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  • Mice  (12)
  • Female  (4)
  • American Association for the Advancement of Science (AAAS)  (14)
  • EDP Sciences
  • 2015-2019  (4)
  • 1990-1994  (6)
  • 1985-1989  (4)
  • 1970-1974
  • 1945-1949
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  • 1
    Publication Date: 1990-04-06
    Description: The epidermal growth factor (EGF) receptor (EGFR) can efficiently couple with mitogenic signaling pathways when it is transfected into interleukin-3 (IL-3)-dependent 32D hematopoietic cells. When expression vectors for erbB-2, which is structurally related to EGFR, or its truncated counterpart, delta NerbB-2, were introduced into 32D cells, neither was capable of inducing proliferation. This was despite overexpression and constitutive tyrosine kinase activity of their products at levels associated with potent transformation of fibroblast target cells. Thus, EGFR and erbB-2 couple with distinct mitogenic signaling pathways. The region responsible for the specificity of intracellular signal transduction was localized to a 270-amino acid stretch encompassing their respective tyrosine kinase domains. Thus, tissue- or cell-specific regulation of growth factor receptor signaling can occur at a point after the initial interaction of growth factor with receptor. Such specificity in signal transduction may account for the selection of certain oncogenes in some malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Fiore, P P -- Segatto, O -- Taylor, W G -- Aaronson, S A -- Pierce, J H -- New York, N.Y. -- Science. 1990 Apr 6;248(4951):79-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2181668" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Division ; Cell Line ; DNA/genetics ; DNA, Recombinant ; Fibroblasts/cytology/metabolism ; Gene Expression ; Genetic Vectors ; Hematopoietic Stem Cells/cytology/metabolism ; Immunoblotting ; Mice ; *Mitogens ; Molecular Sequence Data ; Protein-Tyrosine Kinases/genetics/*physiology ; Proto-Oncogene Proteins/genetics/*physiology ; Receptor, Epidermal Growth Factor/genetics/*physiology ; Sequence Homology, Nucleic Acid ; Signal Transduction ; Transfection
    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
    Publication Date: 2015-10-17
    Description: Human skin relies on cutaneous receptors that output digital signals for tactile sensing in which the intensity of stimulation is converted to a series of voltage pulses. We present a power-efficient skin-inspired mechanoreceptor with a flexible organic transistor circuit that transduces pressure into digital frequency signals directly. The output frequency ranges between 0 and 200 hertz, with a sublinear response to increasing force stimuli that mimics slow-adapting skin mechanoreceptors. The output of the sensors was further used to stimulate optogenetically engineered mouse somatosensory neurons of mouse cortex in vitro, achieving stimulated pulses in accordance with pressure levels. This work represents a step toward the design and use of large-area organic electronic skins with neural-integrated touch feedback for replacement limbs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tee, Benjamin C-K -- Chortos, Alex -- Berndt, Andre -- Nguyen, Amanda Kim -- Tom, Ariane -- McGuire, Allister -- Lin, Ziliang Carter -- Tien, Kevin -- Bae, Won-Gyu -- Wang, Huiliang -- Mei, Ping -- Chou, Ho-Hsiu -- Cui, Bianxiao -- Deisseroth, Karl -- Ng, Tse Nga -- Bao, Zhenan -- New York, N.Y. -- Science. 2015 Oct 16;350(6258):313-6. doi: 10.1126/science.aaa9306.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Electrical Engineering, Stanford University, Stanford, CA, USA. ; Department of Materials Science and Engineering, Stanford University, Stanford, CA, USA. ; Department of Bioengineering, Stanford University, Stanford, CA, USA. ; Department of Chemistry, Stanford University, Stanford, CA, USA. ; Department of Chemical Engineering, Stanford University, Stanford, CA, USA. ; Xerox Palo Alto Research Center, Palo Alto, CA, USA. ; Department of Chemical Engineering, Stanford University, Stanford, CA, USA. zbao@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26472906" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebral Cortex/cytology/physiology ; Hand/anatomy & histology/innervation/physiology ; Humans ; In Vitro Techniques ; *Mechanoreceptors ; Mice ; *Neural Prostheses ; Optogenetics ; Pressure ; Skin/*innervation ; *Touch ; Transcutaneous Electric Nerve Stimulation/*methods ; Transistors, Electronic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 1985-06-28
