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Medizinische Hochschule Hannover | Carl-Neuberg-Str.1 | 30625 Hannover | Tel.:(+49) 0511-532-0

Receptor Biology and Signal Transduction

 

 

Principal Investigator

 

 

Dr. Johann Meyer
Hannover Medical School
Experimental Hematology
OE 6960
Carl-Neuberg-Str. 1
D-30625 Hannover
Germany                                                                        

 

E-Mail: Meyer.Johann[at]mh-hannover.de
Fon: +49 (0)511/ 532 5145
Fax: +49 (0)511/ 532 5105

 

 

Receptor biology and signal transduction

 

Group Members: Johann Meyer, Elke Barczak, Tamaryin Godinho

 

Contributing Principal Investigator: Zhixiong Li

 

Proliferation, differentiation and apoptosis in the hematopoietic system is tightly controlled by cytokines and their corresponding receptors. There are numerous examples of aberrantly elevated and/or sustained activations of cytokine receptors (gain of function) that are the causative events in haematological malignancies. The mechanisms of activation range from aberrant expression of cytokines and/or receptors (autocrine activation) over point mutations (eg. thrombopoietin receptor (Mpl) mutations in MPD) and deletions/insertions (e.g. FLT-ITD) to chromosomal rearrangements (e.g. TEL-PDGFR). Knowledge about how signalling networks from constitutive activated receptors are altered is important for the development of cancer therapies. On the other hand modifications of cytokine receptors could be useful in cell therapy. Therefore our group has two main research areas. To define the molecular mechanisms that leads to receptor activation and aberrant signalling. Our special interests in this regard are the neurotrophin receptor system (Trks) and Mpl. The other research focus is to engineer cytokine receptor variants which are potentially useful in cell therapy approaches.

 

 

 

 

            MPL receptor

     

       

       

         

         

         

        • belongs to cytokine receptor superfamily (EpoR, GH and Prolactin receptor)


        • has no intrinsic kinase activity, instead associated with JAK2 kinase


        • characteristic WSXWS motif

         

         

                                           

          

         

         

        Selected own references: Meyer et al. Growth factors 2002; Horn et al., Oncogene 2003; Beutel et al., Br J Haematol 2005; Meyer et al., Leukemia 2007; Li et al., Blood 2009

         

         

         

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