Key gene function against cell death discovered
- Date:
- November 22, 2011
- Source:
- Medical University of Vienna
- Summary:
- Scientists have discovered that two genes (TSC/Tuberin and PRAS40) are extremely important regulators in the development of stem cells: if these genes are switched off, the stem cells do not develop but instead die a programmed cell death.
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A team of researchers at the MedUni Vienna's Institute of Medical Genetics has discovered that two genes (TSC/Tuberin and PRAS40) are extremely important regulators in the development of stem cells: if these genes are switched off, the stem cells do not develop but instead die a programmed cell death.
The group led by Markus Hengstschläger, Director of the Institute of Medical Genetics at the MedUni Vienna, has been able to prove in a paper now published in the journal Human Molecular Genetics, that stem cells need both of these proteins to develop and be involved in the regeneration and differentiation processes in cells.
The human body maintains a stable equilibrium between cell death and the breakdown of tissue and the regeneration of tissue from stem cells. Stem cells have the potential to develop into other types of cells such as skin, muscle or nerve cells and are therefore crucial for the rebuilding of tissue. A human stomach cells, for example, lives only two days. Skin cells live for up to four weeks. A lung cell dies after around 80 days and a red blood cell dies after around 120 days.
The two proteins TSC (tuberin) and PRAS40 are crucial for this development, deciding whether the stem cell develops correctly or undergoes apoptosis, a form of programmed cell death. They act, as it were, as 'gatekeepers'.
Story Source:
Materials provided by Medical University of Vienna. Note: Content may be edited for style and length.
Journal Reference:
- C. Fuchs, M. Rosner, H. Dolznig, M. Mikula, N. Kramer, M. Hengstschlager. Tuberin and PRAS40 are anti-apoptotic gatekeepers during early human amniotic fluid stem cell differentiation. Human Molecular Genetics, 2011; DOI: 10.1093/hmg/ddr535
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