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  • Articles  (195)
  • Male  (195)
  • Cell & Developmental Biology
  • American Association for the Advancement of Science (AAAS)  (195)
  • 1995-1999  (195)
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  • Articles  (195)
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  • American Association for the Advancement of Science (AAAS)  (195)
  • Wiley-Blackwell  (240)
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  • 1
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    A single ataxia telangiectasia gene with a product similar to PI-3 kinase (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-23
    Description: A gene, ATM, that is mutated in the autosomal recessive disorder ataxia telangiectasia (AT) was identified by positional cloning on chromosome 11q22-23. AT is characterized by cerebellar degeneration, immunodeficiency, chromosomal instability, cancer predisposition, radiation sensitivity, and cell cycle abnormalities. The disease is genetically heterogeneous, with four complementation groups that have been suspected to represent different genes. ATM, which has a transcript of 12 kilobases, was found to be mutated in AT patients from all complementation groups, indicating that it is probably the sole gene responsible for this disorder. A partial ATM complementary DNA clone of 5.9 kilobases encoded a putative protein that is similar to several yeast and mammalian phosphatidylinositol-3' kinases that are involved in mitogenic signal transduction, meiotic recombination, and cell cycle control. The discovery of ATM should enhance understanding of AT and related syndromes and may allow the identification of AT heterozygotes, who are at increased risk of cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Savitsky, K -- Bar-Shira, A -- Gilad, S -- Rotman, G -- Ziv, Y -- Vanagaite, L -- Tagle, D A -- Smith, S -- Uziel, T -- Sfez, S -- Ashkenazi, M -- Pecker, I -- Frydman, M -- Harnik, R -- Patanjali, S R -- Simmons, A -- Clines, G A -- Sartiel, A -- Gatti, R A -- Chessa, L -- Sanal, O -- Lavin, M F -- Jaspers, N G -- Taylor, A M -- Arlett, C F -- Miki, T -- Weissman, S M -- Lovett, M -- Collins, F S -- Shiloh, Y -- HG00882/HG/NHGRI NIH HHS/ -- NS31763/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1995 Jun 23;268(5218):1749-53.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, Sackler School of Medicine, Tel Aviv University, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7792600" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Ataxia Telangiectasia/*genetics ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle ; Cell Cycle Proteins ; Chromosome Mapping ; Chromosomes, Artificial, Yeast ; *Chromosomes, Human, Pair 11 ; Cloning, Molecular ; DNA, Complementary/genetics ; DNA-Binding Proteins ; Female ; Genetic Complementation Test ; Genetic Predisposition to Disease ; Heterozygote ; Humans ; Male ; Meiosis ; Molecular Sequence Data ; Neoplasms/genetics ; Nucleic Acid Hybridization ; Phosphatidylinositol 3-Kinases ; Phosphotransferases (Alcohol Group Acceptor)/chemistry/*genetics/physiology ; *Protein-Serine-Threonine Kinases ; Proteins/chemistry/*genetics/physiology ; Radiation Tolerance ; Sequence Deletion ; Signal Transduction ; Tumor Suppressor Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Distinct mechanism for antidepressant activity by blockade of central substance P receptors (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-11
    Description: The localization of substance P in brain regions that coordinate stress responses and receive convergent monoaminergic innervation suggested that substance P antagonists might have psychotherapeutic properties. Like clinically used antidepressant and anxiolytic drugs, substance P antagonists suppressed isolation-induced vocalizations in guinea pigs. In a placebo-controlled trial in patients with moderate to severe major depression, robust antidepressant effects of the substance P antagonist MK-869 were consistently observed. In preclinical studies, substance P antagonists did not interact with monoamine systems in the manner seen with established antidepressant drugs. These findings suggest that substance P may play an important role in psychiatric disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kramer, M S -- Cutler, N -- Feighner, J -- Shrivastava, R -- Carman, J -- Sramek, J J -- Reines, S A -- Liu, G -- Snavely, D -- Wyatt-Knowles, E -- Hale, J J -- Mills, S G -- MacCoss, M -- Swain, C J -- Harrison, T -- Hill, R G -- Hefti, F -- Scolnick, E M -- Cascieri, M A -- Chicchi, G G -- Sadowski, S -- Williams, A R -- Hewson, L -- Smith, D -- Carlson, E J -- Hargreaves, R J -- Rupniak, N M -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1640-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Merck Research Laboratories, West Point, PA 19456, USA. Mark_Kramer@merck.