    Description: The search for new congeners of the leading anticancer drug doxorubicin has led to an analog that is approximately 1000 times more potent, noncardiotoxic at therapeutic dose levels, and non-cross-resistant with doxorubicin. The new anthracycline, 3'-deamino-3'-(3-cyano-4-morpholinyl)doxorubicin (MRA-CN), is produced by incorporation of the 3' amino group of doxorubicin in a new cyanomorpholinyl ring. The marked increase in potency was observed against human ovarian and breast carcinomas in vitro; it was not accompanied by an increase in cardiotoxicity in fetal mouse heart cultures. Doxorubicin and MRA-CN both produced typical cardiac ultrastructural and biochemical changes, but at equimolar concentrations. In addition, MRA-CN was not cross-resistant with doxorubicin in a variant of the human sarcoma cell line MES-SA selected for resistance to doxorubicin. Thus antitumor efficacy was dissociated from both cardiotoxicity and cross-resistance by this modification of anthracycline structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikic, B I -- Ehsan, M N -- Harker, W G -- Friend, N F -- Brown, B W -- Newman, R A -- Hacker, M P -- Acton, E M -- CA 24543/CA/NCI NIH HHS/ -- CA 32250/CA/NCI NIH HHS/ -- CA 33303/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Jun 28;228(4707):1544-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4012308" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antineoplastic Agents ; Breast Neoplasms/drug therapy ; Cell Line ; Chemical Phenomena ; Chemistry ; Dose-Response Relationship, Drug ; Doxorubicin/adverse effects/*analogs & derivatives/therapeutic use ; Female ; Heart/drug effects ; Humans ; Isoenzymes ; L-Lactate Dehydrogenase/analysis ; Mice ; Myocardium/enzymology ; Ovarian Neoplasms/drug therapy ; Pregnancy
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 1986-04-25
    Description: Anterior pituitaries from the dwarf mouse strain "little" did not release growth hormone or accumulate adenosine 3',5'-monophosphate (cyclic AMP) in response to human and rat growth hormone-releasing factor (GRF). Dibutyryl cyclic AMP, as well as the adenylate cyclase stimulators forskolin and cholera toxin, markedly stimulated growth hormone (GH) release. The basis of the GH deficiency in the little mouse may therefore be a defect in an early stage of GRF-stimulated GH release related either to receptor binding or to the function of the hormone-receptor complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jansson, J O -- Downs, T R -- Beamer, W G -- Frohman, L A -- AM 17947/AM/NIADDK NIH HHS/ -- AM 30667/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 25;232(4749):511-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3008329" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Colforsin/pharmacology ; Cyclic AMP/analysis ; Dwarfism, Pituitary/*physiopathology ; Female ; Growth Hormone-Releasing Hormone/metabolism/pharmacology/physiology/secretion ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains/*physiology ; Pituitary Gland, Anterior/analysis/drug effects/physiopathology/secretion ; Receptors, Cell Surface/metabolism/*physiology ; *Receptors, Neuropeptide ; *Receptors, Pituitary Hormone-Regulating Hormone
    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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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1991-09-06
    Description: Alloimmune mice (mice that have been exposed to cells from another murine strain) were shown to make antibodies against gp120 and p24 of human immunodeficiency virus (HIV), and mice of the autoimmune strains MRL-lpr/lpr and MRL-(+)/+ made antibodies against gp120. This is surprising because the mice were not exposed to HIV. Furthermore, anti-anti-MHC antibodies (molecules that have shapes similar to those of major histocompatibility complex molecules) were detected in both alloimmune sera and MRL mice. These results are discussed in the context of a possible role for allogeneic stimuli in the pathogenesis of acquired immunodeficiency syndrome, as suggested by an idiotypic network model.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kion, T A -- Hoffmann, G W -- New York, N.Y. -- Science. 1991 Sep 6;253(5024):1138-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of British Columbia, Vancouver, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1909456" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; *Antibody Formation ; Autoimmune Diseases/genetics/*immunology/microbiology ; Enzyme-Linked Immunosorbent Assay ; Gene Products, gag/*immunology ; HIV Antibodies/*biosynthesis ; HIV Antigens/*immunology ; HIV Core Protein p24 ; HIV Envelope Protein gp120/*immunology ; Histocompatibility Antigens Class II/*immunology ; Isoantibodies/*biosynthesis ; *Major Histocompatibility Complex ; Mice ; Mice, Inbred BALB C ; Mice, Inbred CBA ; Mice, Mutant Strains ; T-Lymphocytes/immunology ; Viral Core Proteins/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 1989-06-02
