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- W2610269969 abstract "Abstract : Traumatic brain injury (TBI) is a major cause of long-term disability. Acute TBI prompts a constellation of dysfunctional processes, collectively known as secondary injury mechanisms. A hallmark secondary injury in TBI is a prolonged imbalance in calcium homeostasis, resulting in a dramatic influx of calcium into brain cells. This influx elicits the generation of damaging reactive oxygen species. Protein carbonylation and citrullination are pathological post-translational modifications that can result from intracellular calcium overload. These modifications have been proposed to play a role in neurodegenerative disorders, including Alzheimers disease, and multiple sclerosis. Both carbonylation and citrullination can contribute to ongoing dysfunction, either through direct loss of protein function or via immune-based mechanisms where proteins specifically modified by citrullination become targeted by the adaptive immune system. This work investigated carbonylation and citrullination in a rodent model of TBI. We have identified specific regions and cell types susceptible to these modifications following TBI." @default.
- W2610269969 created "2017-05-12" @default.
- W2610269969 creator A5052824715 @default.
- W2610269969 date "2015-05-04" @default.
- W2610269969 modified "2023-09-24" @default.
- W2610269969 title "Protein Modification: A Proposed Mechanism for the Long-Term Pathogenesis of Traumatic Brain Injury" @default.
- W2610269969 doi "https://doi.org/10.21236/ad1012716" @default.
- W2610269969 hasPublicationYear "2015" @default.
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