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733503" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Amygdala/drug effects/metabolism ; Animals ; Antidepressive Agents, Second-Generation/adverse ; effects/metabolism/pharmacology/*therapeutic use ; Behavior, Animal/drug effects ; Brain/drug effects/metabolism ; Depressive Disorder/*drug therapy/etiology/metabolism ; Female ; Gerbillinae ; Guinea Pigs ; Humans ; Male ; Middle Aged ; Morpholines/adverse effects/metabolism/pharmacology/*therapeutic use ; *Neurokinin-1 Receptor Antagonists ; Norepinephrine/physiology ; Paroxetine/therapeutic use ; Receptors, Neurokinin-1/metabolism ; Serotonin/physiology ; Stress, Psychological/drug therapy ; Substance P/*antagonists & inhibitors/metabolism ; Vocalization, Animal/drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Immune system impairment and hepatic fibrosis in mice lacking the dioxin-binding Ah receptor (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-05-05
    Description: The aryl hydrocarbon (Ah) receptor (AHR) mediates many carcinogenic and teratogenic effects of environmentally toxic chemicals such as dioxin. An AHR-deficient (Ahr-/-) mouse line was constructed by homologous recombination in embryonic stem cells. Almost half of the mice died shortly after birth, whereas survivors reached maturity and were fertile. The Ahr-/- mice showed decreased accumulation of lymphocytes in the spleen and lymph nodes, but not in the thymus. The livers of Ahr-/- mice were reduced in size by 50 percent and showed bile duct fibrosis Ahr-/- mice were also nonresponsive with regard to dioxin-mediated induction of genes encoding enzymes that catalyze the metabolism of foreign compounds. Thus, the AHR plays an important role in the development of the liver and the immune system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fernandez-Salguero, P -- Pineau, T -- Hilbert, D M -- McPhail, T -- Lee, S S -- Kimura, S -- Nebert, D W -- Rudikoff, S -- Ward, J M -- Gonzalez, F J -- P30 ES06096/ES/NIEHS NIH HHS/ -- R01 ES06811/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1995 May 5;268(5211):722-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7732381" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Gene Expression Regulation/physiology ; Immunity/*physiology ; Liver/*physiology ; Liver Cirrhosis, Experimental/genetics/pathology ; Lymphoid Tissue/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Receptors, Aryl Hydrocarbon/genetics/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Control of autoimmune diabetes in NOD mice by GAD expression or suppression in beta cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-15
    Description: Glutamic acid decarboxylase (GAD) is a pancreatic beta cell autoantigen in humans and nonobese diabetic (NOD) mice. beta Cell-specific suppression of GAD expression in two lines of antisense GAD transgenic NOD mice prevented autoimmune diabetes, whereas persistent GAD expression in the beta cells in the other four lines of antisense GAD transgenic NOD mice resulted in diabetes, similar to that seen in transgene-negative NOD mice. Complete suppression of beta cell GAD expression blocked the generation of diabetogenic T cells and protected islet grafts from autoimmune injury. Thus, beta cell-specific GAD expression is required for the development of autoimmune diabetes in NOD mice, and modulation of GAD might, therefore, have therapeutic value in type 1 diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoon, J W -- Yoon, C S -- Lim, H W -- Huang, Q Q -- Kang, Y -- Pyun, K H -- Hirasawa, K -- Sherwin, R S -- Jun, H S -- DK 45735/DK/NIDDK NIH HHS/ -- DK 53015-01/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 May 14;284(5417):1183-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral and Immunopathogenesis of Diabetes, Julia McFarlane Diabetes Research Centre, Faculty of Medicine, University of Calgary, Calgary, Alberta T2N 4N1, Canada. yoon@ucalgary.