    Description: The target of the CD8+ T cell-dependent immunity that protects mice immunized with irradiation-attenuated malaria sporozoites has not been established. Immune BALB/c mice were shown to develop malaria-specific, CD8+ T cell-dependent inflammatory infiltrates in their livers after challenge with Plasmodium berghei sporozoites. Spleen cells from immune BALB/c and C57BL/6 mice eliminated hepatocytes infected with the liver stage of P. berghei in vitro. The activity against infected hepatocytes is not inhibited by antibodies to interferon-gamma and is not present in culture supernatants. It is genetically restricted, an indication that malaria antigens on the hepatocyte surface are recognized by immune T effector cells. Subunit vaccine development will require identification of the antigens recognized by these T cells and a method of immunization that induces such immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, S L -- Isenbarger, D -- Long, G W -- Sedegah, M -- Szarfman, A -- Waters, L -- Hollingdale, M R -- van der Meide, P H -- Finbloom, D S -- Ballou, W R -- New York, N.Y. -- Science. 1989 Jun 2;244(4908):1078-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Infectious Diseases Department, Naval Medical Research Institute, Bethesda, MD 20814.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2524877" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology ; Antibodies, Protozoan/analysis ; Antigens, Protozoan/genetics/immunology ; H-2 Antigens/immunology ; *Immunization ; Interferon-gamma/immunology/pharmacology ; Liver/immunology/*parasitology ; Malaria/*immunology/parasitology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Plasmodium berghei/*immunology ; Recombinant Proteins ; Spleen/immunology ; T-Lymphocytes, Regulatory/*immunology ; Vaccines/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 1991-06-28
    Description: Trypanosoma brucei, the protozoan parasite responsible for African sleeping sickness, evades the host immune response through the process of antigenic variation. The variant antigen, known as the variant surface glycoprotein (VSG), is anchored to the cell surface by a glycosyl phosphatidylinositol (GPI) structure that contains myristate (n-tetradecanoate) as its only fatty acid component. The utilization of heteroatom-containing analogs of myristate was studied both in a cell-free system and in vivo. Results indicated that the specificity of fatty acid incorporation depends on chain length rather than on hydrophobicity. One analog, 10-(propoxy)decanoic acid, was highly toxic to trypanosomes in culture although it is nontoxic to mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doering, T L -- Raper, J -- Buxbaum, L U -- Adams, S P -- Gordon, J I -- Hart, G W -- Englund, P T -- 5T32GM07309/GM/NIGMS NIH HHS/ -- AI21334/AI/NIAID NIH HHS/ -- AI27179/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1991 Jun 28;252(5014):1851-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, Johns Hopkins Medical School, Baltimore, MD 21210.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1829548" target="_blank"〉PubMed〈/a〉
    Keywords: Acyl Coenzyme A/metabolism ; Animals ; Cell-Free System ; Glycolipids/metabolism ; Glycosylphosphatidylinositols ; Kinetics ; Mice ; Myristic Acid ; Myristic Acids/*metabolism/*pharmacology ; Phosphatidylinositols/metabolism ; Structure-Activity Relationship ; Trypanosoma brucei brucei/*drug effects/metabolism/ultrastructure
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 1993-08-13
