14
    Description: Isoniazid (isonicotinic acid hydrazide, INH) is one of the most widely used antituberculosis drugs, yet its precise target of action on Mycobacterium tuberculosis is unknown. A missense mutation within the mycobacterial inhA gene was shown to confer resistance to both INH and ethionamide (ETH) in M. smegmatis and in M. bovis. The wild-type inhA gene also conferred INH and ETH resistance when transferred on a multicopy plasmid vector to M. smegmatis and M. bovis BCG. The InhA protein shows significant sequence conservation with the Escherichia coli enzyme EnvM, and cell-free assays indicate that it may be involved in mycolic acid biosynthesis. These results suggest that InhA is likely a primary target of action for INH and ETH.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Banerjee, A -- Dubnau, E -- Quemard, A -- Balasubramanian, V -- Um, K S -- Wilson, T -- Collins, D -- de Lisle, G -- Jacobs, W R Jr -- AI27160/AI/NIAID NIH HHS/ -- UO1AI30189/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Jan 14;263(5144):227-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Albert Einstein College of Medicine, Bronx, NY 10461.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8284673" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacterial Proteins/chemistry/*genetics ; Base Sequence ; Cloning, Molecular ; Drug Resistance, Microbial/*genetics ; Ethionamide/metabolism/*pharmacology ; *Genes, Bacterial ; Isoniazid/metabolism/*pharmacology ; Molecular Sequence Data ; Mutation ; Mycobacterium/drug effects/genetics ; Mycobacterium bovis/drug effects/genetics ; Mycobacterium tuberculosis/chemistry/drug effects/*genetics/metabolism ; Mycolic Acids/metabolism ; Open Reading Frames ; *Oxidoreductases ; Sequence Alignment
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    Zinc finger phage: affinity selection of fingers with new DNA-binding specificities (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-04
    Description: A phage display system was developed and used to select zinc finger proteins with altered DNA-binding specificities. The three zinc fingers of the Zif268 protein were expressed on the surface of filamentous phage, and a library of variants was prepared by randomizing critical amino acids in the first zinc finger. Affinity selections, using DNA sites with base changes in the region recognized by the first finger, yielded Zif268 variants that bound tightly and specifically to the new sites. This phage system provides a tool for the study of protein-DNA interactions and may offer a general method for selecting zinc finger proteins that recognize desired target sites on double-stranded DNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rebar, E J -- Pabo, C O -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):671-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303274" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacteriophages/genetics ; Base Sequence ; Cloning, Molecular ; DNA/*metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Genetic Variation ; Genetic Vectors ; Molecular Sequence Data ; Protein Binding ; Transcription Factors/chemistry/genetics/*metabolism ; Zinc Fingers/genetics/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Control of topographic retinal axon branching by inhibitory membrane-bound molecules (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-05
    Description: Retinotopic map development in nonmammalian vertebrates appears to be controlled by molecules that guide or restrict retinal axons to correct locations in their targets. However, the retinotopic map in the superior colliculus (SC) of the rat is developed instead by a topographic bias in collateral branching and arborization. Temporal retinal axons extending across alternating membranes from the topographically correct rostral SC or the incorrect caudal SC of embryonic rats preferentially branch on rostral membranes. Branching preference is due to an inhibitory phosphatidylinositol-linked molecule in the caudal SC. Thus, position-encoding membrane-bound molecules may establish retinotopic maps in mammals by regulating axon branching, not by directing axon growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roskies, A L -- O'Leary, D D -- NEI RO1 EY07025/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 5;265(5173):799-803.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory, Salk Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8047886" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Carbocyanines ; Cells, Cultured ; Embryonic and Fetal Development/physiology ; Fluorescent Dyes ; Phosphatidylinositol Diacylglycerol-Lyase ; Phosphoric Diester Hydrolases ; Rats ; Rats, Sprague-Dawley ; Retinal Ganglion Cells/*physiology ; Superior Colliculi/embryology
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    Anergic T cells as suppressor cells in vitro (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: T cell-mediated suppression is an established phenomenon, but its underlying mechanisms are obscure. An in vitro system was used to test the possibility that anergic T cells can act as specific suppressor cells. Anergic human T cells caused inhibition of antigen-specific and allospecific T cell proliferation. In order for the inhibition to occur, the anergic T cells had to be specific for the same antigen-presenting cells (APCs) as the T cells that were suppressed. The mechanism of this suppression appears to be competition for the APC surface and for locally produced interleukin-2.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lombardi, G -- Sidhu, S -- Batchelor, R -- Lechler, R -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1587-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Royal Postgraduate Medical School, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202711" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen-Presenting Cells/immunology ; Cell Line ; Cells, Cultured ; *Clonal Anergy ; Humans ; Interleukin-10/immunology ; Interleukin-2/immunology/secretion ; Interleukin-4/immunology ; Lymphocyte Activation ; Recombinant Proteins/immunology ; T-Lymphocytes, Helper-Inducer/*immunology ; T-Lymphocytes, Regulatory/*immunology ; Transforming Growth Factor beta/immunology
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    Generation of lymphohematopoietic cells from embryonic stem cells in culture (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-19
    Description: An efficient system was developed that induced the differentiation of embryonic stem (ES) cells into blood cells of erythroid, myeloid, and B cell lineages by coculture with the stromal cell line OP9. This cell line does not express functional macrophage colony-stimulating factor (M-CSF). The presence of M-CSF had inhibitory effects on the differentiation of ES cells to blood cells other than macrophages. Embryoid body formation or addition of exogenous growth factors was not required, and differentiation was highly reproducible even after the selection of ES cells with the antibiotic G418. Combined with the ability to genetically manipulate ES cells, this system will facilitate the study of molecular mechanisms involved in development and differentiation of hematopoietic cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakano, T -- Kodama, H -- Honjo, T -- New York, N.Y. -- Science. 1994 Aug 19;265(5175):1098-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry, Faculty of Medicine, Kyoto University Yoshida, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8066449" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/cytology ; Base Sequence ; Cell Differentiation ; Cell Line ; Cells, Cultured ; Culture Media ; Erythrocytes/cytology ; Erythropoiesis ; Gene Rearrangement ; *Hematopoiesis ; Hematopoietic Stem Cells/*cytology ; Lymphocytes/*cytology ; Macrophage Colony-Stimulating Factor/pharmacology ; Macrophages/cytology ; Mesoderm/cytology ; Mice ; Molecular Sequence Data ; Recombinant Proteins/pharmacology ; Stromal Cells/cytology
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    Differential effects of apolipoproteins E3 and E4 on neuronal growth in vitro (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-06
    Description: Apolipoprotein E4 (apoE4), one of the three common isoforms of apoE, has been implicated in Alzheimer's disease. The effects of apoE on neuronal growth were determined in cultures of dorsal root ganglion neurons. In the presence of beta-migrating very low density lipoproteins (beta-VLDL), apoE3 increased neurite outgrowth, whereas apoE4 decreased outgrowth. The effects of apoE3 or apoE4 in the presence of beta-VLDL were prevented by incubation with a monoclonal antibody to apoE or by reductive methylation of apoE, both of which block the ability of apoE to interact with lipoprotein receptors. The data suggest that receptor-mediated binding or internalization (or both) of apoE-enriched beta-VLDL leads to isoform-specific differences in interactions with cellular proteins that affect neurite outgrowth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nathan, B P -- Bellosta, S -- Sanan, D A -- Weisgraber, K H -- Mahley, R W -- Pitas, R E -- HL 41633/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 May 6;264(5160):850-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Cardiovascular Disease, University of California, San Francisco 94141-9100.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171342" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoprotein E3 ; Apolipoprotein E4 ; Apolipoproteins E/metabolism/*pharmacology ; Cells, Cultured ; Culture Media, Serum-Free ; Fetus ; Ganglia, Spinal ; Lipoproteins, VLDL/pharmacology ; Neurites/*drug effects/ultrastructure ; Neurons/cytology/*drug effects ; Rabbits ; Receptors, LDL/metabolism
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    iaglu, a gene from Zea mays involved in conjugation of growth hormone indole-3-acetic acid (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-16