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10325232" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Autoantigens/genetics/*immunology/physiology ; Autoimmunity ; DNA, Antisense ; Diabetes Mellitus, Type 1/*enzymology/*immunology/pathology ; Female ; Gene Expression ; Glutamate Decarboxylase/genetics/*immunology/physiology ; Insulin/blood/metabolism ; Islets of Langerhans/*enzymology/immunology/metabolism/pathology ; Islets of Langerhans Transplantation ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; T-Lymphocytes/immunology ; Transgenes
    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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    Bone marrow as a potential source of hepatic oval cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-15
    Description: Bone marrow stem cells develop into hematopoietic and mesenchymal lineages but have not been known to participate in production of hepatocytes, biliary cells, or oval cells during liver regeneration. Cross-sex or cross-strain bone marrow and whole liver transplantation were used to trace the origin of the repopulating liver cells. Transplanted rats were treated with 2-acetylaminofluorene, to block hepatocyte proliferation, and then hepatic injury, to induce oval cell proliferation. Markers for Y chromosome, dipeptidyl peptidase IV enzyme, and L21-6 antigen were used to identify liver cells of bone marrow origin. From these cells, a proportion of the regenerated hepatic cells were shown to be donor-derived. Thus, a stem cell associated with the bone marrow has epithelial cell lineage capability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petersen, B E -- Bowen, W C -- Patrene, K D -- Mars, W M -- Sullivan, A K -- Murase, N -- Boggs, S S -- Greenberger, J S -- Goff, J P -- New York, N.Y. -- Science. 1999 May 14;284(5417):1168-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15261, USA. bryon+@pitt.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10325227" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Acetylaminofluorene/pharmacology ; Animals ; Bone Marrow Cells/*cytology ; Bone Marrow Transplantation ; Carbon Tetrachloride/pharmacology ; Cell Differentiation ; Cell Division ; DNA-Binding Proteins/genetics ; Dipeptidyl Peptidase 4/metabolism ; Epithelial Cells/cytology ; Female ; Hematopoietic Stem Cells/cytology ; In Situ Hybridization ; Liver/*cytology/drug effects/physiology ; *Liver Regeneration ; Liver Transplantation ; Male ; *Nuclear Proteins ; Polymerase Chain Reaction ; Rats ; Rats, Inbred F344 ; Rats, Inbred Lew ; Sex-Determining Region Y Protein ; Stem Cells/*cytology ; *Transcription Factors ; Y Chromosome
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  • 6
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    Dissociating pain from its anticipation in the human brain (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-18
    Description: The experience of pain is subjectively different from the fear and anxiety caused by threats of pain. Functional magnetic resonance imaging in healthy humans was applied to dissociate neural activation patterns associated with acute pain and its anticipation. Expectation of pain activated sites within the medial frontal lobe, insular cortex, and cerebellum distinct from, but close to, locations mediating pain experience itself. Anticipation of pain can in its own right cause mood changes and behavioral adaptations that exacerbate the suffering experienced by chronic pain patients. Selective manipulations of activity at these sites may offer therapeutic possibilities for treating chronic pain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ploghaus, A -- Tracey, I -- Gati, J S -- Clare, S -- Menon, R S -- Matthews, P M -- Rawlins, J N -- New York, N.Y. -- Science. 1999 Jun 18;284(5422):1979-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Functional Magnetic Resonance Imaging of the Brain, Department of Clinical Neurology, University of Oxford, Oxford OX3 9DU, UK. alex@fmrib.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10373114" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Anxiety/*physiopathology ; Brain/*physiology ; Brain Mapping ; Cerebellum/physiology ; Cerebral Cortex/physiology ; Cues ; Female ; Frontal Lobe/physiology ; Humans ; Magnetic Resonance Imaging ; Male ; Pain/*physiopathology/*psychology ; Pain Measurement ; Perception/*physiology
