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  • Articles  (34)
  • Gene Expression Regulation  (34)
  • American Association for the Advancement of Science (AAAS)  (34)
  • Springer
  • 2005-2009
  • 1985-1989  (34)
  • 1989  (14)
  • 1987  (20)
Collection
  • Articles  (34)
Source
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (34)
  • Springer
Years
  • 2005-2009
  • 1985-1989  (34)
Year
Journal
Topic
  • 1
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    Neurotoxicity of a fragment of the amyloid precursor associated with Alzheimer's disease (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-07-28
    Description: Amyloid deposition in senile plaques and the cerebral vasculature is a marker of Alzheimer's disease. Whether amyloid itself contributes to the neurodegenerative process or is simply a by-product of that process is unknown. Pheochromocytoma (PC12) and fibroblast (NIH 3T3) cell lines were transfected with portions of the gene for the human amyloid precursor protein. Stable PC12 cell transfectants expressing a specific amyloid-containing fragment of the precursor protein gradually degenerated when induced to differentiate into neuronal cells with nerve growth factor. Conditioned medium from these cells was toxic to neurons in primary hippocampal cultures, and the toxic agent could be removed by immunoabsorption with an antibody directed against the amyloid polypeptide. Thus, a peptide derived from the amyloid precursor may be neurotoxic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yankner, B A -- Dawes, L R -- Fisher, S -- Villa-Komaroff, L -- Oster-Granite, M L -- Neve, R L -- HD 18655/HD/NICHD NIH HHS/ -- HD 18658/HD/NICHD NIH HHS/ -- NS 01240/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Jul 28;245(4916):417-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Harvard Medical School, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2474201" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*etiology/pathology ; Amyloid/genetics/*physiology ; Blotting, Northern ; Cell Line ; Fibroblasts ; Gene Expression Regulation ; Humans ; Immunoblotting ; Neurons/pathology ; Nucleic Acid Hybridization ; Pheochromocytoma ; Protein Precursors/genetics/*physiology ; RNA/analysis/genetics ; Restriction Mapping ; Transfection ; Tumor Cells, Cultured
    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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    Tissue distribution and developmental expression of the messenger RNA encoding angiogenin (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-17
    Description: New blood vessel growth occurs during normal fetal development and in diseases such as cancer and diabetes. The polypeptide angiogenin induces new blood vessel growth in two biological assays and may play a role in the vascular development of the fetus and in the neovascularization that accompanies diseases and wound healing. A complementary DNA probe for human angiogenin was used to examine the tissue distribution of angiogenin messenger RNA (mRNA) in the developing rat and in selected transformed cell lines. Angiogenin mRNA was detected predominantly in adult liver but was also detectable at low levels in other tissues. The expression of the angiogenin gene in rat liver was found to be developmentally regulated; mRNA levels were low in the developing fetus, increased in the neonate, and maximal in the adult. The amount of angiogenin mRNA in human HT-29 colon carcinoma and SK-HEP hepatoma cells was not greater than that in normal rat liver. These results demonstrate that angiogenin is predominantly expressed in adult liver, that the pattern of angiogenin gene expression is not temporally related to vascular development in the rat, and that the transformed cells studied do not contain more angiogenin mRNA than does normal liver. If angiogenin activity is controlled at the transcriptional level, the results of this study suggest that the primary function of angiogenin in vivo may be in processes other than the regulation of vascular growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weiner, H L -- Weiner, L H -- Swain, J L -- HL26831/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 17;237(4812):280-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2440105" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Animals ; Cell Line ; Gene Expression Regulation ; Humans ; Liver/physiology ; Neoplasm Proteins/*genetics ; Neovascularization, Pathologic ; RNA, Messenger/genetics ; Rats ; *Ribonuclease, Pancreatic ; Tissue Distribution
    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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  • 3
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    Expression of functional nerve growth factor receptors after gene transfer (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-01-20
    Description: Nerve growth factor (NGF) interacts with both high affinity (Kd = 10(-10)-10(-11)M) and low affinity (Kd = 10(-8)-10(-9)M) receptors; the binding of NGF to the high affinity receptor is correlated with biological actions of NGF. To determine whether a single NGF binding protein is common to both forms of the receptor, a full-length receptor cDNA was introduced in the NR18 cell line, an NGF receptor-deficient variant of the PC12 pheochromocytoma cell line. The transformant displayed (i) both high and low affinity receptors detectable by receptor binding; (ii) an affinity cross-linking pattern with 125I-labeled NGF similar to that of the parent PC12 cell line; and (iii) biological responsiveness to NGF as assayed by induction of c-fos transcription. These findings support the hypothesis that a single binding protein is common to both forms of the NGF receptor and suggest that an additional protein is required to produce the high affinity form of the NGF receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hempstead, B L -- Schleifer, L S -- Chao, M V -- HD23315/HD/NICHD NIH HHS/ -- NS-21072/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1989 Jan 20;243(4889):373-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology/Oncology, 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/2536190" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blotting, Northern ; Cloning, Molecular ; Gene Expression Regulation ; Nerve Growth Factors/pharmacology ; Pheochromocytoma ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins c-fos ; Rats ; Receptors, Cell Surface/*genetics/metabolism ; Receptors, Nerve Growth Factor ; Transformation, Genetic ; Tumor Cells, Cultured