    Description: Plants contain most of the growth hormone indole-3-acetic acid (IAA) in conjugated forms believed to be inactive in promoting growth. The iaglu gene, which controls the first step in the biosynthesis of the IAA conjugates of Zea mays, encodes (uridine 5'-diphosphate-glucose:indol-3-ylacetyl)-beta-D-glucosyl transferase. Protein synthesized by Escherichia coli that contained cloned 1-O-beta-D-indol-3-ylacetyl-glucose complementary DNA (cDNA) was catalytically active. The predicted amino acid sequence of the cDNA was confirmed by amino-terminal sequencing of the purified enzyme. Homologous nucleotide sequences were found in all plants tested. The blockage or enhancement of iaglu expression may permit regulation of plant growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Szerszen, J B -- Szczyglowski, K -- Bandurski, R S -- New York, N.Y. -- Science. 1994 Sep 16;265(5179):1699-701.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Botany and Plant Pathology, Michigan State University, East Lansing 48824.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8085154" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cloning, Molecular ; DNA, Complementary ; Escherichia coli/genetics ; *Genes, Plant ; Genome ; Glucosyltransferases/chemistry/*genetics/metabolism ; Glycosylation ; Indoleacetic Acids/*metabolism ; Molecular Sequence Data ; Phosphorylation ; Recombinant Proteins/metabolism ; Sequence Alignment ; Zea mays/*genetics/metabolism
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    Control of angiogenesis in fibroblasts by p53 regulation of thrombospondin-1 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-09
    Description: As normal cells progress toward malignancy, they must switch to an angiogenic phenotype to attract the nourishing vasculature that they depend on for their growth. In cultured fibroblasts from Li-Fraumeni patients, this switch was found to coincide with loss of the wild-type allele of the p53 tumor suppressor gene and to be the result of reduced expression of thrombospondin-1 (TSP-1), a potent inhibitor of angiogenesis. Transfection assays revealed that p53 can stimulate the endogenous TSP-1 gene and positively regulate TSP-1 promoter sequences. These data indicate that, in fibroblasts, wild-type p53 inhibits angiogenesis through regulation of TSP-1 synthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dameron, K M -- Volpert, O V -- Tainsky, M A -- Bouck, N -- CA52750/CA/NCI NIH HHS/ -- CA64239/CA/NCI NIH HHS/ -- P01 CA34936/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Sep 9;265(5178):1582-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology-Immunology, Northwestern University Medical School, Chicago, IL 60611.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7521539" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Cells, Cultured ; Fibroblasts/*metabolism ; *Gene Expression Regulation ; *Genes, p53 ; Humans ; Li-Fraumeni Syndrome ; Membrane Glycoproteins/biosynthesis/*genetics/physiology ; *Neovascularization, Pathologic ; Phenotype ; Promoter Regions, Genetic ; Thrombospondins ; Transfection
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    Ku80: product of the XRCC5 gene and its role in DNA repair and V(D)J recombination (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-02
    Description: The radiosensitive mutant xrs-6, derived from Chinese hamster ovary cells, is defective in DNA double-strand break repair and in ability to undergo V(D)J recombination. The human XRCC5 DNA repair gene, which complements this mutant, is shown here through genetic and biochemical evidence to be the 80-kilodalton subunit of the Ku protein. Ku binds to free double-stranded DNA ends and is the DNA-binding component of the DNA-dependent protein kinase. Thus, the Ku protein is involved in DNA repair and in V(D)J recombination, and these results may also indicate a role for the Ku-DNA-dependent protein kinase complex in those same processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taccioli, G E -- Gottlieb, T M -- Blunt, T -- Priestley, A -- Demengeot, J -- Mizuta, R -- Lehmann, A R -- Alt, F W -- Jackson, S P -- Jeggo, P A -- AI 20047/AI/NIAID NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1442-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Children's Hospital, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073286" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, Nuclear ; Base Sequence ; CHO Cells ; Cell Survival/radiation effects ; Cloning, Molecular ; Cricetinae ; DNA Damage ; *DNA Helicases ; DNA Repair/*genetics ; DNA-Binding Proteins/*genetics/metabolism ; *Genes, Immunoglobulin ; Genetic Complementation Test ; Humans ; Hybrid Cells ; Molecular Sequence Data ; Nuclear Proteins/*genetics/metabolism ; Receptors, Antigen, T-Cell/*genetics ; *Recombination, Genetic ; Transfection
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    Ability of HIV to promote a TH1 to TH0 shift and to replicate preferentially in TH2 and TH0 cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-08
    Description: Both interferon gamma (IFN-gamma) produced by T helper 1 (TH1) lymphocytes and interleukin-4 (IL-4) produced by TH2 lymphocytes were reduced in either bulk circulating mononuclear cells or mitogen-induced CD4+ T cell clones from the peripheral blood of individuals infected with human immunodeficiency virus (HIV). There was a preferential reduction in clones producing IL-4 and IL-5 in the advanced phases of infection. However, enhanced proportions of CD4+ T cell clones producing both TH1-type and TH2-type cytokines (TH0 clones) were generated from either skin-infiltrating T cells that had been activated in vivo or peripheral blood T cells stimulated by antigen in vitro when cells were isolated from HIV-infected individuals. All TH2 and most TH0 clones supported viral replication, although viral replication was not detected in any of the TH1 clones infected in vitro with HIV. These results suggest that HIV (i) does not induce a definite TH1 to TH2 switch, but can favor a shift to the TH0 phenotype in response to recall antigens, and (ii) preferentially replicates in CD4+ T cells producing TH2-type cytokines (TH2 and TH0).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maggi, E -- Mazzetti, M -- Ravina, A -- Annunziato, F -- de Carli, M -- Piccinni, M P -- Manetti, R -- Carbonari, M -- Pesce, A M -- del Prete, G -- New York, N.Y. -- Science. 1994 Jul 8;265(5169):244-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Clinical Immunology and Allergy, University of Florence, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023142" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology ; Cell Line ; Cells, Cultured ; HIV/*physiology ; HIV Infections/*immunology/microbiology ; HIV Seropositivity/immunology ; Humans ; Immunologic Memory ; Interferon-gamma/*biosynthesis ; Interleukin-4/biosynthesis ; Interleukin-5/biosynthesis ; Interleukins/*biosynthesis ; Lymphocyte Activation ; Phenotype ; T-Lymphocytes, Helper-Inducer/*immunology/microbiology ; Virus Replication
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    Engineered biosynthesis of a complete macrolactone in a heterologous host (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-22
    Description: Macrocyclic polyketides have been subjects of great interest in synthetic and biosynthetic chemistry because of their structural complexity and medicinal activities. With expression of the entire 6-deoxyerythronolide B synthase (DEBS) (10,283 amino acids) in a heterologous host, substantial quantities of 6-deoxyerythronolide B (6dEB), the aglycone of the macrolide antibiotic erythromycin, and 8,8a-deoxyoleandolide, a 14-membered lactone ring identical to 6dEB except for a methyl group side chain in place of an ethyl unit, were synthesized in Streptomyces coelicolor. The biosynthetic strategy utilizes a genetic approach that facilitates rapid structural manipulation of DEBS or other modular polyketide synthases (PKSs), including those found in actinomycetes with poorly developed genetic methods. From a technological viewpoint, this approach should allow the rational design of biosynthetic products and may eventually lead to the generation of diverse polyketide libraries by means of combinatorial cloning of naturally occurring and mutant PKS modules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kao, C M -- Katz, L -- Khosla, C -- New York, N.Y. -- Science. 1994 Jul 22;265(5171):509-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical Engineering, Stanford University, CA 94305-5025.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036492" target="_blank"〉PubMed〈/a〉
    Keywords: Acyl Coenzyme A/metabolism ; Base Sequence ; Binding Sites ; Cloning, Molecular ; Drug Design ; Erythromycin/*analogs & derivatives/biosynthesis/isolation & purification ; Escherichia coli/genetics ; Genes, Bacterial ; Genetic Engineering ; Genetic Vectors ; Molecular Sequence Data ; Multienzyme Complexes/chemistry/*genetics/metabolism ; Multigene Family ; Mutation ; Oleandomycin/*analogs & derivatives/biosynthesis/isolation & purification ; Recombinant Proteins/metabolism ; Streptomyces/enzymology/genetics ; Structure-Activity Relationship
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    c-Fos: a key regulator of osteoclast-macrophage lineage determination and bone remodeling (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-21
