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Oncogenes and Growth Factors Abstracts

  
 
The discovery of oncogenes in the late 1970s represented a primary break through in unraveling the mechanisms that cause cancerous cell growth- and this database enables scientists to keep abreast of both experimental and clinical literature focusing on mechanisms of oncogenes and growth factors. Conceived by two NIH scientist, Oncogenes and Growth Factors Abstracts covers every aspect of oncogene research into the molecular basis of malignant transformations. This journal will prove indispensable insuggesting new directions for research and helping scientists avoid deadends or costly duplication of work. A necessity for molecular biologists researching cell growth and oncogenesis, Oncogenes and Growth Factors Abstracts will also be valuable to researchers in immunology, virology, bacteriology, genetics, and other related fields.

Subject Coverage
    Oncogenes, Growth Factors and Growth Factor Receptors associated with:
    • Tyrosine kinase activity
    • Serine-threonine kinase activity
    • Tyrosine phosphatase activity
    • Serine-threonine phosphatase activity
    • Cell cycle and DNA repair
    Also includes:
    • Guanine nucleotide-binding proteins
    • Guanine nucleotide exchange factors
    • Nuclear oncogenes and DNA-binding proteins
    • Viral oncogenes
    • Tumor suppressor genes and Anti-oncogenes
    • Metastasis
Dates of Coverage
    June 1989 - present
Update Frequency
    Monthly, with approximately 200 new records added
Size
    Over 0 records as of May 2013
Print Equivalent
    Oncogenes and Growth Factors Abstracts (1989 - 1996)
Supplier
    Proquest
    789 E. Eisenhower Parkway
    P.O. Box 1346
    Ann Arbor, MI 48106-1346
    Tel: +1-734-761-4700
Sample Record

    TI:

    Title
    Cell adhesion and prostate tumor-suppressor activity of TSLL2/IGSF4C, an immunoglobulin superfamily molecule homologous to TSLC1/IGSF4

    AU:

    Author
    Williams, YN; Masuda, M; Sakurai-Yageta, M; Maruyama, T; Shibuya, M; Murakami, Y

    AF:

    Author Affiliation
    Tumor Suppression and Functional Genomics Project, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan, ymurakam@gan2.ncc.go.jp

    SO:

    Source
    Oncogene [Oncogene]. Vol. 25, no. 10, pp. 1446-1453. 9 Mar 2006

    IS:

    ISSN
    0950-9232

    DE:

    Descriptors
    Prostate cancer; Immunoglobulins; Cell adhesion; IGSF4 protein; Urinary bladder; renal tubules; Brain; Cell adhesion molecules; Calcium; Confocal microscopy; Loss of heterozygosity; Homology

    AB:

    Abstract
    The TSLL2/IGSF4C encodes an immunoglobulin (Ig) superfamily molecule showing significant homology with a lung tumor suppressor, TSLC1. The TSLL2 protein of 55kDa is mainly expressed in the kidney, bladder, and prostate in addition to the brain. Here, we report the biological significance of TSLL2 in the urinary tissues. An immunohistochemical study reveals that TSLL2 is expressed at the cell-cell attachment sites in the renal tubules, the transitional epithelia of the bladder, and the glandular epithelia of the prostate. Confocal microscopy analysis demonstrates that TSLL2 is localized in the lateral membranes in polarized Mardin-Darby canine kidney (MDCK) cells. TSLL2 forms homo-dimers and its overexpression induces aggregation of suspended MDCK cells in a Ca super(2+)/Mg super(2+)-independent manner, suggesting that it is involved in cell adhesion through homophilic trans-interaction. The TSLL2 gene is mapped on the chromosomal region 19q13.2, whose loss of heterozygosity has been frequently reported in prostate cancer. TSLL2 protein is lost in nine of nine primary prostate cancers and in a prostate cancer cell, PPC-1. Introduction of TSLL2 into PPC-1 strongly suppresses subcutaneous tumor formation in nude mice. These results suggest that TSLL2 is a new member of the Ig superfamily cell adhesion molecules and is a tumor-suppressor candidate in prostate cancer.

    LA:

    Language
    English

    SL:

    Summary Language
    English

    PY:

    Publication Year
    2006

    PT:

    Publication Type
    Journal Article

    PB:

    Publisher
    Nature Publishing Group, The Macmillan Building, 4 Crinan Street, London
    N1 9XW, UK, feedback@nature.com, http://www.nature.com/

    DO:

    DOI
    10.1038/sj.onc.1209192

    CL:

    Classification
    B 26416 Other tumor suppressor genes/antioncogenes

    UD:

    Update
    200605

    SF:

    Subfile
    Oncogenes & Growth Factors Abstracts

    AN:

    Accession Number
    6759117

    PG:

    Journal Pages
    1446-1453

    JV:

    Journal Volume
    25

    JI:

    Journal Issue
    10
Field Codes
    The following field codes are found in the records of this database.Here they are listed in alphabetical order by two-letter code. See Field Codes and Search Examples for detailed descriptions and search examples.

    AB = Abstract IS = ISSN
    AF = Author Affiliation LA = Language
    AN = Accession Number NT = Notes
    AU = Authors NU = Other Numbers
    CA = Corporate Author OT = Original Title
    CF = Conference PB = Publisher
    CL =Classification Code PT = Publication Type
    DE = Descriptors PY = Publication Year
    ED= Editor SF = Subfile Name
    EM = EntryMonth SL = Summary Language
    ER =Environmental Regime SO = Source
    IB = ISBN TI = Title
    ID = Identifiers TR= Asfa Input Center Number
 
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