Targeting mitochondrial DNA repair for novel anti-cancer therapies (Q84259): Difference between revisions
Jump to navigation
Jump to search
(Changed label, description and/or aliases in 1 language: translated_label) |
(Changed label, description and/or aliases in 2 languages: Changing unique label-description pair) |
||
| description / en | description / en | ||
Project in Poland | Project Q84259 in Poland | ||
| description / pl | description / pl | ||
Projekt w Polsce | Projekt Q84259 w Polsce | ||
Revision as of 05:23, 29 October 2020
Project Q84259 in Poland
| Language | Label | Description | Also known as |
|---|---|---|---|
| English | Targeting mitochondrial DNA repair for novel anti-cancer therapies |
Project Q84259 in Poland |
Statements
3,200,000.0 zloty
0 references
3,200,000.0 zloty
0 references
100.0 percent
0 references
1 March 2018
0 references
28 February 2023
0 references
UNIWERSYTET GDAŃSKI
0 references
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)
0 references
Mitochondrial DNA, partially associated with mitochondrial inner membrane, is at the heart of ROS production thus, relative to boring, 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. (English)
14 October 2020
0 references
Identifiers
POIR.04.04.00-00-3E44/17
0 references