    Description: Mice lacking the proto-oncogene c-fos develop the bone disease osteopetrosis. Fos mutant mice were found to have a block in the differentiation of bone-resorbing osteoclasts that was intrinsic to hematopoietic cells. Bone marrow transplantation rescued the osteopetrosis, and ectopic c-fos expression overcame this differentiation block. The lack of Fos also caused a lineage shift between osteoclasts and macrophages that resulted in increased numbers of bone marrow macrophages. These results identify Fos as a key regulator of osteoclast-macrophage lineage determination in vivo and provide insights into the molecular mechanisms underlying metabolic bone diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grigoriadis, A E -- Wang, Z Q -- Cecchini, M G -- Hofstetter, W -- Felix, R -- Fleisch, H A -- Wagner, E F -- New York, N.Y. -- Science. 1994 Oct 21;266(5184):443-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Molecular Pathology (IMP), Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Transplantation ; Bone Remodeling/*physiology ; Cell Differentiation ; Cells, Cultured ; Genes, fos ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*cytology ; Macrophages/*cytology ; Mice ; Mice, Mutant Strains ; Osteoclasts/*cytology ; Osteogenesis ; Osteopetrosis/metabolism/pathology ; Proto-Oncogene Proteins c-fos/genetics/*physiology
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    Slow repair of pyrimidine dimers at p53 mutation hotspots in skin cancer (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-11
    Description: Ultraviolet light has been linked with the development of human skin cancers. Such cancers often exhibit mutations in the p53 tumor suppressor gene. Ligation-mediated polymerase chain reaction was used to analyze at nucleotide resolution the repair of cyclobutane pyrimidine dimers along the p53 gene in ultraviolet-irradiated human fibroblasts. Repair rates at individual nucleotides were highly variable and sequence-dependent. Slow repair was seen at seven of eight positions frequently mutated in skin cancer, suggesting that repair efficiency may strongly contribute to the mutation spectrum in a cancer-associated gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tornaletti, S -- Pfeifer, G P -- ES06070/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1436-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beckman Rsearch Institute of the City of Hope, Department of Biology, Duarte, CA 91010.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128225" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; *DNA Repair ; Exons ; *Genes, p53 ; HeLa Cells ; Humans ; Mutation ; Phosphoglycerate Kinase/genetics ; Polymerase Chain Reaction ; Pyrimidine Dimers/*metabolism ; Skin/metabolism/*radiation effects ; Skin Neoplasms/*genetics/metabolism ; Ultraviolet Rays
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    Soluble beta-amyloid induction of Alzheimer's phenotype for human fibroblast K+ channels (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-08
    Description: Although beta-amyloid is the main constituent of neurite plaques and may play a role in the pathophysiology of Alzheimer's disease, mechanisms by which soluble beta-amyloid might produce early symptoms such as memory loss before diffuse plaque deposition have not been implicated. Treatment of fibroblasts with beta-amyloid (10 nM) induced the same potassium channel dysfunction previously shown to occur specifically in fibroblasts from patients with Alzheimer's disease--namely, the absence of a 113-picosiemen potassium channel. A tetraethylammonium-induced increase of intracellular concentrations of calcium, [Ca2+]i, a response that depends on functional 113-picosiemen potassium channels, was also eliminated or markedly reduced by 10 nM beta-amyloid. Increased [Ca2+]i induced by high concentrations of extracellular potassium and 166-picosiemen potassium channels were unaffected by 10 nM beta-amyloid. In Alzheimer's disease, then, beta-amyloid might alter potassium channels and thus impair neuronal function to produce symptoms such as memory loss by a means other than plaque formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Etcheberrigaray, R -- Ito, E -- Kim, C S -- Alkon, D L -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):276-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Adaptive Systems, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146663" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*metabolism ; Amyloid beta-Peptides/*pharmacology ; Bombesin/pharmacology ; Calcium/metabolism ; Cell Line ; Cells, Cultured ; Dimethyl Sulfoxide/pharmacology ; Female ; Fibroblasts/*drug effects/metabolism ; Humans ; Male ; Phenotype ; Potassium Channel Blockers ; Potassium Channels/*drug effects/metabolism ; Potassium Chloride/pharmacology ; Solubility ; Tetraethylammonium ; Tetraethylammonium Compounds/pharmacology
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    Aberrant neurites and synaptic vesicle protein deficiency in synapsin II-depleted neurons (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-05-13
    Description: Synapsin I and synapsin II are neuron-specific phosphoproteins that have a role in the regulation of neurotransmitter release and in the formation of nerve terminals. After depletion of synapsin II by antisense oligonucleotides, rat hippocampal neurons in culture were unable to consolidate their minor processes and did not elongate axons. These aberrant morphological changes were accompanied by an abnormal distribution of intracellular filamentous actin (F-actin). In addition, synapsin II suppression resulted in a selective decrease in the amounts of several synaptic vesicle-associated proteins. These data suggest that synapsin II participates in cytoskeletal organization during the early stages of nerve cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferreira, A -- Kosik, K S -- Greengard, P -- Han, H Q -- New York, N.Y. -- Science. 1994 May 13;264(5161):977-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurological Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178158" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Base Sequence ; *Calcium-Binding Proteins ; Cells, Cultured ; Hippocampus/cytology ; Membrane Glycoproteins/*metabolism ; Microtubule-Associated Proteins/metabolism ; Molecular Sequence Data ; Nerve Tissue Proteins/*metabolism ; Neurites/*physiology ; Neurons/*cytology/metabolism/ultrastructure ; Oligonucleotides, Antisense/pharmacology ; Rats ; Synapsins/genetics/*metabolism ; Synaptophysin/*metabolism ; Synaptotagmins ; Tubulin/metabolism ; tau Proteins/metabolism
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    Sea urchin egg receptor for sperm: sequence similarity of binding domain and hsp70 (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-03-05
    Description: Fertilization depends on cell surface recognition proteins that interact and thereby mediate binding and subsequent fusion of the sperm and egg. Overlapping complementary DNA's encoding the egg plasma membrane receptor for sperm from the sea urchin Strongylocentrotus purpuratus were cloned and sequenced. Analysis of the deduced primary structure suggests that the receptor is a transmembrane protein with a short cytoplasmic domain. This domain showed no sequence similarity to known protein sequences. In contrast, the extracellular, sperm binding domain of the receptor did show sequence similarity to the heat shock protein 70 (hsp70) family of proteins. Recombinant protein representing this portion of the receptor bound to the sperm protein, binding, and also inhibited fertilization in a species-specific manner; beads coated with the protein became specifically bound to acrosome-reacted sperm. These data provide a basis for detailed investigations of molecular interactions that occur in gamete recognition and egg activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Foltz, K R -- Partin, J S -- Lennarz, W J -- HD18590/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 5;259(5100):1421-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of California, Santa Barbara 93106.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8383878" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cloning, Molecular ; Female ; Fertilization ; Heat-Shock Proteins/*genetics ; Humans ; Male ; Molecular Sequence Data ; Ovum/physiology ; Receptors, Cell Surface/*genetics/metabolism ; Recombinant Proteins/metabolism ; Restriction Mapping ; Sea Urchins ; Sequence Homology, Amino Acid ; Sperm-Ovum Interactions ; Spermatozoa/cytology/physiology
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    Role of intracellular calcium in NI-35-evoked collapse of neuronal growth cones (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-01
    Description: A myelin-associated protein from the central nervous system, the neurite growth inhibitor NI-35, inhibits regeneration of lesioned neuronal fiber tracts in vivo and growth of neurites in vitro. Growth cones of cultured rat dorsal root ganglion neurons arrested their growth and collapsed when exposed to liposomes containing NI-35. Before morphological changes, the concentration of free intracellular calcium ([Ca2+]i) showed a rapid and large increase in growth cones exposed to liposomes containing NI-35. Neither an increase in [Ca2+]i nor collapse of growth cones was detected in the presence of antibodies to NI-35. Dantrolene, an inhibitor of calcium release from caffeine-sensitive intracellular calcium stores, protected growth cones from collapse evoked by NI-35. Depletion of these caffeine-sensitive intracellular calcium stores prevented the increase in [Ca2+]i evoked by NI-35. The NI-35-evoked cascade of intracellular messengers that mediates collapse of growth cones includes the crucial step of calcium release from intracellular stores.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bandtlow, C E -- Schmidt, M F -- Hassinger, T D -- Schwab, M E -- Kater, S B -- NS24683/NS/NINDS NIH HHS/ -- NS28323/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):80-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brain Research Institute, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8418499" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caffeine/pharmacology ; Calcium/*metabolism ; Cells, Cultured ; Drug Carriers ; Fura-2 ; Ganglia, Spinal/*physiology ; Growth Inhibitors/*pharmacology ; Kinetics ; Liposomes ; Nerve Fibers/drug effects/*physiology/ultrastructure ; Neurons/drug effects/*physiology/ultrastructure ; Rats
