UbiGolD SIGNED
Deciphering ubiquitin-dependent regulation of Golgi homeostasis control in neurodegeneration
Total Cost €
0EC-Contrib. €
0Partnership
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Project "UbiGolD" data sheet
The following table provides information about the project.
| Coordinator |
WEIZMANN INSTITUTE OF SCIENCE
Organization address contact info |
| Coordinator Country | Israel [IL] |
| Total cost | 185˙464 € |
| EC max contribution | 185˙464 € (100%) |
| Programme |
1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility) |
| Code Call | H2020-MSCA-IF-2018 |
| Funding Scheme | MSCA-IF-EF-ST |
| Starting year | 2019 |
| Duration (year-month-day) | from 2019-04-01 to 2021-03-31 |
Partnership
Take a look of project's partnership.
| # | ||||
|---|---|---|---|---|
| 1 | WEIZMANN INSTITUTE OF SCIENCE | IL (REHOVOT) | coordinator | 185˙464.00 |
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Project objective
Alzheimer’s disease (AD) is the most common neurodegenerative disorder which affects 47 million patients worldwide. However, the underlying molecular mechanisms leading to sporadic-AD remain unknown and preventive treatment is not yet available. Lately, the ubiquitin-proteasome system has been implicated in AD. Dr. Merbl’s laboratory recently discovered a novel mechanism of Golgi-localized proteasomal degradation that controls Golgi integrity under stress. As the Golgi apparatus is the major hub required for protein secretion and plasma membrane localization, its proper function is crucial for maintaining cellular homeostasis and controlled cell-cell communication. This intriguing finding may be of instrumental importance to evidence of Golgi fragmentation which is observed in neurons in neurodegeneration diseases including AD as the Merbl lab identified that the ubiquitin-proteasome system is required for Golgi fragmentation. My goal is to identify regulatory mechanisms of ubiquitin E3 ligases that are involved in Golgi fragmentation in neurons. Specifically, I aim to identify critical determinants that regulate Golgi homeostasis and integrity under changing pH and calcium concentration and decipher their role in AD using CRISPR gene manipulation, pH-dependent immunofluorescence and biochemical methods and state-of-the-art proteomic and glycomic techniques. Elucidating ubiquitin-dependent regulation of Golgi fragmentation in neurodegeneration and AD would advance our understanding not only of Golgi biology and provide new possibilities for therapeutic intervention for neurodegeneration.
Publications
| year | authors and title | journal | last update |
|---|---|---|---|
| 2020 |
Avital Eisenberg-Lerner, Ron Benyair, Noa Hizkiahou, Neta Nudel, Roey Maor, Matthias P. Kramer, Merav D. Shmueli, Inbal Zigdon, Marina Cherniavsky Lev, Adi Ulman, Jitka Yehudith Sagiv, Molly Dayan, Bareket Dassa, Mercedes Rosenwald, Idit Shachar, Jie Li, Yanzhuang Wang, Nili Dezorella, Suman Khan, Ziv Porat, Eyal Shimoni, Ori Avinoam, Yifat Merbl Golgi organization is regulated by proteasomal degradation published pages: , ISSN: 2041-1723, DOI: 10.1038/s41467-019-14038-9 |
Nature Communications 11/1 | 2020-04-15 |
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