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Last Updated on Tuesday, 20 June 2017 12:01

Bachelor- und Masterarbeiten (in German)

Dabei handelt es sich um eine Gruppe von sporadischen und erblichen Krankheiten der Skelett -und Herzmuskulatur, die zu schweren körperlichen Behinderungen und vorzeitigem Tod führen. Die Arbeiten werden in enger Kollaboration mit klinischen Partnern (Uni-Klinik, Erlangen) durchgeführt.

Notwendige Qualifikation: Bachelor in ILS, Biologie oder Biochemie.

Wünschenswerte Qualifikation: Grundkenntnisse in MATLAB, Konfokalmikroskopie und Zellkultur. Kenntnisse in computergestützter Bildgebung und Bildauswertung sind vorteilhaft, aber nicht Bedingung.

Bemerkungen: Die Stelle soll zum Master (M.Sc.) der Bewerberin/des Bewerbers führen. Aufgabe des Masterstudenten(in) ist es, mechanische Messungen an skeletalen Myoblasten und Myotuben von zwei der häufigsten humanpathogenen Mutationen (R155C VCP und W2710X filamin C) mittels Traktionsmikroskopie, Magnetbead-Mikrorheologie und einem Zellstretcher in Kombination mit Konfokalmikroskopie mit hoher zeitlicher und räumlicher Auflösung durchzuführen.

Für Auskünfte kontaktieren Sie bitte Prof. Wolfgang Goldmann, PhD, Biophysics Group der FAU, Center for Medical Physics und Technology, Henkestr 91, 91052 Erlangen. Phone: (+49) (0)9131-85-25605 fax: (+49) (0)9131-85-25601 email: This email address is being protected from spambots. You need JavaScript enabled to view it.

Dilated cardiomyopathy caused by mutations in A-type lamins.

Dilated cardiomyopathy is one of the leading causes of heart failure in Europe. Despite of the conventional medical care, there is no definitive and satisfactory treatment for the progressive cardiac dilatation and loss of contractility in LMNA cardiomyopathy short of heart transplantation. LMNA gene encodes nuclear A-type lamins, which are the main constituents of the nuclear lamina. To explain how mutations in proteins of the nuclear envelope can cause a disease of the heart, it has been proposed that nuclear envelope abnormalities bring about cellular fragility and a decrease in the mechanical resistance to stress, which could partially explain the cardiac muscle disease, considering that the heart muscle is constantly subjected to mechanical force.

In preliminary work, we showed that there is an abnormal activation of stress-activated ERK1/2 signaling in hearts that carry LMNA mutations. Administration of drugs inhibiting ERK1/2 signaling improves cardiac ejection fraction in mice and blunts further increase in left ventricular dilatation. These studies clearly show that the abnormal ERK1/2 activation is involved in the pathophysiology of LMNA dilated cardiomyopathy.

It is therefore important to further our knowledge on the pathophysiology of cardiomyopathies and to determine the influence of external/internal stress in order to unveil molecular/cellular mechanisms to target future therapeutic approaches. 

Required qualifications: Bachelor in ILS, biology or biochemistry.

Desirable qualifications:  Basic knowledge of MATLAB, confocal microscopy and cell culture. Knowledge in computer-aided imaging and image analysis are advantageous, but not essential.