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    Origin recognition complex (ORC) in transcriptional silencing and DNA replication in S. cerevisiae (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-12-17
    Description: In Saccharomyces cerevisiae, the HMR-E silencer blocks site-specific interactions between proteins and their recognition sequences in the vicinity of the silencer. Silencer function is correlated with the firing of an origin of replication at HMR-E. An essential gene with a role in transcriptional silencing was identified by means of a screen for mutations affecting expression of HMR. This gene, known as ORC2, was shown to encode a component of the origin recognition complex that binds yeast origins of replication. A temperature-sensitive mutation in ORC2 disrupted silencing in cells grown at the permissive temperature. At the restrictive temperature, the orc2-1 mutation caused cell cycle arrest at a point in the cell cycle indicative of blocks in DNA replication. The orc2-1 mutation also resulted in the enhanced mitotic loss of a plasmid, suggestive of a defect in replication. These results provide strong evidence for an in vivo role of ORC in both chromosomal replication and silencing, and provide a link between the mechanism of silencing and DNA replication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Foss, M -- McNally, F J -- Laurenson, P -- Rine, J -- GM31105/GM/NIGMS NIH HHS/ -- P30ES01896-12/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1993 Dec 17;262(5141):1838-44.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266071" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Cell Cycle ; Cloning, Molecular ; *DNA Replication ; DNA, Fungal/genetics/metabolism ; *DNA-Binding Proteins ; Fungal Proteins/chemistry/*genetics/metabolism ; *Gene Expression Regulation, Fungal ; *Genes, Fungal ; Molecular Sequence Data ; Mutation ; Origin Recognition Complex ; Phenotype ; Plasmids ; *Replicon ; Repressor Proteins/chemistry/*genetics/metabolism ; Saccharomyces cerevisiae/cytology/*genetics/metabolism ; Saccharomyces cerevisiae Proteins ; Transcription, Genetic
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    Expression cloning and signaling properties of the rat glucagon receptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-12
    Description: Glucagon and the glucagon receptor are a primary source of control over blood glucose concentrations and are especially important to studies of diabetes in which the loss of control over blood glucose concentrations clinically defines the disease. A complementary DNA clone for the glucagon receptor was isolated by an expression cloning strategy, and the receptor protein was expressed in several kidney cell lines. The cloned receptor bound glucagon and caused an increase in the intracellular concentration of adenosine 3', 5'-monophosphate (cAMP). The cloned glucagon receptor also transduced a signal that led to an increased concentration of intracellular calcium. The glucagon receptor is similar to the calcitonin and parathyroid hormone receptors. It can transduce signals leading to the accumulation of two different second messengers, cAMP and calcium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jelinek, L J -- Lok, S -- Rosenberg, G B -- Smith, R A -- Grant, F J -- Biggs, S -- Bensch, P A -- Kuijper, J L -- Sheppard, P O -- Sprecher, C A -- New York, N.Y. -- Science. 1993 Mar 12;259(5101):1614-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ZymoGenetics Inc., Seattle, WA 98105.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8384375" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/pharmacology ; Cell Line ; Cloning, Molecular ; Cricetinae ; Cyclic AMP/metabolism ; Glucagon/metabolism/*pharmacology ; Kidney ; Kinetics ; Liver/*metabolism ; Molecular Sequence Data ; Rats ; Receptors, Gastrointestinal Hormone/genetics/metabolism/*physiology ; Receptors, Glucagon ; *Signal Transduction ; Transfection
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    Inhibition of Rev-mediated HIV-1 expression by an RNA binding protein encoded by the interferon-inducible 9-27 gene (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-26
    Description: Interferon inhibits expression of human immunodeficiency virus type-1 (HIV-1) through unknown mechanisms. A gene inducible by interferon-alpha (IFN-alpha) and interferon-gamma (IFN-gamma) was isolated by screening of a human complementary DNA library for proteins binding to the Rev-responsive element (RRE) of HIV-1. The product of this gene, RBP9-27, was shown to bind RNA in vitro and to inhibit HIV-1 expression after transfection into human cells. RBP9-27 primarily inhibited Rev-dependent posttranscriptional steps of viral gene expression. Thus, RBP9-27 is a cellular factor that antagonizes Rev function. These results suggest an interferon-induced antiviral mechanism operating through the induction of RNA binding proteins such as RBP9-27. Elucidation of RBP9-27 function may lead to a better understanding of the mechanism of interferon action during HIV-1 infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Constantoulakis, P -- Campbell, M -- Felber, B K -- Nasioulas, G -- Afonina, E -- Pavlakis, G N -- N0-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Feb 26;259(5099):1314-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Retrovirus Section, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7680491" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cloning, Molecular ; *Gene Expression Regulation, Viral ; Genes, env ; *Genes, rev ; HIV-1/*genetics ; Humans ; Interferons/pharmacology ; *Membrane Proteins ; Molecular Sequence Data ; Oligodeoxyribonucleotides/chemistry ; RNA-Binding Proteins/*genetics ; Regulatory Sequences, Nucleic Acid
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    Microbial competition: Escherichia coli mutants that take over stationary phase cultures (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-03-19
    Description: Many microorganisms, including Escherichia coli, can survive extended periods of starvation. The properties of cells that survived prolonged incubation in stationary phase were studied by mixture of 10-day-old (aged) cultures with 1-day-old (young) cultures of the same strain of Escherichia coli. Mutants from the aged cultures that could grow eventually took over the population, which resulted in the death of the cells from the young cultures. This phenotype was conferred by mutations in rpoS, which encodes a putative stationary phase-specific sigma factor. These rapid population shifts have implications for the studies of microbial evolution and ecology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zambrano, M M -- Siegele, D A -- Almiron, M -- Tormo, A -- Kolter, R -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1757-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7681219" target="_blank"〉PubMed〈/a〉
    Keywords: Acridine Orange ; Alleles ; Amino Acid Sequence ; Cloning, Molecular ; Escherichia coli/*genetics/*growth & development/physiology ; Hydrogen Peroxide/metabolism ; Molecular Sequence Data ; *Mutation ; Peroxidase/metabolism ; Phenotype ; Sigma Factor/chemistry/*genetics ; Staining and Labeling ; Time Factors
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    A genetic linkage map of the mouse: current applications and future prospects (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-10-01
    Description: Technological advances have made possible the development of high-resolution genetic linkage maps for the mouse. These maps in turn offer exciting prospects for understanding mammalian genome evolution through comparative mapping, for developing mouse models of human disease, and for identifying the function of all genes in the organism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Copeland, N G -- Jenkins, N A -- Gilbert, D J -- Eppig, J T -- Maltais, L J -- Miller, J C -- Dietrich, W F -- Weaver, A -- Lincoln, S E -- Steen, R G -- HG00198/HG/NHGRI NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 1;262(5130):57-66.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211130" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; *Chromosome Mapping ; Cloning, Molecular ; Crosses, Genetic ; Female ; Genetic Markers ; *Genome ; Human Genome Project ; Humans ; Male ; Mice/*genetics ; Multigene Family ; Muridae/*genetics ; Mutation ; Neoplasms/genetics
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    Altered fluid transport across airway epithelium in cystic fibrosis (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-10-15
    Description: In cystic fibrosis (CF), absence or dysfunction of a phosphorylation-regulated chloride channel [CF transmembrane conductance regulator (CFTR)] leads to the loss or reduction of chloride secretion into the airways. Active sodium absorption is also increased in CF, and both of these ion transport changes could alter fluid transport across the airways. Under baseline conditions, cultured human airway epithelia from normal individuals absorbed fluid, and this absorption was increased in epithelia from patients with CF. In normal and CF epithelial cultures fluid absorption was inhibited by amiloride. Adenosine 3',5'-monophosphate stimulated fluid secretion in normal epithelial cultures but not in cultures from individuals with CF. In contrast, fluid secretion induced by nucleotide triphosphates (uridine triphosphate or adenosine triphosphate) was unaltered in cultures of epithelia from patients with CF, suggesting an approach to the treatment of CF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jiang, C -- Finkbeiner, W E -- Widdicombe, J H -- McCray, P B Jr -- Miller, S S -- HL 42368/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 15;262(5132):424-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211164" target="_blank"〉PubMed〈/a〉