    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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    Cloning and expression of a Xenopus embryonic gap junction protein (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-03-03
    Description: Gap junctions in the early amphibian embryo may play a fundamental role in the regulation of differentiation by mediating the cell-to-cell transfer of chemical signals. A complementary DNA encoding a gap junction present in Xenopus oocytes and early embryos has now been cloned and sequenced. This protein sequence is homologous to the well-characterized gap junction structural proteins rat connexin32 and connexin43. RNA blot analysis of total Xenopus oocyte RNA showed hybridization to a single 1.6-kilobase band. This messenger RNA is abundant in oocytes, decreases to levels below the sensitivity of our assay by stage 15 (18 hours), and is not detectable in RNA from a number of adult organs. To confirm that the oocyte cDNA encodes a gap junction channel, the protein was over expressed in Xenopus oocytes by injection of RNA synthesized in vitro. Pairs of RNA-injected oocytes formed many more time- and voltage-sensitive cell-cell channels than water-injected pairs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ebihara, L -- Beyer, E C -- Swenson, K I -- Paul, D L -- Goodenough, D A -- GM18974/GM/NIGMS NIH HHS/ -- GM37751/GM/NIGMS NIH HHS/ -- HL28958-06/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Mar 3;243(4895):1194-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2466337" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Communication ; *Cloning, Molecular ; Connexins ; DNA Probes ; Electric Conductivity ; Female ; Gene Expression Regulation ; Intercellular Junctions/physiology ; Membrane Proteins/*genetics/physiology ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Oocytes/analysis/physiology ; RNA/analysis ; RNA, Messenger/analysis ; Rats ; Tissue Distribution ; Xenopus/*embryology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    HTLV x gene mutants exhibit novel transcriptional regulatory phenotypes (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-06
    Description: The human T-cell leukemia viruses, HTLV-I and HTLV-II, contain a gene, termed x, with transcriptional regulatory function. The properties of the x proteins were analyzed by constructing mutant genes containing site-directed deletions and point mutations. The results demonstrate that the amino terminal 17 amino acids of the x protein constitute part of a functional domain that is critical for the transcriptional activating properties of the protein. Within this region, substitution of a leucine residue for a proline residue results in major changes in the trans-activation phenotype of the protein. The mutant HTLV-II x protein, though incapable of activating the HTLV-II long terminal repeat, will block trans-activation of the HTLV-II long terminal repeat by the wild-type protein. The altered phenotype of this mutant suggests a potential negative regulatory function of the x protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wachsman, W -- Cann, A J -- Williams, J L -- Slamon, D J -- Souza, L -- Shah, N P -- Chen, I S -- CA 30388/CA/NCI NIH HHS/ -- CA 32727/CA/NCI NIH HHS/ -- CA 38597/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Feb 6;235(4789):674-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3027894" target="_blank"〉PubMed〈/a〉
    Keywords: Deltaretrovirus/*genetics ; Gene Expression Regulation ; *Genes, Viral ; Mutation ; Transcription Factors/*genetics ; Transcription, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    In situ detection of beta-galactosidase in lenses of transgenic mice with a gamma-crystallin/lacZ gene (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-23
    Description: Transgenic mice carrying the gamma 2-crystallin promoter fused to the coding region of the bacterial lacZ gene were generated. The offspring of three founder mice expressed high levels of the enzyme solely in the central nuclear fiber cells of the lens as measured by an in situ assay for the detection of beta-galactosidase activity. These results suggest that gamma 2-crystallin sequences between -759 to +45 contain essential information required for appropriate tissue-specific and temporal regulation of the mouse gamma 2-crystallin gene. In a broader context, this study also demonstrates the utility of beta-galactosidase hybrid gene constructs for monitoring the activity of gene regulatory elements in transgenic mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goring, D R -- Rossant, J -- Clapoff, S -- Breitman, M L -- Tsui, L C -- New York, N.Y. -- Science. 1987 Jan 23;235(4787):456-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3099390" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cataract/enzymology ; Crystallins/*genetics ; Galactosidases/*genetics ; Gene Expression Regulation ; *Lac Operon ; Lens, Crystalline/*physiology ; Mice ; Promoter Regions, Genetic ; Recombinant Fusion Proteins/*genetics ; Recombinant Proteins/*genetics ; Tissue Distribution ; Transfection ; beta-Galactosidase/*genetics/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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  • 7
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    Amyloid beta protein gene: cDNA, mRNA distribution, and genetic linkage near the Alzheimer locus (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-20
