Loss of Pten, a tumor suppressor, causes the strong inhibition of autophagy without affecting LC3 lipidation

• Published in: Autophagy Vol. 4; no. 5; pp. 692 - 700
• Main Authors: Ueno, Takashi, Sato, Wataru, Horie, Yasuo, Komatsu, Masaaki, Tanida, Isei, Yoshida, Mitsutaka, Ohshima, Shigetoshi, Mak, Tak Wah, Watanabe, Sumio, Kominami, Eiki
• Format: Journal Article
• Language: English
• Published: United States Taylor & Francis 01.07.2008
• Subjects: Animals; Apoptosis Regulatory Proteins - antagonists & inhibitors; Apoptosis Regulatory Proteins - physiology; Autophagy - genetics; Autophagy - physiology; Binding; Biology; Bioscience; Calcium; Cancer; Cell; Cells, Cultured; Cycle; Genes, Tumor Suppressor - physiology; Hepatocytes - metabolism; Hepatocytes - pathology; Insulin - physiology; Landes; Lipid Metabolism - physiology; Mice; Mice, Inbred C57BL; Mice, Transgenic; Microtubule-Associated Proteins - metabolism; Organogenesis; Phagosomes - metabolism; Proteins; PTEN Phosphohydrolase - antagonists & inhibitors; PTEN Phosphohydrolase - deficiency; PTEN Phosphohydrolase - genetics; Signal Transduction - genetics; Starvation - metabolism

1Pten (phosphatase and tensin homolog deleted on chromosome ten), a tumor suppressor, is a phosphatase with a variety of substrate specificities. Its function as a negative regulator of the class I phosphatidyl-inositol 3-kinase/Akt pathway antagonizes insulin-dependent cell signaling. The targeted...