    Keywords: Absorption ; Adenosine Triphosphate/pharmacology ; Adolescent ; Adult ; Amiloride/pharmacology ; Body Fluids/*metabolism ; Cells, Cultured ; Cyclic AMP/pharmacology ; Cystic Fibrosis/*metabolism ; Epithelial Cells ; Epithelium/metabolism ; Female ; Humans ; Male ; Middle Aged ; Nasal Mucosa/cytology/*metabolism ; Sodium/metabolism ; Sodium Channels/metabolism ; Trachea/cytology/*metabolism ; Uridine Triphosphate/pharmacology
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    Fusion between transcription factor CBF beta/PEBP2 beta and a myosin heavy chain in acute myeloid leukemia (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-20
    Description: The pericentric inversion of chromosome 16 [inv(16)(p13q22)] is a characteristic karyotypic abnormality associated with acute myeloid leukemia, most commonly of the M4Eo subtype. The 16p and 16q breakpoints were pinpointed by yeast artificial chromosome and cosmid cloning, and the two genes involved in this inversion were identified. On 16q the inversion occurred near the end of the coding region for CBF beta, also known as PEBP2 beta, a subunit of a heterodimeric transcription factor regulating genes expressed in T cells; on 16p a smooth muscle myosin heavy chain (SMMHC) gene (MYH11) was interrupted. In six of six inv(16) patient samples tested, an in-frame fusion messenger RNA was demonstrated that connected the first 165 amino acids of CBF beta with the tail region of SMMHC. The repeated coiled coil of SMMHC may result in dimerization of the CBF beta fusion protein, which in turn would lead to alterations in transcriptional regulation and contribute to leukemic transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, P -- Tarle, S A -- Hajra, A -- Claxton, D F -- Marlton, P -- Freedman, M -- Siciliano, M J -- Collins, F S -- CA55164/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Aug 20;261(5124):1041-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8351518" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; *Chromosome Inversion ; *Chromosomes, Human, Pair 16 ; Cloning, Molecular ; Core Binding Factor Alpha 1 Subunit ; Core Binding Factor beta Subunit ; Core Binding Factors ; Cosmids ; DNA-Binding Proteins/*genetics ; Humans ; In Situ Hybridization, Fluorescence ; Leukemia, Myelomonocytic, Acute/*genetics ; Molecular Sequence Data ; Muscle, Smooth/chemistry ; Myosins/*genetics ; *Neoplasm Proteins ; Polymerase Chain Reaction ; Protein Multimerization ; Restriction Mapping ; Transcription Factor AP-2 ; Transcription Factors/*genetics
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    Identification of the von Hippel-Lindau disease tumor suppressor gene (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-28
    Description: A gene discovered by positional cloning has been identified as the von Hippel-Lindau (VHL) disease tumor suppressor gene. A restriction fragment encompassing the gene showed rearrangements in 28 of 221 VHL kindreds. Eighteen of these rearrangements were due to deletions in the candidate gene, including three large nonoverlapping deletions. Intragenic mutations were detected in cell lines derived from VHL patients and from sporadic renal cell carcinomas. The VHL gene is evolutionarily conserved and encodes two widely expressed transcripts of approximately 6 and 6.5 kilobases. The partial sequence of the inferred gene product shows no homology to other proteins, except for an acidic repeat domain found in the procyclic surface membrane glycoprotein of Trypanosoma brucei.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Latif, F -- Tory, K -- Gnarra, J -- Yao, M -- Duh, F M -- Orcutt, M L -- Stackhouse, T -- Kuzmin, I -- Modi, W -- Geil, L -- New York, N.Y. -- Science. 1993 May 28;260(5112):1317-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunobiology, National Cancer Institute-Frederick Cancer Research and Development Center (NCI-FCRDC), Frederick, MD 21702-1201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493574" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Carcinoma, Renal Cell/genetics ; Chromosomes, Human, Pair 3 ; Cloning, Molecular ; Gene Deletion ; *Genes, Tumor Suppressor ; Humans ; Kidney Neoplasms/genetics ; Membrane Glycoproteins/chemistry/*genetics ; Molecular Sequence Data ; Mutation ; Open Reading Frames ; Pedigree ; Polymorphism, Genetic ; Tumor Cells, Cultured ; von Hippel-Lindau Disease/*genetics
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  • 80
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    Reversal of left-right asymmetry: a situs inversus mutation (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-30
    Description: A recessive mutation was identified in a family of transgenic mice that resulted in a reversal of left-right polarity (situs inversus) in 100 percent of the homozygous transgenic mice tested. Sequences that flanked the transgenic integration site were cloned and mapped to mouse chromosome 4, between the Tsha and Hxb loci. During early embryonic development, the direction of postimplantation turning, one of the earliest manifestations of left-right asymmetry, was reversed in homozygous transgenic embryos. This insertional mutation identifies a gene that controls embryonic turning and visceral left-right polarity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yokoyama, T -- Copeland, N G -- Jenkins, N A -- Montgomery, C A -- Elder, F F -- Overbeek, P A -- HD25340/HD/NICHD NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 30;260(5108):679-82.〈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/8480178" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Chromosome Mapping ; Cloning, Molecular ; Embryonic and Fetal Development/*genetics ; Female ; *Genes, Recessive ; Homozygote ; Male ; Mice ; Mice, Transgenic ; Mutagenesis, Insertional ; Situs Inversus/*genetics
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  • 81
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    Requirement for a GTPase-activating protein in vesicle budding from the endoplasmic reticulum (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-05
    Description: The binding and hydrolysis of guanosine triphosphate (GTP) by the small GTP-binding protein Sar1p is required to form transport vesicles from the endoplasmic reticulum (ER) in Saccharomyces cerevisiae. Experiments revealed that an interaction between Sar1p and the Sec23p subunit of an oligomeric protein is also required for vesicle budding. The isolated Sec23p subunit and the oligomeric complex stimulated guanosine triphosphatase (GTPase) activity of Sar1p 10- to 15-fold but did not activate two other small GTP-binding proteins involved in vesicle traffic (Ypt1p and ARF). Activation of GTPase was inhibited by an antibody to Sec23p but not by an antibody that inhibits the budding activity of the other subunit of the Sec23p complex. Also, activation was thermolabile in pure samples of Sec23p that were isolated from two independent sec23 mutant strains. It appears that Sec23p represents a new class of GTPase-activating protein because its sequence shows no similarity to any known member of this family.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoshihisa, T -- Barlowe, C -- Schekman, R -- New York, N.Y. -- Science. 1993 Mar 5;259(5100):1466-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8451644" target="_blank"〉PubMed〈/a〉
    Keywords: COP-Coated Vesicles ; Cloning, Molecular ; Endoplasmic Reticulum/*metabolism/ultrastructure ; Fungal Proteins/genetics/metabolism ; GTP-Binding Proteins/genetics/*metabolism ; GTPase-Activating Proteins ; Genes, Fungal ; Kinetics ; Macromolecular Substances ; *Monomeric GTP-Binding Proteins ; Mutagenesis ; Proteins/*metabolism ; Saccharomyces cerevisiae/genetics/*metabolism ; *Saccharomyces cerevisiae Proteins ; Spheroplasts/metabolism ; Vesicular Transport Proteins
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  • 82
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    GDNF: a glial cell line-derived neurotrophic factor for midbrain dopaminergic neurons (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-21
    Description: A potent neurotrophic factor that enhances survival of midbrain dopaminergic neurons was purified and cloned. Glial cell line-derived neurotrophic factor (GDNF) is a glycosylated, disulfide-bonded homodimer that is a distantly related member of the transforming growth factor-beta superfamily. In embryonic midbrain cultures, recombinant human GDNF promoted the survival and morphological differentiation of dopaminergic neurons and increased their high-affinity dopamine uptake. These effects were relatively specific; GDNF did not increase total neuron or astrocyte numbers nor did it increase transmitter uptake by gamma-aminobutyric-containing and serotonergic neurons. GDNF may have utility in the treatment of Parkinson's disease, which is marked by progressive degeneration of midbrain dopaminergic neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, L F -- Doherty, D H -- Lile, J D -- Bektesh, S -- Collins, F -- New York, N.Y. -- Science. 1993 May 21;260(5111):1130-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Synergen, Inc., Boulder, CO 80301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493557" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Astrocytes/cytology/drug effects ; Base Sequence ; Cell Differentiation/drug effects ; Cell Line ; Cell Survival/drug effects ; Cells, Cultured ; Cloning, Molecular ; Dopamine/*biosynthesis ; Glial Cell Line-Derived Neurotrophic Factor ; Humans ; Mesencephalon/cytology/*drug effects/metabolism ; Molecular Sequence Data ; Molecular Weight ; *Nerve Growth Factors ; Nerve Tissue Proteins/chemistry/genetics/isolation & purification/*pharmacology ; Neuroglia/*metabolism ; Neurons/cytology/*drug effects/metabolism ; Parkinson Disease/drug therapy ; Rats
