Explore the words cloud of the CRISTONE project. It provides you a very rough idea of what is the project "CRISTONE" about.
The following table provides information about the project.
UNIVERSITE DE GENEVE
|Coordinator Country||Switzerland [CH]|
|Total cost||265˙840 €|
|EC max contribution||265˙840 € (100%)|
1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
|Duration (year-month-day)||from 2017-09-01 to 2020-08-31|
Take a look of project's partnership.
|1||UNIVERSITE DE GENEVE||CH (GENEVE)||coordinator||265˙840.00|
|2||YESHIVA UNIVERSITY||US (NEW YORK)||partner||0.00|
Cancer is responsible for 8.5 million deaths worldwide each year, representing a considerable burden for society. In cancer cells, tumor repression genes are deactivated by epigenetic mechanisms. The accessibility of DNA to transcription factors is determined in part by the chemical modifications of histones, proteins that pack DNA into condensed chromatin. When histones are deacetylated by histone deacetylases (HDACs), the chromatin structure is even more packed, preventing gene expression. HDAC inhibitors are epigenetic drugs currently in the market, able to increase histone acetylation, unpacking DNA for gene transcription. However, the specific mechanisms leading to the success or failure of those drugs are poorly understood, leading to unpredictable therapeutic outcomes. HDAC inhibitors are expected to interact with HDACs in the cell nucleus. However, fluorescence-labeling has revealed HDAC inhibitors to locate mostly outside the nucleus in living cells, suggesting that their genomic effects represent only part of their activities. This project aims at developing a set of tools, using a modified genome-editing method and a fluorescent chemical probe combined with genome-wide assays to understand specifically the genomic mechanisms of HDAC inhibitors. We will develop the CRISTONE (CRISPR-based HDAC inhibitor targeted to histones) tool to allow targeted HDAC inhibition. We will target an HDAC1 inhibitor (a histone tail peptide) specifically to repressed loci in the genome of HDAC1-overexpressing HEK 293T cells. To understanding the transcriptional consequences of targeted and untargeted HDAC1 inhibition, the CRISTONE effects will be compared to those of a new fluorescent chemical probe capable of inhibiting nuclear HDACs. To assess the cellular phenotypic outcome, we will test the genome-wide cellular effects on transcription and chromatin accessibility, giving insights into the specific effects of genomic, targeted HDAC inhibition.
|year||authors and title||journal||last update|
Andrew D. Johnston, Claudia A. SimÃµes-Pires, Taylor V. Thompson, Masako Suzuki, John M. Greally
Functional genetic variants can mediate their regulatory effects through alteration of transcription factor binding
published pages: , ISSN: 2041-1723, DOI: 10.1038/s41467-019-11412-5
|Nature Communications 10/1||2019-08-29|
Are you the coordinator (or a participant) of this project? Plaese send me more information about the "CRISTONE" project.
For instance: the website url (it has not provided by EU-opendata yet), the logo, a more detailed description of the project (in plain text as a rtf file or a word file), some pictures (as picture files, not embedded into any word file), twitter account, linkedin page, etc.
Send me an email (email@example.com) and I put them in your project's page as son as possible.
Thanks. And then put a link of this page into your project's website.
The information about "CRISTONE" are provided by the European Opendata Portal: CORDIS opendata.
Contraception meets the environment: everyday contraceptive practices, politics, and futures in a toxic ageRead More
Narrative, Writing, and the Teotihuacan Language: Exploring Language History Through Phylogenetics, Epigraphy and IconographyRead More
Positive and Negative Asymmetry in Intergroup Contact: Its Impact on Linguistic Forms of Communication and Physiological ResponsesRead More