Q84259 (Q84259): Difference between revisions
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(Removed claim: financed by (P890): European Union (Q1)) |
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| Property / financed by: European Union / rank | |||
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| Property / financed by: Directorate-General for Regional and Urban Policy / rank | |||
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Revision as of 18:53, 8 February 2020
Project in Poland financed by DG Regio
| Language | Label | Description | Also known as |
|---|---|---|---|
| English | No label defined |
Project in Poland financed by DG Regio |
Statements
3,200,000.0 zloty
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3,200,000.0 zloty
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100.0 percent
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1 March 2018
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28 February 2023
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UNIWERSYTET GDAŃSKI
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Mitochondrial DNA, partially associated with mitochondrial inner membrane, is at the heart of ROS production thus, relative to nuDNA, mtDNA contains high levels of oxidative damage. Many of these damages are mutagenic and cause disease. Located on the inner membrane, base excision repair pathway is a major defense mechanism against oxidative damage. EXOG, a membrane-bound 5'-exo/endonuclease, is crucial for mtDNA repair. Depletion of EXOG causes accumulation of DNA damage in the mitochondria, but not in the nucleus, increases oxidative stress and mitochondrial dysfunction and leads to cell death. We propose that N-terminal transmembrane domain of EXOG anchors BER repairosome to mitochondrial inner membrane and modulates crucial 5'exonuclease activity of the enzyme. Because preservation of mtDNA integrity in cancer cells is a key for cancer progression, we aim to develop inhibitors to specifically halt function of EXOG and increase sensitivity to traditional chemotherapeutics. (Polish)
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Identifiers
POIR.04.04.00-00-3E44/17
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