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  • 83
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    The pluses of subtraction (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myers, R M -- New York, N.Y. -- Science. 1993 Feb 12;259(5097):942-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of California, San Francisco 94143-0444.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8094900" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; DNA/*chemistry ; DNA Probes ; Female ; Gene Deletion ; Humans ; Male ; Nucleic Acid Hybridization/*methods ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length
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  • 84
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    Death gives birth to the nervous system. But how? (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1993 Feb 5;259(5096):762-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430328" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/physiology ; Caenorhabditis elegans/embryology/genetics ; Cell Death/*physiology ; Cells, Cultured ; Embryo, Nonmammalian/physiology ; Nerve Growth Factors/physiology ; Nervous System/cytology/*embryology ; Neurons/cytology/*physiology ; Protein-Tyrosine Kinases/genetics ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins c-bcl-2 ; Proto-Oncogenes
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  • 85
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    Enhancement by histamine of NMDA-mediated synaptic transmission in the hippocampus (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-02
    Description: Histamine is a neuromodulator in the brain, and the hippocampus is one of the regions of the brain that is innervated by histaminergic neurons. When applied to cultured hippocampal neurons, histamine selectively increased by up to tenfold the amplitude of the component of synaptic transmission that was mediated by N-methyl-D-aspartate (NMDA) receptors. Spontaneous miniature synaptic currents and the current elicited by applied NMDA also were enhanced, indicating that the histamine effect was expressed primarily postsynaptically. These results suggest that histamine may modulate processes involving NMDA receptors, such as the induction of long-term potentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bekkers, J M -- New York, N.Y. -- Science. 1993 Jul 2;261(5117):104-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, John Curtin School of Medical Research, Australian National Univresity, Canberra, ACT.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8391168" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cells, Cultured ; Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology ; Hippocampus/cytology/drug effects/*physiology ; Histamine/*pharmacology ; Ion Channel Gating/drug effects ; N-Methylaspartate/*metabolism/pharmacology ; Rats ; Receptors, Histamine/physiology ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/*physiology ; Synaptic Transmission/*drug effects ; Virulence Factors, Bordetella/pharmacology
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  • 86
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    Rapid assessment of drug susceptibilities of Mycobacterium tuberculosis by means of luciferase reporter phages (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-07
    Description: Effective chemotherapy of tuberculosis requires rapid assessment of drug sensitivity because of the emergence of multidrug-resistant Mycobacterium tuberculosis. Drug susceptibility was assessed by a simple method based on the efficient production of photons by viable mycobacteria infected with specific reporter phages expressing the firefly luciferase gene. Light production was dependent on phage infection, expression of the luciferase gene, and the level of cellular adenosine triphosphate. Signals could be detected within minutes after infection of virulent M. tuberculosis with reporter phages. Culture of conventional strains with antituberculosis drugs, including isoniazid or rifampicin, resulted in extinction of light production. In contrast, light signals after luciferase reporter phage infection of drug-resistant strains continued to be produced. Luciferase reporter phages may help to reduce the time required for establishing antibiotic sensitivity of M. tuberculosis strains from weeks to days and to accelerate screening for new antituberculosis drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jacobs, W R Jr -- Barletta, R G -- Udani, R -- Chan, J -- Kalkut, G -- Sosne, G -- Kieser, T -- Sarkis, G J -- Hatfull, G F -- Bloom, B R -- AI27235/AI/NIAID NIH HHS/ -- AI28927/AI/NIAID NIH HHS/ -- UO1AI30189/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 May 7;260(5109):819-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Albert Einstein College of Medicine, Bronx, NY 10461.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8484123" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Antitubercular Agents/*pharmacology ; Cloning, Molecular ; Drug Resistance, Microbial ; Luciferases/genetics/metabolism ; *Luminescent Measurements ; Microbial Sensitivity Tests/*methods ; Mycobacteriophages/genetics ; Mycobacterium/genetics/metabolism ; Mycobacterium bovis/drug effects/genetics/metabolism ; Mycobacterium tuberculosis/*drug effects/genetics/metabolism
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  • 87
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    Interleukin-7: a cofactor for V(D)J rearrangement of the T cell receptor beta gene (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-02
    Description: The diversity of the T cell receptor repertoire is generated by rearrangement of gene elements in immature thymocytes. To identify a thymic signal that induces this rearrangement, a variety of agents were tested for their ability to induce rearrangement of the T cell receptor beta gene in suspensions of thymocytes from mouse embryos at day 14 of gestation. Of 16 agents tested, only interleukin-7 (IL-7) induced V(D)J gene rearrangement and sustained expression of the RAG-1 and RAG-2 genes, which are known to control rearrangement. These data implicate IL-7, a cytokine that is abundantly expressed in embryonic thymus, in driving gene rearrangement during early T cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muegge, K -- Vila, M P -- Durum, S K -- New York, N.Y. -- Science. 1993 Jul 2;261(5117):93-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biological Carcinogenesis and Development Program, Program Resources Inc./Dyncorp, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7686307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Cell Survival/drug effects ; Cells, Cultured ; *DNA-Binding Proteins ; Gene Expression ; *Gene Rearrangement, beta-Chain T-Cell Antigen Receptor ; Genes, RAG-1 ; Hematopoietic Cell Growth Factors/pharmacology ; Interleukin-7/*pharmacology ; Ionomycin/pharmacology ; Mice ; Molecular Sequence Data ; Organ Culture Techniques ; Proteins/genetics ; Stem Cell Factor ; T-Lymphocytes/cytology/*immunology ; Tetradecanoylphorbol Acetate/pharmacology ; Thymus Gland/embryology/immunology ; Tumor Cells, Cultured
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  • 88
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    Neuroprotective effects of glutamate antagonists and extracellular acidity (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-04
    Description: Glutamate antagonists protect neurons from hypoxic injury both in vivo and in vitro, but in vitro studies have not been done under the acidic conditions typical of hypoxia-ischemia in vivo. Consistent with glutamate receptor antagonism, extracellular acidity reduced neuronal death in murine cortical cultures that were deprived of oxygen and glucose. Under these acid conditions, N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate-kainate antagonists further reduced neuronal death, such that some neurons tolerated prolonged oxygen and glucose deprivation almost as well as did astrocytes. Neuroprotection induced by this combination exceeded that induced by glutamate antagonists alone, suggesting that extracellular acidity has beneficial effects beyond the attenuation of ionotropic glutamate receptor activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaku, D A -- Giffard, R G -- Choi, D W -- NS 01425/NS/NINDS NIH HHS/ -- NS 26907/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 4;260(5113):1516-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8389056" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Death/drug effects ; Cell Hypoxia/physiology ; Cells, Cultured ; Cerebral Cortex/cytology ; *Excitatory Amino Acid Antagonists ; Extracellular Space/*metabolism ; Glucose/deficiency ; *Hydrogen-Ion Concentration ; L-Lactate Dehydrogenase/metabolism ; Mice ; Nerve Degeneration/drug effects ; Neurons/*drug effects/enzymology ; Receptors, AMPA ; Receptors, Kainic Acid ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors
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  • 89
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    Molecular mechanism of transcription-repair coupling (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-04-02