    Description: The amyloid beta protein has been identified as an important component of both cerebrovascular amyloid and amyloid plaques of Alzheimer's disease and Down syndrome. A complementary DNA for the beta protein suggests that it derives from a larger protein expressed in a variety of tissues. Overexpression of the gene in brain tissue from fetuses with Down syndrome (trisomy 21) can be explained by dosage since the locus encoding the beta protein maps to chromosome 21. Regional localization of this gene by both physical and genetic mapping places it in the vicinity of the genetic defect causing the inherited form of Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanzi, R E -- Gusella, J F -- Watkins, P C -- Bruns, G A -- St George-Hyslop, P -- Van Keuren, M L -- Patterson, D -- Pagan, S -- Kurnit, D M -- Neve, R L -- AG00029/AG/NIA NIH HHS/ -- HD10658/HD/NICHD NIH HHS/ -- HD20118/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Feb 20;235(4791):880-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2949367" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics ; Amino Acid Sequence ; Amyloid/*genetics ; Amyloidosis/genetics ; Brain/physiopathology ; Chromosome Mapping ; *Chromosomes, Human, Pair 21 ; DNA/genetics ; Down Syndrome/genetics ; Gene Expression Regulation ; Genetic Linkage ; Humans ; RNA, Messenger/genetics ; Tissue Distribution ; Transcription, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    AP1/jun function is differentially induced in promotion-sensitive and resistant JB6 cells (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-05-05
    Description: Tumor promoters may bring about events that lead to neoplastic transformation by inducing specific promotion-relevant effector genes. Functional activation of the transacting transcription factor AP-1 by the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) may play an essential role in this process. Clonal genetic variants of mouse epidermal JB6 cells that are genetically susceptible (P+) or resistant (P-) to promotion of transformation by TPA were transfected with 3XTRE-CAT, a construct that has AP-1 cis-enhancer sequences attached to a reporter gene encoding chloramphenicol acetyltransferase (CAT). Transfected JB6 P+, but not P- variants, showed TPA-inducible CAT synthesis. Epidermal growth factor, another transformation promoter in JB6 cells, also caused P+ specific induction of CAT gene expression. These results demonstrate an association between induced AP-1 function and sensitivity to promotion of neoplastic transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bernstein, L R -- Colburn, N H -- New York, N.Y. -- Science. 1989 May 5;244(4904):566-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins University, Department of Biology, Baltimore, MD 21218.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2541502" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cell Transformation, Neoplastic ; Chloramphenicol O-Acetyltransferase/genetics ; Cloning, Molecular ; DNA-Binding Proteins/genetics/*physiology ; Epidermal Growth Factor/pharmacology ; Epidermis ; Gene Expression Regulation ; Genetic Variation ; Kinetics ; Mice ; Nucleic Acid Hybridization ; Plasmids ; Promoter Regions, Genetic ; Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-jun ; Simplexvirus/genetics ; Tetradecanoylphorbol Acetate/*pharmacology ; Transcription Factors/genetics/*physiology ; Transfection
    Print ISSN: 0036-8075
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  • 9
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    Switch protein alters specificity of RNA polymerase containing a compartment-specific sigma factor (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-01-27
    Description: During sporulation in Bacillus subtilis, expression of developmental genes spoIVCB and cotD is induced in the mother cell compartment of the sporangium at morphological stages IV and V, respectively. A 27-kilodalton RNA polymerase sigma factor called sigma K (or sigma 27) has been found that causes weak transcription of spoIVCB and strong transcription of cotD. A 14-kD protein was also discovered that changes the specificity of sigma K-containing RNA polymerase, greatly stimulating spoIVCB transcription and markedly repressing cotD transcription. Both sigma K and the 14-kD protein are products of genes known to be required for expression of specific genes in the mother cell. Thus, sigma K directs gene expression in the mother cell and it is proposed that inactivation or sequestering of the 14-kD protein switches the temporal pattern of gene expression during the transition from stages IV to V of development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kroos, L -- Kunkel, B -- Losick, R -- GM18568/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1989 Jan 27;243(4890):526-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Developmental Biology, Harvard University, Cambridge, Massachusetts 02138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2492118" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacillus subtilis/*genetics/physiology ; Cloning, Molecular ; DNA-Directed RNA Polymerases/*genetics/isolation & purification ; Electrophoresis, Polyacrylamide Gel ; Gene Expression Regulation ; Molecular Sequence Data ; Promoter Regions, Genetic ; Sigma Factor/*genetics/isolation & purification ; Spores, Bacterial/genetics ; Transcription Factors/*genetics ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 10
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    Gene signals relapse of breast, ovarian cancers (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-05-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1989 May 12;244(4905):654-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2566202" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics/pathology ; Female ; *Gene Amplification ; Gene Expression Regulation ; Humans ; Lymph Nodes/pathology ; *Neoplasm Recurrence, Local ; Ovarian Neoplasms/*genetics ; Prognosis ; Proto-Oncogene Proteins/*genetics ; *Proto-Oncogenes ; Receptor, ErbB-2
    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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