Martin Sattler, PhD

Martin Sattler, PhD

Researcher

Contact Information

Office Phone Number

(617) 632-4382

Fax

(617) 632-4388

Biography

Martin Sattler, PhD

Dr. Sattler received his PhD in biochemistry from the University of Hannover, Germany, in 1992. He then completed a postdoctoral study designing bacterial expression vectors for large-scale protein purification at the GBF, Braunschweig, Germany. In 1993, he began his second postdoctoral fellowship in Dr. James Griffin's laboratory, studying signal transduction pathways activated by BCR/ABL.

Researcher

Physician

Instructor in Medicine, Harvard Medical School

Recent Awards

  • Jose Carreras International Leukemia Foundation, Fellowship 1996

Research

    Mechanisms of Cell Transformation

    A systematic analysis of several key targets of the transforming tyrosine kinase BCR/ABL has been conducted in recent years. For example, activation of c-CBL, SHP2, and CRKL by BCR/ABL has defined the mechanism that leads to activation of phosphatidylinositol 3'-kinase (PI3K) in BCR/ABL-transformed cells. However, one of the major questions that is unanswered in the biology of chronic myeloid leukemia (CML) is why BCR/ABL causes a myeloproliferative phenotype.PI3K/SHIP pathwayThere is a fine balance between phosphatases and kinases in the homeostatic mechanism of the cell. The lipid kinase PI3K is important in the regulation of a variety of cellular events through the formation of bioactive lipids. PI3K regulates cell migration, viability, differentiation, cell growth, and apoptosis. It is activated in many transformed cells, and its activity has been shown to be crucial for transformation in many systems. Levels of bioactive lipids formed by PI3K are, in part, down-regulated by the inositol 5-phosphatase SHIP. In CML cells, the level of SHIP is reduced by more than 90%. Interestingly, disruption of the SHIP gene in mice leads to a phenotype similar to that of CML. To better understand the role of SHIP, it will be necessary to study its role in signaling events that promote cell growth and regulate gene expression and myeloid differentiation.Reactive oxygen speciesROS are believed to play a crucial role in the regulation of cellular processes. Elevated levels of ROS may support cell growth, whereas even higher levels may lead to apoptosis or necrosis. Relative levels of ROS are likely to be increased in most diseases, but the importance in disease pathology is unknown. Recent evidence suggests that many key signaling pathways contain proteins with redox-sensitive thiol groups that regulate their activities. However, ROS are likely to synergize with cellular events without themselves being able to induce cell growth. Therefore, it is of special interest to dissect the signaling events and pathways influenced by ROS, including gene targets that can be up-regulated or down-regulated in response to ROS.

    Locations

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    Dana-Farber Cancer Institute

    450 Brookline Avenue Mayer 540 Boston, MA 02215
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    Dana-Farber Cancer Institute

    Location Avtar

    Dana-Farber Cancer Institute

    450 Brookline Avenue Mayer 540 Boston, MA 02215
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    42.3374, -71.1082

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