    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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  • 7
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    Monoallelic expression of the interleukin-2 locus (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-16
    Description: The lymphokine interleukin-2 (IL-2) is responsible for autocrine cell cycle progression and regulation of immune responses. Uncontrolled secretion of IL-2 results in adverse reactions ranging from anergy, to aberrant T cell activation, to autoimmunity. With the use of fluorescent in situ hybridization and single-cell polymerase chain reaction in cells with different IL-2 alleles, IL-2 expression in mature thymocytes and T cells was found to be tightly controlled by monoallelic expression. Because IL-2 is encoded at a nonimprinted autosomal locus, this result represents an unusual regulatory mode for controlling the precise expression of a single gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hollander, G A -- Zuklys, S -- Morel, C -- Mizoguchi, E -- Mobisson, K -- Simpson, S -- Terhorst, C -- Wishart, W -- Golan, D E -- Bhan, A K -- Burakoff, S J -- P01 CA39542-09/CA/NCI NIH HHS/ -- R01 AI17258-18/AI/NIAID NIH HHS/ -- R01 DK47677/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Mar 27;279(5359):2118-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pediatric Immunology, Department of Research and Children's Hospital, Basel University Medical School, 4031 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9516115" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; CD4-Positive T-Lymphocytes/cytology/*immunology ; Concanavalin A/pharmacology ; DNA Replication ; Female ; Flow Cytometry ; *Gene Expression Regulation ; Heterozygote ; In Situ Hybridization, Fluorescence ; Interleukin-2/biosynthesis/*genetics ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Muridae ; Mutation ; Polymerase Chain Reaction ; S Phase ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 8
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    Embryonic stem cell lines derived from human blastocysts (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-06
    Description: Human blastocyst-derived, pluripotent cell lines are described that have normal karyotypes, express high levels of telomerase activity, and express cell surface markers that characterize primate embryonic stem cells but do not characterize other early lineages. After undifferentiated proliferation in vitro for 4 to 5 months, these cells still maintained the developmental potential to form trophoblast and derivatives of all three embryonic germ layers, including gut epithelium (endoderm); cartilage, bone, smooth muscle, and striated muscle (mesoderm); and neural epithelium, embryonic ganglia, and stratified squamous epithelium (ectoderm). These cell lines should be useful in human developmental biology, drug discovery, and transplantation medicine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thomson, J A -- Itskovitz-Eldor, J -- Shapiro, S S -- Waknitz, M A -- Swiergiel, J J -- Marshall, V S -- Jones, J M -- New York, N.Y. -- Science. 1998 Nov 6;282(5391):1145-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wisconsin Regional Primate Research Center, University of Wisconsin, Madison, WI 53715, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9804556" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Tumor-Associated, Carbohydrate ; Blastocyst/*cytology ; *Cell Culture Techniques ; Cell Differentiation ; *Cell Line ; Cryopreservation ; Ectoderm/cytology ; Endoderm/cytology ; Female ; Glycosphingolipids/analysis ; Graft Rejection ; Humans ; Karyotyping ; Male ; Mesoderm/cytology ; Mice ; Mice, SCID ; Stage-Specific Embryonic Antigens ; Stem Cell Transplantation ; Stem Cells/chemistry/*cytology ; Telomerase/metabolism ; Teratoma/etiology ; Trophoblasts/cytology
    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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  • 9
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    Mutations in the SMAD4/DPC4 gene in juvenile polyposis (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-06