    Description: Lesions in the transcribed strand block transcription and are repaired more rapidly than lesions in the nontranscribed (coding) strand which do not block RNA polymerase (RNAP). It has been shown previously that in Escherichia coli the mfd (mutation frequency decline) gene is necessary for strand-specific repair. The mfd gene was cloned and sequenced and the Mfd protein was purified and used to reconstitute strand-specific repair in a completely defined system. The mfd gene encodes a protein of 130 kilodaltons and contains the so-called "helicase motifs," a leucine zipper motif, and regions of sequence similarity to UvrB and RecG proteins. The Mfd protein was shown to (i) displace RNAP stalled at a lesion in an adenosine triphosphate-dependent reaction, (ii) bind to the damage recognition subunit (UvrA) of the excision nuclease, and (iii) stimulate the repair of the transcribed strand only when transcription is taking place. Thus, Mfd appears to target the transcribed strand for repair by recognizing a stalled RNAP and actively recruiting the repair enzyme to the transcription blocking lesion as it dissociates the stalled RNAP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selby, C P -- Sancar, A -- New York, N.Y. -- Science. 1993 Apr 2;260(5104):53-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill 27599.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8465200" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacterial Proteins/chemistry/*genetics/metabolism ; Base Sequence ; Binding Sites ; Cloning, Molecular ; *DNA Helicases ; DNA Repair/*genetics ; DNA, Bacterial/metabolism ; DNA-Directed RNA Polymerases/metabolism ; Endodeoxyribonucleases/metabolism ; Escherichia coli/*genetics ; *Escherichia coli Proteins ; Leucine Zippers ; Molecular Sequence Data ; Multienzyme Complexes/chemistry/genetics ; Mutation/genetics ; Transcription Factors/chemistry/*genetics/metabolism ; *Transcription, Genetic
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  • 90
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    Antagonism of catecholamine receptor signaling by expression of cytoplasmic domains of the receptors (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-05
    Description: The actions of many hormones and neurotransmitters are mediated by the members of a superfamily of receptors coupled to heterotrimeric guanine nucleotide-binding proteins (G proteins). These receptors are characterized by a highly conserved topographical arrangement in which seven transmembrane domains are connected by intracellular and extracellular loops. The interaction between these receptors and G proteins is mediated in large part by the third intracellular loop of the receptor. Coexpression of the third intracellular loop of the alpha 1B-adrenergic receptor with its parent receptor inhibited receptor-mediated activation of phospholipase C. The inhibition extended to the closely related alpha 1C-adrenergic receptor subtype, but not the phospholipase C-coupled M1 muscarinic acetylcholine receptor nor the adenylate cyclase-coupled D1A dopamine receptor. These results suggest that the receptor-G protein interface may represent a target for receptor antagonist drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luttrell, L M -- Ostrowski, J -- Cotecchia, S -- Kendall, H -- Lefkowitz, R J -- HL16037/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 5;259(5100):1453-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8383880" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Cloning, Molecular ; Cyclic AMP/metabolism ; Cytoplasm/metabolism ; GTP-Binding Proteins/*metabolism ; Globins/genetics ; Glutathione Transferase/genetics/metabolism ; Humans ; Inositol Phosphates/metabolism ; Kinetics ; Molecular Sequence Data ; Muscarinic Antagonists ; Oligodeoxyribonucleotides ; Plasmids ; Protein Structure, Secondary ; Receptors, Adrenergic, alpha/genetics/*metabolism ; Receptors, Dopamine D1/antagonists & inhibitors/genetics/*metabolism ; Receptors, Muscarinic/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Transfection ; Type C Phospholipases/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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  • 91
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    Inhibition of viral replication by interferon-gamma-induced nitric oxide synthase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-10
    Description: Interferons (IFNs) induce antiviral activity in many cell types. The ability of IFN-gamma to inhibit replication of ectromelia, vaccinia, and herpes simplex-1 viruses in mouse macrophages correlated with the cells' production of nitric oxide (NO). Viral replication was restored in IFN-gamma-treated macrophages exposed to inhibitors of NO synthase. Conversely, epithelial cells with no detectable NO synthesis restricted viral replication when transfected with a complementary DNA encoding inducible NO synthase or treated with organic compounds that generate NO. In mice, an inhibitor of NO synthase converted resolving ectromelia virus infection into fulminant mousepox. Thus, induction of NO synthase can be necessary and sufficient for a substantial antiviral effect of IFN-gamma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karupiah, G -- Xie, Q W -- Buller, R M -- Nathan, C -- Duarte, C -- MacMicking, J D -- CA43610/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1445-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7690156" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/*biosynthesis/metabolism ; Animals ; Arginine/analogs & derivatives/pharmacology ; Cell Line ; Cells, Cultured ; Ectromelia virus/drug effects/*physiology ; Ectromelia, Infectious/microbiology ; Enzyme Induction ; Female ; Humans ; Interferon-gamma/*pharmacology ; Macrophages/*microbiology ; Mice ; Mice, Inbred C57BL ; Nitric Oxide/metabolism/pharmacology ; Nitric Oxide Synthase ; Simplexvirus/drug effects/physiology ; Transfection ; Vaccinia virus/drug effects/physiology ; *Virus Replication/drug effects ; omega-N-Methylarginine
    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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  • 92
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    Developmental regulation of neural response to FGF-1 and FGF-2 by heparan sulfate proteoglycan (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-02
    Description: Murine neural precursor cells and cell lines derived from them are stimulated by members of the heparin-binding fibroblast growth factor (FGF) family. The activity of FGF is regulated by heparan sulfate proteoglycans (HSPGs), and this interaction is an essential prerequisite for the binding of growth factor to the signal transducing receptors. Messenger RNA for FGF-2 was detectable in the neuroepithelium at embryonic day 9, and the HSPGs produced by these cells at this time preferentially bound FGF-2. However, at embryonic day 11, when messenger RNA for FGF-1 was first detectable, there was a switch in the binding specificity of the HSPG to FGF-1. Thus, a single species of HSPG undergoes a rapid, tightly controlled change in growth factor-binding specificity concomitant with the temporal expression of the FGFs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nurcombe, V -- Ford, M D -- Wildschut, J A -- Bartlett, P F -- New York, N.Y. -- Science. 1993 Apr 2;260(5104):103-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7682010" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Culture Media, Conditioned ; Epithelium/chemistry/embryology ; Fibroblast Growth Factor 1/genetics/*pharmacology ; Fibroblast Growth Factor 2/genetics/*pharmacology ; Gene Expression ; Gestational Age ; Heparan Sulfate Proteoglycans ; Heparitin Sulfate/*pharmacology ; Mice ; Molecular Weight ; Nervous System/chemistry/*embryology/metabolism ; Neurons/cytology ; Polysaccharide-Lyases/metabolism ; Proteoglycans/*pharmacology ; RNA, Messenger/analysis ; Signal Transduction/physiology ; Stem Cells/cytology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 93
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    AIDS theories (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Curtis, T -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):14.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8418488" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines ; Acquired Immunodeficiency Syndrome/immunology/*transmission ; Animals ; Cells, Cultured ; *Hiv-1 ; Haplorhini ; Humans ; Kidney ; Male
    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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  • 94
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    The Caenorhabditis elegans unc-17 gene: a putative vesicular acetylcholine transporter (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-30
    Description: Mutations in the unc-17 gene of the nematode Caenorhabditis elegans produce deficits in neuromuscular function. This gene was cloned and complementary DNAs were sequenced. On the basis of sequence similarity to mammalian vesicular transporters of biogenic amines and of localization to synaptic vesicles of cholinergic neurons in C. elegans, unc-17 likely encodes the vesicular transporter of acetylcholine. Mutations that eliminated all unc-17 gene function were lethal, suggesting that the acetylcholine transporter is essential. Molecular analysis of unc-17 mutations will allow the correlation of specific parts of the gene (and the protein) with observed functional defects. The mutants will also be useful for the isolation of extragenic suppressors, which could identify genes encoding proteins that interact with UNC-17.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alfonso, A -- Grundahl, K -- Duerr, J S -- Han, H P -- Rand, J B -- R01 GM038679/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 30;261(5121):617-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Molecular and Cell Biology, Oklahoma Medical Research Foundation, Oklahoma City 73104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8342028" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*metabolism ; Alleles ; Amino Acid Sequence ; Animals ; Caenorhabditis elegans/chemistry/cytology/*genetics ; *Caenorhabditis elegans Proteins ; Carrier Proteins/analysis/chemistry/*genetics ; Cloning, Molecular ; *Genes, Helminth ; Helminth Proteins/analysis/chemistry/*genetics ; *Membrane Transport Proteins ; Molecular Sequence Data ; Mutation ; Neurons/*chemistry ; Parasympathetic Nervous System/chemistry ; Phenotype ; Sequence Alignment ; Synaptic Vesicles/*chemistry ; Vesicular Acetylcholine Transport Proteins ; *Vesicular Transport Proteins
