Targeting Mitochondrial DNA repair for novel anti-cancer therapy (Q84259): Difference between revisions
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(Created claim: summary (P836): Mitochondrial DNA, participating with with Mitochondrial inner membrane, is at the heart of the output of thus, relative to nausea, mtDNA contains high levels of reproductive age.Any of these dacages are mutagenicity and cause disease.Accommodated on the inner membrane, base decision repair path is a major defence against reproductive damage.EXOG, and membranes bound 5 '-exo/endonuccrelease, is crucial for mtDNA repairs.Removal of EXOG causes ac...) |
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| Property / summary | |||
Mitochondrial DNA, participating with with Mitochondrial inner membrane, is at the heart of the output of thus, relative to nausea, mtDNA contains high levels of reproductive age.Any of these dacages are mutagenicity and cause disease.Accommodated on the inner membrane, base decision repair path is a major defence against reproductive damage.EXOG, and membranes bound 5 '-exo/endonuccrelease, is crucial for mtDNA repairs.Removal of EXOG causes accumulation of DNA damage in the mitochondria, but not in the nucleus, increases meaningful stress and Mitochondrial dysfunction and leads are cell demoath.By means that N terminal, the transmembrane domain of EXOG BER reporirosome to Mitochondrial to Mitochondrial and modulates rcial 5'excucrelease activity of the Enzyme.Cause Conservation of mtDNA integrates in cancer progression is a key for cancer progression. (English) | |||
| Property / summary: Mitochondrial DNA, participating with with Mitochondrial inner membrane, is at the heart of the output of thus, relative to nausea, mtDNA contains high levels of reproductive age.Any of these dacages are mutagenicity and cause disease.Accommodated on the inner membrane, base decision repair path is a major defence against reproductive damage.EXOG, and membranes bound 5 '-exo/endonuccrelease, is crucial for mtDNA repairs.Removal of EXOG causes accumulation of DNA damage in the mitochondria, but not in the nucleus, increases meaningful stress and Mitochondrial dysfunction and leads are cell demoath.By means that N terminal, the transmembrane domain of EXOG BER reporirosome to Mitochondrial to Mitochondrial and modulates rcial 5'excucrelease activity of the Enzyme.Cause Conservation of mtDNA integrates in cancer progression is a key for cancer progression. (English) / rank | |||
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Revision as of 10:02, 4 March 2020
Project in Poland financed by DG Regio
| Language | Label | Description | Also known as |
|---|---|---|---|
| English | Targeting Mitochondrial DNA repair for novel anti-cancer therapy |
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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Mitochondrial DNA, participating with with Mitochondrial inner membrane, is at the heart of the output of thus, relative to nausea, mtDNA contains high levels of reproductive age.Any of these dacages are mutagenicity and cause disease.Accommodated on the inner membrane, base decision repair path is a major defence against reproductive damage.EXOG, and membranes bound 5 '-exo/endonuccrelease, is crucial for mtDNA repairs.Removal of EXOG causes accumulation of DNA damage in the mitochondria, but not in the nucleus, increases meaningful stress and Mitochondrial dysfunction and leads are cell demoath.By means that N terminal, the transmembrane domain of EXOG BER reporirosome to Mitochondrial to Mitochondrial and modulates rcial 5'excucrelease activity of the Enzyme.Cause Conservation of mtDNA integrates in cancer progression is a key for cancer progression. (English)
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Identifiers
POIR.04.04.00-00-3E44/17
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