Studiegids

nl en

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

Vak
2013-2014

The balance between cell survival and cell death is carefully controlled by cellular signaling pathways during development and physiological as well as pathological processes. It is perhaps counterintuitive that cell death is not necessarily a bad thing in the organism. For instance, it not only contributes to aging but also plays an essential role in embryonic development to carve out tissue architectures. Likewise, on the one hand cell death in response to genotoxic insults can deplete (stem) cell pools causing tissue degeneration but on the other hand it clears the body of cells carrying damaged DNA that may otherwise cause cancer.

In this caput program, the different forms of cell death are discussed as well as some of the essential cell signaling pathways controlling those forms. Lectures are combined with paper discussions to reach the following end goals of the course:

  • Knowledge of the different types of cell death

  • Knowledge of the signaling pathways in control of the various cellular survival/death decisions

  • Understanding of apoptosis, necrosis, and autophagy

  • Understanding of the role of p53, caspases, and the Bcl2 family in these forms of cell death

  • Understanding of the role of the immune system as a regulator of cell death pathways

The course includes an oral presentation and a written examination.

Coordinator

Dr. E. Danen

Toegangseisen

Basic Cell Biology and Biochemistry.

Onderwijsvorm

Lectures

Literatuur

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.

Toetsing

Oral presentation and written examination on April 16th 2014.

Rooster

The course will be given on Wednesdays from February 12th to April 2nd, 2014 and exam on April 16th 2014. See roster for details.

Inschrijving

Application via uSis.