Rudolph Research Group
The research project "Longevity and Aging-Associated Genes in Adult Stem Cell Aging" (ERC Advanced Grant) determines the influence of longevity and aging-associated genes on stem cell aging by employing reverse genetic screening approaches. In vivo and ex vivo RNAi will identify genes and molecular mechanisms that affect the function of stem cells in aging mice or genetically engineered mouse models of accelerated accumulation of molecular damages and stem cell dysfunction. Analysis of primary human stem cells from young vs. old donors will delineate whether the identified genes and mechanisms are conserved in humans.
Reverse genetic approaches of aging/longevity-associated genes have not been conducted in adult mammalian stem cells. Our group gained significant expertise in analyzing molecular mechanisms of stem cell maintenance and function as well as in conducting RNAi screens in different murine stem cell compartments. Our studies will delineate novel mechanisms of stem cell aging and its implication for defects in organ homeostasis and regeneration during aging.
A second project deals with checkpoints and stem cell function upon telomere dysfunction. This project is part of the Marie Curie Initial Training Network "Chronic DNA damage in Ageing" (CodeAge) of the EU 7th Framework Program. The aim is to identify novel checkpoints that limit maintenance and function of adult stem cells in response to telomere dysfunction. Like this, we gain an understanding of the molecular processes that are affected by these checkpoints and generate a rational basis to select novel targets for compound screens aiming to identify novel compounds for regenerative therapies.
For example, Exo1- and p21-independent checkpoints limit stem cell function, organ maintenance and lifespan of aging telomere dysfunctional mice. We have recently shown that Exo1 or p21 deletion can improve the maintenance and function of adult stem cells in response to telomere dysfunction. However, the exact nature of these checkpoints remains unknown. Understanding Exo1- and p21-independent checkpoints in response to telomere dysfunction is expected to identify targets for future therapies aiming to improve stem cell function and organ maintenance in the context of telomere dysfunction and aging.
In late life, hematopoietic stem cells partly lose their functionality, especially the capability to build immune cells, which is thought to contribute to the development of immune defects and increased risk of infections in the elderly. At the same time, a weakened immune system can accelerate aging, since damaged body cells are no longer detected and eliminated by the immune cells. Hence, old and defect cells can live and proliferate for a longer time, thus leading to organ and tissue dysfunction or an increasing risk to come down with cancer.
Our lab is team member in two cooperative research projects funded by the SAW program of the Leibniz foundation. One project is part of a postdoc network on aging induced impairments in regeneration focusing on “Genes regulating hematopoietic stem cells quiescence and aging”. The other project is part of a collaborative project between different Leibniz Institutes to foster interactions within the Leibniz Research Alliance “Healthy Aging”. The project from our laboratory focuses on the targeting of senescent cells in order to improve organ maintenance.
|Karl Lenhard Rudolph||+49 3641 email@example.com||Group Leader|
|Stefan Tümpel||+49 3641 firstname.lastname@example.org||Staff Scientist|
|Vasily Romanov||+49 3641 email@example.com||Postdoc|
|Mei-Fang Wu||+49 3641 firstname.lastname@example.org||Postdoc|
|Elias Amro||+49 3641 email@example.com||Doctoral Student|
|Seerat Bajwa||+49 3641 firstname.lastname@example.org||Doctoral Student|
|Friedrich Becker||+49 3641 email@example.com||Doctoral Student|
|Phillip Gerald Calmes||+49 3641 firstname.lastname@example.org||Doctoral Student|
|Yulin Chen||+49 3641 email@example.com||Doctoral Student|
|Zhiyang Chen||+49 3641 firstname.lastname@example.org||Doctoral Student|
|Sarmistha Deb||+49 3641 email@example.com||Doctoral Student|
|George Garside||+49 3641 firstname.lastname@example.org||Doctoral Student|
|Bing Han||+49 3641 email@example.com||Doctoral Student|
|Nicolas Huber||+49 3641 firstname.lastname@example.org||Doctoral Student|
|Ilwook Kim||+49 3641 email@example.com||Doctoral Student|
|Sospeter Ngoci Njeru||+49 3641 firstname.lastname@example.org||Doctoral Student|
|Omid Omrani||+49 3641 email@example.com||Doctoral Student|
|Aruna Shukla||+49 3641 firstname.lastname@example.org||Doctoral Student|
|Miaomiao Suo||+49 3641 email@example.com||Doctoral Student|
|Jiangnan Yang||+49 3641 firstname.lastname@example.org||Doctoral Student|
|Ali Hyder Baig||+49 3641 email@example.com||Scientist|
|Nadine Pömpner||+49 3641 firstname.lastname@example.org||Research Engineer|
|Sebastian Benkhoff||+49 3641 email@example.com||Technical Assistant|
|Sabrina Eichwald||+49 3641 firstname.lastname@example.org||Technical Assistant|
|Arshia Berryemail@example.com||Master Student|
|Chen-Jen Hsu||+49 3641 firstname.lastname@example.org||Master Student|