    Description: Familial juvenile polyposis is an autosomal dominant disease characterized by a predisposition to hamartomatous polyps and gastrointestinal cancer. Here it is shown that a subset of juvenile polyposis families carry germ line mutations in the gene SMAD4 (also known as DPC4), located on chromosome 18q21.1, that encodes a critical cytoplasmic mediator in the transforming growth factor-beta signaling pathway. The mutant SMAD4 proteins are predicted to be truncated at the carboxyl-terminus and lack sequences required for normal function. These results confirm an important role for SMAD4 in the development of gastrointestinal tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Howe, J R -- Roth, S -- Ringold, J C -- Summers, R W -- Jarvinen, H J -- Sistonen, P -- Tomlinson, I P -- Houlston, R S -- Bevan, S -- Mitros, F A -- Stone, E M -- Aaltonen, L A -- New York, N.Y. -- Science. 1998 May 15;280(5366):1086-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, University of Iowa College of Medicine, Iowa City, IA 52242, USA. james-howe@uiowa.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9582123" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Membrane/metabolism ; Cell Nucleus/metabolism ; Chromosome Mapping ; Chromosomes, Human, Pair 18 ; Colorectal Neoplasms/*genetics ; *DNA-Binding Proteins ; Female ; Frameshift Mutation ; Gastrointestinal Neoplasms/*genetics ; Genes, DCC ; *Genes, Tumor Suppressor ; Genetic Predisposition to Disease ; Germ-Line Mutation ; Hamartoma Syndrome, Multiple/*genetics ; Humans ; Intestinal Polyps/*genetics ; Male ; Pedigree ; Polymerase Chain Reaction ; Sequence Deletion ; Signal Transduction ; Smad4 Protein ; Trans-Activators/chemistry/*genetics/metabolism ; Transforming Growth Factor beta/metabolism
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  • 10
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    PTEN, a putative protein tyrosine phosphatase gene mutated in human brain, breast, and prostate cancer (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-28
    Description: Mapping of homozygous deletions on human chromosome 10q23 has led to the isolation of a candidate tumor suppressor gene, PTEN, that appears to be mutated at considerable frequency in human cancers. In preliminary screens, mutations of PTEN were detected in 31% (13/42) of glioblastoma cell lines and xenografts, 100% (4/4) of prostate cancer cell lines, 6% (4/65) of breast cancer cell lines and xenografts, and 17% (3/18) of primary glioblastomas. The predicted PTEN product has a protein tyrosine phosphatase domain and extensive homology to tensin, a protein that interacts with actin filaments at focal adhesions. These homologies suggest that PTEN may suppress tumor cell growth by antagonizing protein tyrosine kinases and may regulate tumor cell invasion and metastasis through interactions at focal adhesions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, J -- Yen, C -- Liaw, D -- Podsypanina, K -- Bose, S -- Wang, S I -- Puc, J -- Miliaresis, C -- Rodgers, L -- McCombie, R -- Bigner, S H -- Giovanella, B C -- Ittmann, M -- Tycko, B -- Hibshoosh, H -- Wigler, M H -- Parsons, R -- 5R35 CA39829/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1943-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, College of Physicians & Surgeons, Columbia University, 630 West 168 Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072974" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Brain Neoplasms/genetics ; Breast Neoplasms/genetics ; Chromosome Mapping ; *Chromosomes, Human, Pair 10 ; Female ; Frameshift Mutation ; *Genes, Tumor Suppressor ; Glioblastoma/genetics ; Humans ; Male ; Microfilament Proteins/chemistry ; Molecular Sequence Data ; *Mutation ; Neoplasm Transplantation ; Neoplasms/*genetics ; PTEN Phosphohydrolase ; *Phosphoric Monoester Hydrolases ; Phosphotyrosine/metabolism ; Prostatic Neoplasms/genetics ; Protein Tyrosine Phosphatases/chemistry/*genetics/physiology ; Protein-Tyrosine Kinases/antagonists & inhibitors ; Sequence Deletion ; Sequence Homology, Amino Acid ; Transplantation, Heterologous ; Tumor Cells, Cultured ; *Tumor Suppressor 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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