    Description: The apolipoprotein E type 4 allele (APOE-epsilon 4) is genetically associated with the common late onset familial and sporadic forms of Alzheimer's disease (AD). Risk for AD increased from 20% to 90% and mean age at onset decreased from 84 to 68 years with increasing number of APOE-epsilon 4 alleles in 42 families with late onset AD. Thus APOE-epsilon 4 gene dose is a major risk factor for late onset AD and, in these families, homozygosity for APOE-epsilon 4 was virtually sufficient to cause AD by age 80.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corder, E H -- Saunders, A M -- Strittmatter, W J -- Schmechel, D E -- Gaskell, P C -- Small, G W -- Roses, A D -- Haines, J L -- Pericak-Vance, M A -- New York, N.Y. -- Science. 1993 Aug 13;261(5123):921-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Joseph and Kathleen Bryan Alzheimer's Disease Research Center, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8346443" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; Aging ; *Alleles ; Alzheimer Disease/*genetics/metabolism/mortality ; Amyloid beta-Peptides/metabolism ; Apolipoprotein E4 ; Apolipoproteins E/*genetics/physiology ; Female ; *Gene Frequency ; Genotype ; Homozygote ; Humans ; Linkage Disequilibrium ; Male ; Risk Factors ; Survival Rate
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  • 9
    Publication Date: 1989-06-02
    Description: The gene for von Recklinghausen neurofibromatosis (NF1), one of the most common autosomal-dominant disorders of humans, was recently mapped to chromosome 17 by linkage analysis. The identification of two NF1 patients with balanced translocations that involved chromosome 17q11.2 suggests that the disease can arise by gross rearrangement of the NF1 locus, and that the NF1 gene might be identified by cloning the region around these translocation breakpoints. To further define the region of these translocations, a series of chromosome 17 Not I-linking clones has been mapped to proximal 17q and studied by pulsed-field gel electrophoresis. One clone, 17L1 (D17S133), clearly identifies the breakpoint in an NF1 patient with a t(1;17) translocation. A 2.3-megabase pulsed-field map of this region was constructed and indicates that the NF1 breakpoint is only 10 to 240 kilobases away from 17L1. This finding prepares the way for the cloning of NF1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fountain, J W -- Wallace, M R -- Bruce, M A -- Seizinger, B R -- Menon, A G -- Gusella, J F -- Michels, V V -- Schmidt, M A -- Dewald, G W -- Collins, F S -- NS22224/NS/NINDS NIH HHS/ -- NS23410/NS/NINDS NIH HHS/ -- NS23427/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Jun 2;244(4908):1085-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Michigan, Ann Arbor 48109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2543076" target="_blank"〉PubMed〈/a〉
    Keywords: *Chromosome Mapping ; *Chromosomes, Human, Pair 17 ; Cloning, Molecular ; DNA Restriction Enzymes ; Electrophoresis ; Female ; Genetic Linkage ; Humans ; Hybrid Cells ; Male ; Neurofibromatosis 1/*genetics ; *Translocation, Genetic
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  • 10
    Publication Date: 1994-10-07
    Description: In this study, a protein that interacts with sequences encoded by the first exon of the protein kinase Bcr was cloned. The Bcr-associated protein 1 (Bap-1) is a member of the 14-3-3 family of proteins. Bap-1 interacts with full-length c-Bcr and with the chimeric Bcr-Abl tyrosine kinase of Philadelphia chromosome (Ph1)-positive human leukemias. Bap-1 is a substrate for the Bcr serine-threonine kinase and is also phosphorylated on tyrosine by Bcr-Abl but not by c-Abl. Bap-1 may function in the regulation of c-Bcr and may contribute to the transforming activity of Bcr-Abl in vivo. 14-3-3 proteins are essential for cell proliferation and have a role in determining the timing of mitosis in yeast. Through direct binding to sequences present in Bcr and in other proteins implicated in signaling, the mammalian 14-3-3 proteins may link specific signaling protein components to mitogenic and cell-cycle control pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reuther, G W -- Fu, H -- Cripe, L D -- Collier, R J -- Pendergast, A M -- CA61033/CA/NCI NIH HHS/ -- DK01965/DK/NIDDK NIH HHS/ -- GM07184/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Oct 7;266(5182):129-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939633" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Animals ; Cell Division ; Cell Line ; Cell Transformation, Neoplastic ; Fusion Proteins, bcr-abl/*metabolism ; Humans ; Mice ; Phosphorylation ; Poly(ADP-ribose) Polymerases/metabolism ; Protein-Tyrosine Kinases/*metabolism ; Proteins/isolation & purification/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-bcr ; Rats ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; *Tyrosine 3-Monooxygenase
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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