Due to the Corona virus education methods or examination can deviate. For the latest news please check the course page in Brightspace.

Prospectus

nl en

Molecular Mechanisms of Cell Death (formerly Molecular Mechanisms of Apoptosis)

Course
2012-2013

The cells in our bodies are in a constant process of renewal. Therefore “old” cells have to die. Also, infected or transformed cells need to be removed. Cells can kill themselves by activation of programmed cell death also named “apoptosis”. This is a very complex, tightly regulated process that secures that cells die at the right moment without an effect on total body function. Disturbance of the apoptotic process is related to numerous diseases like cancer, neurodegeneration and AIDS. A better understanding of the molecular mechanisms that control apoptosis could identify new therapeutic targets for pharmaceutical intervention in apoptosis.
The contents of the caput course are the biochemical and cell biological processes that are involved in apoptosis.
We will start with an introduction about the concept “apoptosis in living organisms” including the role of apoptosis in health and disease. In the next series of sessions the various mechanisms in induction, commitment and execution of apoptosis will be discussed including death receptors, Bcl-2 family members, p53, stress response proteins, caspases and signal transduction pathways.
The course includes an oral presentation and a written examination.

Coordinator

Prof. Dr. B. van de Water

Admittance demands

Basic Cell Biology and Biochemistry.

Method of instruction

Lectures

Required reading

Former bachelor students of ‘Bio-Farmaceutische Wetenschappen’ can use the following book for additional reading:

‘Mechanistic Toxicology’ by Urs A Boelsterli, Publishers: Taylor and Francis, ISBN 0-415-28459-7.

Examination

Oral presentation and written examination on April 17, 2013.

Time table

The course will be given on Wednesdays from February 11 to April 3, 2013. See roster for details.

Application

Application via uSis.