MD TP38: Regulation of cell migration by endothelin receptor type A
Endothelin-1 type A receptor (ETAR) antagonists (e.g. ambrisentan) are currently approved by the U.S Food and Drug administration, representing a well-tolerated treatment of pulmonary arterial hypertension for patients with connective tissue diseases such as systemic sclerosis. Noteworthy, increased numbers of infiltrating neutrophils have been associated with worse clinical outcome in PAH patients.
In another context, several studies have reported that endothelin-1 and its receptor ETAR also play a central role in the development of tumour cell invasion and metastasis. However, the effects of pharmacological ETAR antagonists on migration of neutrophils and tumour cells remain to be determined.
The objective is to analyse the effects of two ETAR antagonists on migration of neutrophils and tumour cell lines.
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- MD TP1 - Ig Glycolysation
- MD TP2 - Immunoprivilege
- MD TP3 - ANA antibodies
- MD TP4 - Autoantibody prevalence
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- MD TP7 - Neutrophil signalling
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- MD TP34 - PI3K-subunits in EBA
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- MD TP36 - Signaling cascades in keratinocytes
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- MD TP38 - Cell migration regulation
- MD TP39 - mACh-Receptors in systemic sclerosis
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- MD TP48 - Epitope specificity and glycolization
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- MD TP57 - Inhibition of IFN-γ as therapy for epidermolysis bullosa acquisita
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Principal investigator(s)
Mentors
PhD student
Lucy Kappes