Mechanisms underlying the myosin motor’s function /dysfunction in skeletal and cardiac muscles.




​Cytoskeletal motors are ATP-dependent force generating biological machines that perform diverse tasks such as, intracellular cargo transport, muscle contraction, cell division, and whole cell movement etc.

The non-prcessive Myosin-II motors drives contraction of skeletal and cardic muscles, while the processive actin-based molecular motor proteins such as myosin V  is involved in intracellular transport. The principle aim of our research is to gain detailed understanding of the mechanisms by which different motors perform diverse roles.

​With vital roles in nearly all aspects of cellular physiology, motor protein dysfunctions are intricately linked to several myopathies including heart disorder Familial hypertrophic cardiomyopathy (FHC) that affects 1 in 200 individuals worldwide. Clinical phenotypes display a high variability ranging from being asymptomatic, to rapidly progressive failing heart or sudden cardiac death in young individuals and competitive athletes.

We aim to gain comprehensive understanding of functional domains in the myosin head, as a consequence of point mutations and to indentify the primary functional alteration resulting into myocardial disorganization leading to the hypertrophy of left ventricle.

​Our experimental approaches include single molecule biophysical methods such as total internal reflection fluorescence microscopy (TIRFM), zero mode waveguides and optical trapping  to obtain precise kinetic and mechanical insights of the motor proteins.

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Our lab is funded by following grants:

  • German Research Foundation (DFG)
  • Hochschulinterne Förderung (HilF, MHH)
  • Fritz Thyssen Foundation


Labor Mitarbeiter