« Projekte
Signal Transduktion von JAK2-V617F
Finanzierung:
Land (Sachsen-Anhalt) ;
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

Prof. Dr. Fred Schaper

Otto-von-Guericke-Universität Magdeburg

Fakultät für Naturwissenschaften

Institut für Biologie

Universitätsplatz 2

39106

Magdeburg

Tel.+49 391 6750220

Fax:+49 391 6743004

fred.schaper(at)ovgu.de

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