Summary
In this project, I will investigate ineffective erythropoiesis as a contributing factor and potential therapeutic target in the pathogenesis of sickle cell disease (SCD), one of the most prevalent genetic disorders in man and a global health problem. I will employ cutting-edge proteomic and genomic approaches to investigate in detail deregulation of the master erythroid transcription factor GATA1 as a result of oxidative stress in sickle red blood cells, as the basis for ineffective erythropoiesis in SCD. I will also investigate whether restoring GATA1 functions can alleviate ineffective erythropoiesis, thus providing alternative therapeutic opportunities in treating SCD. Lastly, I will generate novel cellular models for SCD from patients that can be used in dissecting the pathophysiology of SCD and in screening for agents that can alleviate IE and sickling. My project will generate novel insight into SCD pathogenesis and tools that can lead to the development of novel therapeutic approaches. My background in SCD cellular pathophysiology is highly complementary to those of my supervisors, Prof. John Strouboulis who is an expert in GATA1 functions in molecular erythropoiesis and Prof. David Rees, who is a world leading clinician in pediatric sickle cell disease. I stand to benefit greatly by receiving excellent training in -omics, functional assays in molecular erythropoiesis and in clinical aspects of SCD, that will enable me to progress into a career as an independent investigator.
Unfold all
/
Fold all
More information & hyperlinks
| Web resources: | https://cordis.europa.eu/project/id/101024970 |
| Start date: | 01-02-2022 |
| End date: | 31-01-2024 |
| Total budget - Public funding: | 212 933,76 Euro - 212 933,00 Euro |
Cordis data
Original description
In this project, I will investigate ineffective erythropoiesis as a contributing factor and potential therapeutic target in the pathogenesis of sickle cell disease (SCD), one of the most prevalent genetic disorders in man and a global health problem. I will employ cutting-edge proteomic and genomic approaches to investigate in detail deregulation of the master erythroid transcription factor GATA1 as a result of oxidative stress in sickle red blood cells, as the basis for ineffective erythropoiesis in SCD. I will also investigate whether restoring GATA1 functions can alleviate ineffective erythropoiesis, thus providing alternative therapeutic opportunities in treating SCD. Lastly, I will generate novel cellular models for SCD from patients that can be used in dissecting the pathophysiology of SCD and in screening for agents that can alleviate IE and sickling. My project will generate novel insight into SCD pathogenesis and tools that can lead to the development of novel therapeutic approaches. My background in SCD cellular pathophysiology is highly complementary to those of my supervisors, Prof. John Strouboulis who is an expert in GATA1 functions in molecular erythropoiesis and Prof. David Rees, who is a world leading clinician in pediatric sickle cell disease. I stand to benefit greatly by receiving excellent training in -omics, functional assays in molecular erythropoiesis and in clinical aspects of SCD, that will enable me to progress into a career as an independent investigator.Status
SIGNEDCall topic
MSCA-IF-2020Update Date
28-04-2024
Images
No images available.
Geographical location(s)
Structured mapping
