Cold Spring Harbor, NY — Cold Spring Harbor Laboratory Press announced the release of The PTEN Family,available on its website in hardcover and ebook formats.
The PTEN protein is a phosphatase that plays important roles as a tumor suppressor by negatively regulating the PI3K/Akt signaling pathway that controls cell proliferation and survival. Impaired PTEN function leads to unrestrained downstream signaling and, in turn, uncontrolled cell growth and cancer. PTEN also has other roles: Recent work has implicated it in a variety of additional biological processes, including control of DNA replication and repair, and in disparate pathological conditions (e.g., autism).
Written and edited by experts in the field, this collection from Cold Spring Harbor Perspectives in Medicine covers all aspects of PTEN biology and its roles in human diseases. The contributors discuss the structural characteristics of PTEN; its functions at the plasma membrane as well as in the cytoplasm and nucleus; the mutations, interacting partners, and posttranslational modifications that affect its expression levels, subcellular localization, and enzymatic activity; and how this activity ultimately leads to changes in cell growth, migration, and morphology, as well as in gene expression, chromatin dynamics, and the maintenance of genomic stability. A historical perspective that covers the initial discovery and subsequent characterization of PTEN is also included.
In addition, the authors discuss the loss of PTEN function in various cancers, as well as in immune, metabolic, and neurological disorders (e.g., autoimmunity, type 2 diabetes, and autism), and consider how this knowledge can be exploited for diagnostic and therapeutic purposes. This volume is therefore essential reading for all cell and molecular biologists, cancer biologists, and pharmacologists interested in PTEN’s remarkable biological complexity and importance in human health.
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Please visit our website at cshlpress.org to access free sample material and for further information on this title.
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