Delayed neuronal death after brain trauma involves p53-dependent inhibition of NF-κB transcriptional activity
نویسندگان
چکیده
منابع مشابه
Delayed neuronal death after brain trauma involves p53-dependent inhibition of NF-kappaB transcriptional activity.
Acute and chronic neurodegeneration, for example, following brain injury or Alzheimer's disease, is characterized by programmed death of neuronal cells. The present study addresses the role and interaction of p53- and NF-kappaB-dependent mechanisms in delayed neurodegeneration following traumatic brain injury (TBI). After experimental TBI in mice p53 rapidly accumulated in the injured brain tis...
متن کاملPhagocytosis executes delayed neuronal death after focal brain ischemia.
Delayed neuronal loss and brain atrophy after cerebral ischemia contribute to stroke and dementia pathology, but the mechanisms are poorly understood. Phagocytic removal of neurons is generally assumed to be beneficial and to occur only after neuronal death. However, we report herein that inhibition of phagocytosis can prevent delayed loss and death of functional neurons after transient brain i...
متن کاملHypoxia-inducible factor-1alpha mediates hypoxia-induced delayed neuronal death that involves p53.
Hypoxia-induced delayed neuronal death is known to require de novo gene expression; however, the molecular mediators that are involved remain undefined. The transcription factor hypoxia-inducible factor-1alpha (HIF-1alpha), in addition to promoting the expression of adaptive genes under conditions of hypoxia, has been implicated as being a necessary component in p53-mediated cell death in tumor...
متن کاملLoss of p53 enhances NF-κB-dependent lamellipodia formation.
Tumor suppressor p53 prevents tumorigenesis and tumor growth by suppressing the activation of several transcription factors, including nuclear factor-κB (NF-κB) and STAT3. On the other hand, p53 stimulates actin cytoskeleton remodeling and integrin-related signaling cascades. Here, we examined the p53-mediated link between regulation of the actin cytoskeleton and activation of NF-κB and STAT3 i...
متن کاملDown-regulation of NF-κB transcriptional activity in HIV-associated kidney disease by BRD4 inhibition.
NF-κB-mediated inflammation is the major pathology in chronic kidney diseases, including HIV-associated nephropathy (HIVAN) that ultimately progresses to end stage renal disease. HIV infection in the kidney induces NF-κB activation, leading to the production of proinflammatory chemokines, cytokines, and adhesion molecules. In this study, we explored selective inhibition of NF-κB transcriptional...
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 Death & Differentiation
سال: 2007
ISSN: 1350-9047,1476-5403
DOI: 10.1038/sj.cdd.4402159