ArticleAntioxidants & redox signaling2011
C-terminus of heat shock cognate 70 interacting protein increases following stroke and impairs survival against acute oxidative stress.
Article in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Association betweenGenes · 2023Article
- CHIP ameliorates neuronal damage in HScientific reports · 2022Article
- AMP-activated protein kinase alpha1 promotes tumor development via FOXP3 elevation in tumor-infiltrating Treg cells.iScience · 2022Article
- CHIP ameliorates cerebral ischemia-reperfusion injury by attenuating necroptosis and inflammation.Aging · 2021Article
- Conserved and Unique Roles of Chaperone-Dependent E3 Ubiquitin Ligase CHIP in Plants.Frontiers in plant science · 2021Review
- CHIP as a therapeutic target for neurological diseases.Cell death & disease · 2020Review
- AAV/BBB-Mediated Gene Transfer of CHIP Attenuates Brain Injury Following Experimental Intracerebral Hemorrhage.Translational stroke research · 2020Article
- Dynamic Phosphorylation of the C Terminus of Hsp70 Regulates the Mitochondrial Import of SOD2 and Redox Balance.Cell reports · 2018Article
- Post-translational modification of OCT4 in breast cancer tumorigenesis.Cell death and differentiation · 2018Article
- Neuronal Preconditioning Requires the Mitophagic Activity of C-terminus of HSC70-Interacting Protein.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Alterations in the E3 ligases Parkin and CHIP result in unique metabolic signaling defects and mitochondrial quality control issues.Neurochemistry international · 2018Review
- Aurora Kinase A Promotes AR Degradation via the E3 Ligase CHIP.Molecular cancer research : MCR · 2017Article
- Article
- rAAV8-733-Mediated Gene Transfer of CHIP/Stub-1 Prevents Hippocampal Neuronal Death in Experimental Brain Ischemia.Molecular therapy : the journal of the American Society of Gene Therapy · 2017Article
- CHIP Is an Essential Determinant of Neuronal Mitochondrial Stress Signaling.Antioxidants & redox signaling · 2015Article
- Aggregation-prone c9FTD/ALS poly(GA) RAN-translated proteins cause neurotoxicity by inducing ER stress.Acta neuropathologica · 2014Article
- E3 ubiquitin ligase CHIP and NBR1-mediated selective autophagy protect additively against proteotoxicity in plant stress responses.PLoS genetics · 2014Article
- The E3 ligase CHIP: insights into its structure and regulation.BioMed research international · 2014Review
- Alteration of isocitrate dehydrogenase following acute ischemic injury as a means to improve cellular energetic status in neuroadaptation.CNS & neurological disorders drug targets · 2013Article
- Redox modification of proteins as essential mediators of CNS autophagy and mitophagy.FEBS letters · 2013Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
The decision to remove or refold oxidized, denatured, or misfolded proteins by heat shock protein 70 and its binding partners is critical to determine cell fate under pathophysiological conditions. Overexpression of the ubiquitin ligase C-terminus of HSC70 interacting protein (CHIP) can compensate for failure of other ubiquitin ligases and enhance protein turnover and survival under chronic neurological stress. The ability of CHIP to alter cell fate after acute neurological injury has not been assessed. Using postmortem human tissue samples, we provide the first evidence that cortical CHIP expression is increased after ischemic stroke. Oxygen glucose deprivation in vitro led to rapid protein oxidation, antioxidant depletion, proteasome dysfunction, and a significant increase in CHIP expression. To determine if CHIP upregulation enhances neural survival, we overexpressed CHIP in vitro and evaluated cell fate 24 h after acute oxidative stress. Surprisingly, CHIP overexpressing cells fared worse against oxidative injury, accumulated more ubiquitinated and oxidized proteins, and experienced decreased proteasome activity. Conversely, using small interfering RNA to decrease CHIP expression in primary neuronal cultures improved survival after oxidative stress, suggesting that increases in CHIP observed after stroke like injuries are likely correlated with diminished survival and may negatively impact the neuroprotective potential of heat shock protein 70.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.