Mitochondria, calcium, and tumor suppressor Fus1: At the crossroad of cancer, inflammation, and autoimmunity

摘要: // Roman Uzhachenko 1 , Anil Shanker 1, 2 Wendell G. Yarbrough 3, 4, 5 Alla V. Ivanova 3 Department of Biochemistry and Cancer Biology, Meharry Medical College, Nashville, Tennessee, United States Vanderbilt-Ingram Comprehensive Center, Vanderbilt University, Surgery, Division Otolaryngology, Yale School Medicine, New Haven, Connecticut, 4 Pathology, Correspondence to: Ivanova, e-mail: alla.ivanova@yale.edu Keywords: Fus1/Tusc2, mitochondria, calcium, tumor suppressor, inflammation, autoimmunity Received: March 23, 2015      Accepted: June 27, Published: July 15, 2015 ABSTRACT Mitochondria present a unique set key intracellular functions such as ATP synthesis, production reactive oxygen species (ROS) Ca 2+ buffering. both encode decode signals these interrelated have direct impact on cell signaling metabolism. High proliferative potential is energy-demanding feature shared by cancer cells activated T lymphocytes. Switch metabolic state mediated alterations in mitochondrial homeostasis plays fundamental role maintenance the state. Recent studies show that suppressors ability to affect controlling autoimmunity. Herein, we discuss established putative mechanisms calcium–dependent regulation activities. We use protein Fus1 case suppressor controls immune response growth via homeostasis. focus handling function highlight crosstalk between accumulation Given important signaling, transport ROS activation NFAT NF-κB transcription factors, outline importance activities this context.