    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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  • 95
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    Released form of CNTF receptor alpha component as a soluble mediator of CNTF responses (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-19
    Description: The alpha component of the receptor for ciliary neurotrophic factor (CNTF) differs from other known growth factor receptors in that it is anchored to cell membranes by a glycosylphosphatidylinositol linkage. One possible function of this type of linkage is to allow for the regulated release of this receptor component. Cell lines not normally responsive to CNTF responded to treatment with a combination of CNTF and a soluble form of the CNTF alpha receptor component. These findings not only demonstrate that the CNTF receptor alpha chain is a required component of the functional CNTF receptor complex but also reveal that it can function in soluble form as part of a heterodimeric ligand. Potential physiological roles for the soluble CNTF receptor are suggested by its presence in cerebrospinal fluid and by its release from skeletal muscle in response to peripheral nerve injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, S -- Aldrich, T H -- Ip, N Y -- Stahl, N -- Scherer, S -- Farruggella, T -- DiStefano, P S -- Curtis, R -- Panayotatos, N -- Gascan, H -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1736-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, Inc., Tarrytown, NY 10591.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7681218" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/drug effects ; Cell Division/drug effects ; Cell Membrane/metabolism ; Ciliary Neurotrophic Factor ; Cloning, Molecular ; Gene Expression ; Glycosylphosphatidylinositols/metabolism ; Growth Inhibitors/pharmacology ; Hematopoietic Stem Cells/cytology/drug effects ; Humans ; Interleukin-6/pharmacology ; Leukemia Inhibitory Factor ; Lymphokines/pharmacology ; Mice ; Muscle Denervation ; Muscles/innervation/metabolism ; Nerve Tissue Proteins/*pharmacology ; Phosphatidylinositol Diacylglycerol-Lyase ; Phosphoric Diester Hydrolases/metabolism ; Phosphotyrosine ; RNA, Messenger/genetics ; Rats ; Receptor, Ciliary Neurotrophic Factor ; Receptors, Cell Surface/chemistry/*physiology ; Signal Transduction/physiology ; Tumor Cells, Cultured ; Tyrosine/analogs & derivatives/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 96
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    A faster walk along the genome (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aldhous, P -- New York, N.Y. -- Science. 1993 May 21;260(5111):1075.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493549" target="_blank"〉PubMed〈/a〉
    Keywords: *Base Sequence ; Cloning, Molecular ; DNA/*genetics ; Oligodeoxyribonucleotides/*genetics ; Sequence Analysis, DNA/*methods
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
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    Beta-adrenergic receptor kinase-2 and beta-arrestin-2 as mediators of odorant-induced desensitization (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-05
    Description: beta-Adrenergic receptor kinase (beta ARK) and beta-arrestin function in the homologous or agonist-activated desensitization of G protein-coupled receptors. The isoforms beta ARK-2 and beta-arrestin-2 are highly enriched in and localized to the dendritic knobs and cilia of the olfactory receptor neurons where the initial events of olfactory signal transduction occur. Odorants induce a rapid and transient elevation of adenosine 3',5'-monophosphate (cAMP), which activates a nonspecific cation channel and produces membrane depolarization. Preincubation of rat olfactory cilia with antibodies raised against beta ARK-2 and beta-arrestin-2 increased the odorant-induced elevation of cAMP and attenuated desensitization. These results suggest that beta ARK-2 and beta-arrestin-2 mediate agonist-dependent desensitization in olfaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawson, T M -- Arriza, J L -- Jaworsky, D E -- Borisy, F F -- Attramadal, H -- Lefkowitz, R J -- Ronnett, G V -- NS 01578-01/NS/NINDS NIH HHS/ -- NS-02131/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Feb 5;259(5096):825-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins Medical Institutions, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8381559" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*metabolism ; *Arrestins ; Cells, Cultured ; Cyclic AMP/metabolism ; *Cyclic AMP-Dependent Protein Kinases ; Cytosol/metabolism ; Dendrites/physiology ; Eye Proteins/*metabolism ; G-Protein-Coupled Receptor Kinase 2 ; GTP-Binding Proteins/*metabolism ; Isoenzymes/metabolism ; Male ; Mechanoreceptors/*physiology ; Neurons/*physiology ; *Odors ; Olfactory Bulb/*physiology ; Protein Kinases/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, beta/*physiology ; Signal Transduction ; *Smell ; Testis/physiology ; Turbinates/*physiology ; beta-Adrenergic Receptor Kinases
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  • 98
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    Proliferation of human smooth muscle cells promoted by lipoprotein(a) (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-11
    Description: Elevated blood concentrations of lipoprotein(a) [Lp(a)] and its constituent, apolipoprotein(a) [apo(a)], constitute a major risk factor for atherosclerosis, but their physiological activities remain obscure. Lp(a) and purified apo(a) stimulated the growth of human smooth muscle cells in culture. This effect resulted from inhibition of plasminogen activation, and consequently the activation by plasmin of latent transforming growth factor-beta, which is an inhibitor of smooth muscle cell growth. Because smooth muscle proliferation is one of the hallmarks of atherosclerotic lesions, these results point to a plausible mechanism for the atherogenic activity of Lp(a).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grainger, D J -- Kirschenlohr, H L -- Metcalfe, J C -- Weissberg, P L -- Wade, D P -- Lawn, R M -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1993 Jun 11;260(5114):1655-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Cambridge, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8503012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoproteins/physiology ; Apoprotein(a) ; Cell Division/drug effects/physiology ; Cells, Cultured ; Fibrinolysin/physiology ; Humans ; Lipoprotein(a)/*physiology ; Muscle, Smooth, Vascular/*cytology/metabolism ; Plasminogen Activators/metabolism ; Rats ; Tamoxifen/pharmacology ; Transforming Growth Factor beta/physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    DNA sequence determination by hybridization: a strategy for efficient large-scale sequencing (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-11
    Description: The concept of sequencing by hybridization (SBH) makes use of an array of all possible n-nucleotide oligomers (n-mers) to identify n-mers present in an unknown DNA sequence. Computational approaches can then be used to assemble the complete sequence. As a validation of this concept, the sequences of three DNA fragments, 343 base pairs in length, were determined with octamer oligonucleotides. Possible applications of SBH include physical mapping (ordering) of overlapping DNA clones, sequence checking, DNA fingerprinting comparisons of normal and disease-causing genes, and the identification of DNA fragments with particular sequence motifs in complementary DNA and genomic libraries. The SBH techniques may accelerate the mapping and sequencing phases of the human genome project.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drmanac, R -- Drmanac, S -- Strezoska, Z -- Paunesku, T -- Labat, I -- Zeremski, M -- Snoddy, J -- Funkhouser, W K -- Koop, B -- Hood, L -- New York, N.Y. -- Science. 1993 Jun 11;260(5114):1649-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biological and Medical Research Division, Argonne National Laboratory, IL 60439.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8503011" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cloning, Molecular ; Humans ; Macaca mulatta ; Molecular Sequence Data ; *Nucleic Acid Hybridization ; Oligonucleotide Probes ; Sequence Analysis, DNA/*methods
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    Ixr1, a yeast protein that binds to platinated DNA and confers sensitivity to cisplatin (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-30
    Description: Structure-specific recognition proteins (SSRPs) bind to DNA containing intrastrand cross-links formed by the anticancer drug cisplatin. A yeast gene encoding an SSRP, designated IXR1, was cloned and sequenced. The Ixr1 protein, a member of the high mobility group-box protein family, bound specifically to DNA modified with cisplatin but not inactive platinum compounds. A yeast strain with an inactivated IXR1 gene was half as sensitive to cisplatin and accumulated one-third as many platinum-DNA lesions after treatment with cisplatin as the parental strain. These findings suggest that SSRPs play a role in mediating the cytotoxicity of cisplatin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, S J -- Kellett, P J -- Lippard, S J -- New York, N.Y. -- Science. 1993 Jul 30;261(5121):603-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8342024" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cisplatin/*metabolism/*pharmacology ; Cloning, Molecular ; DNA/*metabolism ; *DNA Adducts ; DNA, Fungal/*metabolism ; *DNA-Binding Proteins ; Fungal Proteins/chemistry/genetics/*metabolism ; Genes, Fungal ; High Mobility Group Proteins/chemistry/genetics/*metabolism ; Molecular Sequence Data ; Saccharomyces cerevisiae/chemistry/drug effects/genetics/*metabolism ; *Saccharomyces cerevisiae Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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