GADD34 induces cell death through inactivation of Akt following traumatic brain injury

Neuronal cell death contributes significantly to the pathology of traumatic brain injury (TBI) irrespective of the mode or severity of the injury. Activation of a pro-survival protein, Akt, is known to be regulated by an E3 ligase TRAF6 through a process of ubiquitination-coupled phosphorylation at...

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Bibliographic Details
Published in:	Cell death & disease Vol. 4; no. 8; p. e754
Main Authors:	Farook, J M, Shields, J, Tawfik, A, Markand, S, Sen, T, Smith, S B, Brann, D, Dhandapani, K M, Sen, N
Format:	Journal Article
Language:	English
Published:	London Nature Publishing Group UK 01-08-2013 Springer Nature B.V Nature Publishing Group
Subjects:	631/378/1934 631/80/86 692/699/375/1345 Activating Transcription Factor 4 - metabolism Animals Antibodies Apoptosis Biochemistry Biomedical and Life Sciences Brain Injuries - enzymology Cell Biology Cell Culture Cell death Cells, Cultured Cerebral Cortex - enzymology Cerebral Cortex - pathology Endoplasmic Reticulum Stress Excitatory Amino Acid Agonists - pharmacology Homeostasis Immunology Life Sciences Male Mice Mice, Inbred C57BL N-Methylaspartate - pharmacology Neurons - physiology Original original-article Phosphorylation Primary Cell Culture Promoter Regions, Genetic Protein Binding Protein Phosphatase 1 - genetics Protein Phosphatase 1 - metabolism Proto-Oncogene Proteins c-akt - metabolism Reactive Oxygen Species - metabolism TNF Receptor-Associated Factor 6 - metabolism Transcriptional Activation Ubiquitination GADD34 TBI Akt cell death TRAF6
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