These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Phospholipase D and the Mitogen Phosphatidic Acid in Human Disease: Inhibitors of PLD at the Crossroads of Phospholipid Biology and Cancer.
    Author: Gomez-Cambronero J, Shah KN.
    Journal: Handb Exp Pharmacol; 2020; 259():89-113. PubMed ID: 31541319.
    Abstract:
    Lipids are key building blocks of biological membranes and are involved in complex signaling processes such as metabolism, proliferation, migration, and apoptosis. Extracellular signaling by growth factors, stress, and nutrients is transmitted through receptors that activate lipid-modifying enzymes such as the phospholipases, sphingosine kinase, or phosphoinositide 3-kinase, which then modify phospholipids, sphingolipids, and phosphoinositides. One such important enzyme is phospholipase D (PLD), which cleaves phosphatidylcholine to yield phosphatidic acid and choline. PLD isoforms have dual role in cells. The first involves maintaining cell membrane integrity and cell signaling, including cell proliferation, migration, cytoskeletal alterations, and invasion through the PLD product PA, and the second involves protein-protein interactions with a variety of binding partners. Increased evidence of elevated PLD expression and activity linked to many pathological conditions, including cancer, neurological and inflammatory diseases, and infection, has motivated the development of dual- and isoform-specific PLD inhibitors. Many of these inhibitors are reported to be efficacious and safe in cells and mouse disease models, suggesting the potential for PLD inhibitors as therapeutics for cancer and other diseases. Current knowledge and ongoing research of PLD signaling networks will help to evolve inhibitors with increased efficacy and safety for clinical studies.
    [Abstract] [Full Text] [Related] [New Search]