A FATal AP-1 dimer switch in hepatosteatosis
نویسندگان
چکیده
منابع مشابه
A FATal AP-1 dimer switch in hepatosteatosis
Activator protein 1 (AP-1) is a dimeric transcription factor with important roles in specifying genetic and cellular programs. AP-1 refers to a collection of DNAbinding homoand heterodimers formed by members of the JUN (c-Jun, JunB, and JunD) and FOS (c-Fos, FosB, Fra-1, and Fra-2) families, as well as ATF and MAF proteins. AP-1 dimers recognize similar and specific sequence elements in the pro...
متن کاملA Fatal Switch for Corals?
In the late summer of 2005, abnormally warm ocean temperatures led to the most severe coral bleaching event ever documented in the northeast Caribbean. Algae living in symbiotic harmony with their animal hosts were expelled, leaving great expanses of white, or so-called bleached, coral reef. In the 12 months following these high temperatures, disease incidence on corals rose sharply. Within two...
متن کاملPhotodynamic activation as a molecular switch to promote osteoblast cell differentiation via AP-1 activation
In photodynamic therapy (PDT), cells are impregnated with a photosensitizing agent that is activated by light irradiation, thereby photochemically generating reactive oxygen species (ROS). The amounts of ROS produced depends on the PDT dose and the nature of the photosensitizer. Although high levels of ROS are cytotoxic, at physiological levels they play a key role as second messengers in cellu...
متن کاملDown-regulation of c-Fos/c-Jun AP-1 dimer activity by sumoylation.
The inducible transcriptional complex AP-1, composed of c-Fos and c-Jun proteins, is crucial for cell adaptation to many environmental changes. While its mechanisms of activation have been extensively studied, how its activity is restrained is poorly understood. We report here that lysine 265 of c-Fos is conjugated by the peptidic posttranslational modifiers SUMO-1, SUMO-2, and SUMO-3 and that ...
متن کاملNF-κB-to-AP-1 Switch: A Mechanism Regulating Transition From Endothelial Barrier Injury to Repair in Endotoxemic Mice
Endothelial barrier disruption is a hallmark of multiple organ injury (MOI). However, mechanisms governing the restoration of endothelial barrier function are poorly understood. Here, we uncovered an NF-κB-to-AP-1 switch that regulates the transition from barrier injury to repair following endotoxemic MOI. Endothelial NF-κB mediates barrier repair by inhibiting endothelial cell (EC) apoptosis. ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Cell Cycle
سال: 2014
ISSN: 1538-4101,1551-4005
DOI: 10.4161/cc.28514