Signal Transduktion von JAK2-V617F
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The identification of a constitutively active mutant of JAK2, namely JAK2-V617F in the year 2005 was a milestone in the understanding of Philadelphia-chromosome negative myeloproliferative neoplasms. The JAK2-V617F mutation confers cytokine hypersensitivity, constitutive activation of the JAK-STAT pathway, and cytokine independent growth. Since we observed constitutive phosphorylation of Gab1 in the presence of JAK2-V617F but not in the presence of JAK2 we hypothesise that adapter proteins of the Gab family may facilitate JAK2-V617F-mediated MAPK, PI3K and PLC activation. Furthermore, we hypothesize, that Gab adapter proteins play a key role in mediating cytokine hypersensitivity by integrating stimulatory and inhibitory signalling events in dependence of the level of JAK2-V617F expression. Gaining a dynamic view on misregulated signalling in response to JAK2-V617F expression is crucial for understanding JAK2-V617F-dependent-diseases. In this project study the molecular interplay of Gab1 and JAK2-V617F.
Anmerkungen
Förderung im Rahmen des Forschungszentrums Dynamische Systeme an der OvGU
Schlagworte
JAK, STAT, oncogene, signal transduction
Kontakt
Prof. Dr. Fred Schaper
Otto-von-Guericke-Universität Magdeburg
Fakultät für Naturwissenschaften
Universitätsplatz 2
39106
Magdeburg
Tel.:+49 391 6750220
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