The research in the Lammerding lab is focused on subcellular mechanics and the cellular signaling response to mechanical stimulation. In particular, we are studying how mutations in nuclear envelope proteins such as lamin can render cells more sensitive to mechanical stress and affect their mechanotransduction signaling. Insights gained from this work can lead to a better understanding of the molecular mechanism underlying laminopathies, a diverse group of diseases including Emery-Dreifuss muscular dystrophy, Hutchison-Gilford progeria syndrome, and familial partial lipodystrophy.
To achieve these goals, we are developing novel experimental techniques to (i) study nuclear mechanical properties in intact cells and isolated nuclei, to (ii) investigate the physical coupling between the nucleus and the cytoskeleton, and to (iii) examine how changes in these properties can affect the cellular response to mechanical stimulation.
Currently, we are applying these techniques to human skin fibroblasts obtained from laminopathy patients and healthy controls and to fibroblasts and myoblasts from mouse models of these diseases. In addition, we are using mouse models of Emery-Dreifuss muscular dystrophy created in Dr. Colin Stewart’s laboratory to study the in vivo consequences of these cellular defects.

Jan Lammerding, Ph.D.
Instructor in Medicine (HMS)
Associate Biophysicist (BWH)

Office: Partners Research Building, Rm 283
65 Landsdowne St
Cambridge, MA 02139
USA
Phone: (617) 768-8273
Fax: (617) 768-8280
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