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  • Book
    Nandini Dey, Pradip De, Brian Leyland-Jones, editors.
    Contents:
    PI3K-Akt-mTOR Signaling in Cancer and Cancer Therapeutics
    Part 1: PI3K-mTOR Pathway in Cancers
    The mTOR Complexes in Cancer Cell Metabolism
    PI3K-AKT-mTOR Pathway Co-operates with the DNA Damage Repair Pathway: Carcinogenesis in Triple Negative Breast Cancers and Beyond
    The AKT-mTOR Signaling Pathway for Drug Response Prediction and Prognostic Signatures
    Resistance to PI3K Pathway Inhibition
    Part 2: PI3K-mTOR Pathway in Cancer Medicine
    Combination Therapies Targeting the PI3K/AKT/mTOR Pathways
    Phospho-Inositol-3-Kinase Activity and Dysregulation in Pediatric Leukemia and Lymphoma
    HER2 Signaling Network in Advanced Breast Cancer: Opportunities for Combination Therapies
    The PI3K-mTOR Pathway in Prostate Cancer: Biological Significance and Therapeutic Opportunities.
    Digital Access Springer 2016
  • Article
    Jones GE.
    J Bacteriol. 1977 Apr;130(1):128-30.
    The cistron that codes for L-asparaginase I in Saccharomyces cerevisiae (aspl) is not genetically linked to either of the cistrons coding for expression of asparaginase II (asp2 and asp3). Cells containing different combinations of theses enzymes grow at different rates in media in which L-asparagine or D-asparagine is the only source of nitrogen for cell replication. Cells lacking L-asparaginase I but possessing asparaginase II grow more rapidly in medium containing D-asparagine as a nitrogen source than cells containing both enzymes, even though D-asparagine is not a substrate of L-asparaginase I. These results indicate that L-asparaginase I and asparaginase II interact in some way to regulate the utilization of asparagine as a nitrogen source for cell growth.
    Digital Access Access Options