Understanding immune dysfunction in acute myeloid leukemia
- Research Opportunity
- PhD, Honours, Master of Biomedical Science
- Biochemistry and Molecular Biology
- Bio21 Molecular Science and Biotechnology Institute
|A/Prof Justine Minternfirstname.lastname@example.org||83442976||Personal web page|
|Professor Jose Villadangosemail@example.com|
Summary In this project, we will examine molecular mechanisms that regulate flt3 receptor in healthy settings and in a model of AML.
The growth factor receptor tyrosine kinase flt3 is the most frequently mutated gene in acute myeloid leukemia (AML). Flt3 is expressed by immune cells and promotes their function and survival. Patients with flt3 mutations have poorer prognosis and more aggressive disease.
In this project, we will examine molecular mechanisms that regulate flt3 receptor in healthy settings and in a model of AML. We will use microscopy, immunoprecipitation and flow cytometry to examine how the mutated flt3 receptor, compared to wild type receptor, is trafficked inside immune cells. These studies will incorporate the use of CRISPR/Cas9 to delete genes identified in patient studies that are implicated in flt3 function. In addition, we will examine how mutant flt3 impacts the ability of immune cells to elicit effective immunity.
Faculty Research Themes
School Research Themes
PhD, Honours, Master of Biomedical Science
Students who are interested in joining this project will need to consider their elegibility as well as other requirements before contacting the supervisor of this research
For further information about this research, please contact a supervisor.
Research Group / Unit / Centre
Research NodeBio21 Molecular Science and Biotechnology Institute
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