Moisoi 2009 Cell Death Differ: Difference between revisions
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{{Publication | {{Publication | ||
|title=Moisoi N, Klupsch K, Fedele V, East P, Sharma S, Renton A, Plun-Favreau H, Edwards RE, Teismann P, Esposti MD, Morrison AD, Wood NW, Downward J, Martins LM (2009) Mitochondrial dysfunction triggered by loss of HtrA2 results in the activation of a brain-specific transcriptional stress response. Cell Death Differ 16: 449- | |title=Moisoi N, Klupsch K, Fedele V, East P, Sharma S, Renton A, Plun-Favreau H, Edwards RE, Teismann P, Esposti MD, Morrison AD, Wood NW, Downward J, Martins LM (2009) Mitochondrial dysfunction triggered by loss of HtrA2 results in the activation of a brain-specific transcriptional stress response. Cell Death Differ 16:449-64. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed?term=Moisoi%2C%20N.%20et%20al.%20Cell%20Death%20Differ%2016%2C%20449%E2%80%93464%20(2009).%20 PMID: 19023330] | |info=[http://www.ncbi.nlm.nih.gov/pubmed?term=Moisoi%2C%20N.%20et%20al.%20Cell%20Death%20Differ%2016%2C%20449%E2%80%93464%20(2009).%20 PMID: 19023330] | ||
|authors=Moisoi N, Klupsch K, Fedele V, East P, Sharma S, Renton A, Plun-Favreau H, Edwards RE, Teismann P, Esposti MD, Morrison AD, Wood NW, Downward J, Martins LM | |authors=Moisoi N, Klupsch K, Fedele V, East P, Sharma S, Renton A, Plun-Favreau H, Edwards RE, Teismann P, Esposti MD, Morrison AD, Wood NW, Downward J, Martins LM | ||
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|organism=Mouse | |organism=Mouse | ||
|tissues=Nervous system, Liver | |tissues=Nervous system, Liver | ||
|preparations=Isolated | |preparations=Isolated mitochondria | ||
|injuries=RONS | |injuries=Oxidative stress;RONS, Mitochondrial disease | ||
|diseases=Parkinson's | |diseases=Parkinson's | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} |
Revision as of 13:37, 13 February 2015
Moisoi N, Klupsch K, Fedele V, East P, Sharma S, Renton A, Plun-Favreau H, Edwards RE, Teismann P, Esposti MD, Morrison AD, Wood NW, Downward J, Martins LM (2009) Mitochondrial dysfunction triggered by loss of HtrA2 results in the activation of a brain-specific transcriptional stress response. Cell Death Differ 16:449-64. |
Moisoi N, Klupsch K, Fedele V, East P, Sharma S, Renton A, Plun-Favreau H, Edwards RE, Teismann P, Esposti MD, Morrison AD, Wood NW, Downward J, Martins LM (2009) Cell Death Differ
Abstract: Cellular stress responses can be activated following functional defects in organelles such as mitochondria and the endoplasmic reticulum. Mitochondrial dysfunction caused by loss of the serine protease HtrA2 leads to a progressive movement disorder in mice and has been linked to parkinsonian neurodegeneration in humans. Here, we demonstrate that loss of HtrA2 results in transcriptional upregulation of nuclear genes characteristic of the integrated stress response, including the transcription factor CHOP, selectively in the brain. We also show that loss of HtrA2 results in the accumulation of unfolded proteins in the mitochondria, defective mitochondrial respiration and enhanced production of reactive oxygen species that contribute to the induction of CHOP expression and to neuronal cell death. CHOP expression is also significantly increased in Parkinson's disease patients' brain tissue. We therefore propose that this brain-specific transcriptional response to stress may be important in the advance of neurodegenerative diseases. โข Keywords: transcription factor CHOP, Parkinson's Disease, HtrA2 KO mice
โข O2k-Network Lab: UK Leicester Martins LM
Labels:
Pathology: Parkinson's
Stress:Oxidative stress;RONS, Mitochondrial disease
Organism: Mouse
Tissue;cell: Nervous system, Liver
Preparation: Isolated mitochondria
HRR: Oxygraph-2k