MelTec GmbH characterizes protein networks involved in T-cell invasion

Magdeburg, Germany, May 1, 2002 MelTec GmbH, a functional proteomics company, today announced the publication of two scientific studies in the April 2002 issue of the Journal of Theoretical Medicine, describing the protein networks involved in T-cell invasion in Sarcoid myopathy and Polymyositis.

It is known that lymphocytes, because of their innate ability to invade and progressively destroy cells, play an essential role in cellular immune response, autoimmune diseases and transplant rejection. In the current published studies, muscle biopsies from patients suffering from polymyositis and sarcoid myopathy, two diseases characterized by muscle invasion of T-cells and therefore progressive muscle deterioration, have been analyzed. Results showed that characteristic cellular phenotypes were associated with the adhesive mechanism of the invading lymphocytes in sarcoid myopathy and polymyositis.

The ability of MelTecs technology to map simultaneously large numbers of proteins in diverse types of cells should enable us to approach any invasion process, including invasion of malignant cells in cancer and autoimmune diseases, said Walter Schubert, M.D., Founder and Chief Executive Officer of MelTec. These higher level order functions in the cellular proteome cannot be detected using conventional proteomics techniques, which typically use tissue homogenates. Therefore, MELK provides a unique tool for analyzing proteomic information that was not available before, linking cellular topology, protein expression and function.

MELK reads protein networks in the context of whole, intact cells, providing an image of protein locations in the cell, or the cells protein topology. MELK enables the researcher to simultaneously discover the molecular phenotype of cells and the precise position of protein networks, thus enabling closer investigation of the hidden relationships between the structure, molecular expression and function of proteins.

The fir

Contact: Melissa Wainberg
Noonan/Russo Communications

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