Ingeborg Kluge

Tel.: +49 (0)631-205-4273

Fax: +49 (0)631-205-4090

Email: ikluge(at)biologie.uni-kl.de

Bau: 24/105

Sprechzeiten:

Montag bis Donnerstag vormittags

Freitag (gerade Wochen) vormittags

Dr. Markus Räschle

Tel. +49 (0)631-205-5919 (Office 24/107)

Email:Markus.Raeschle[at]bio.uni-kl.de

Research projects

Proteomics of DNA repair

Our group uses cutting-edge mass spectrometry to study DNA repair processes. We comprehensively monitor the assembly of DNA repair complexes on chromatin as it undergoes replication and repair in Xenopus egg extracts. From the proteomic profiles we identify novel factors with potential roles in DNA repair and the maintenance of genome stability. Using a variety of biochemical and cell biological assays we try to pinpoint their precise function during the repair process.

Over the past years this approach has reveal several new genome stability factors with important functions in the repair of psoralen crosslinks. By covering additional DNA repair pathways we aim at obtaining a system-wide view of DNA repair.   

Dr. Maja Kneißig

Tel. +49 (0)631-205-5920 (Office 24/109)

Email:kneissig[at]bio.uni-kl.de

Project description:

Genomic aberrations in cancer cells are thought to arise through a gradual process of mutation and selection. However, recent progress in genomic sequencing technologies has enable the discovery of a radically different phenomenon of genetic instability termed chromotripsis. In this case, massive shattering and random reassembly of single chromosome and/or chromosome regions lead to the formation of highly derivative chromosomes within one cell cycle. What initiates the chromosome damage, and which processes are involved in the repair of the DNA breaks remain unknown. The focus of my study is to understand the cellular and molecular mechanisms of chromotripsis in human cells.

Dr. Galal Metwally

Tel. +49 (0)631-205-5920 (Office 24/109)

Email: gmetwa[at]bio.uni-kl.de

http://www.uni-kl.de/aktuelles/news/news/detail/News/humboldt-stipendiat-erforscht-einfluss-von-veraenderter-chromosomen-anzahl-auf-den-zellzyklus/

Dr. Maria Krivega

Tel. +49 (0)631-205-5920 (Office 24/109)

Email: krivega[at]rhrk.uni-kl.de

Project description:

Human cells can partially tolerate aneuploidy. The presence of an extra chromosome deregulates several physiological pathways and causes proteotoxic stress due to imbalanced protein expression. One of the key changes is upregulation of autophagy, which is a pathway that enables cells to dispose of unnecessary or dysfunctional components. In our group, we aim to uncover the upstream signaling pathways required for autophagy activation and to identify the components that are cleared by autophagy from aneuploid cells.

Menges Paul PhD

Tel. +49 (0)631-205-5920 (Office 24/109)

Email: pmenges[at]rhrk.uni-kl.de

Project description:

Bernhard Sara PhD

Tel. +49 (0)631-205-5920 (Office 24/109)

Email: sbernhar[at]bio.uni-kl.de

Project description:

Cells often undergo tetraploidization during tumorigenesis. Tetraploid cells contain doubled chromosome and centrosome number and are inherently instable. Therefore, tetraploidy is considered to be an intermediate state leading from diploidy to aneuploidy. Proliferation of tetraploid cells is prevented by several molecular mechanisms, but some cells can escape and further proliferate, which then in turn facilitates tumor formation. My work focuses on the molecular mechanisms that allow tetraploid cells to escape the cell cycle arrest and apoptosis. 

Avarello Mario PhD

Tel. +49 (0)631-205-5920 (Office 24/109)

Email: avarello[at]bio.uni-kl.de

Project description:

Aneuploidy affects many aspects of physiology of human cells. DNA replication and repair processes are strongly downregulated in response to aneuploidy; particularly the timely loading of the replicative helicase MCM2-7 helicase is impaired. The focus of my research is to understand what causes this impairment and what are the cellular consequences. 

Chunduri Narendra PhD

Tel. +49 (0)631-205-5920 (Office 24/109)

Email: chunduri(at)bio.uni-kl.de

Project description:

Every time the cell divides, all chromosomes have to be duplicated and segregated equally into the two daughter cells. When there are errors in segregation, the daughter cells will either lose or gain a chromosome. The propagation of these cells is usually limited by activation of the p53 pathway. However, the mechanisms underlying the p53 activation remain unclear. Using aneuploid cells (monosomic and trisomic) as a model system, I will investigate the mechanisms of p53 activation and the impact of p53 on the cellular response to aneuploidy.

Seget Katarzyna PhD

Tel. +49 (0)631-205-5920 (Office 24/109)

Email: seget[at]bio.uni-kl.de

Project description:

Tetraploidy is a state when cells contain doubled chromosome number. Although it can occur physiologically in very specialized tissues such as liver, most tetraploid cells are found in early stages of cancer. In fact, about 40% of solid tumors have undergo tetraploidization at some point during their development. Interestingly, proliferation of tetraploid cells is limited in a p53 - dependent manner. My work focuses on revealing the molecularmechanisms underlying p53 activation and, on the other hand, understanding how some cells escape this fate and progress into cancer.

Sen Sushweta PhD

Tel. +49 (0)631-205-5920 (Office 24/109)

Email: ssen(at)bio.uni-kl.de

Project description:

Dilger Erna

Tel. +49 (0)631-205-4269 (Laboratory 24/138)

Fax +49 (0)631-205-4090

Email: edilger[at]rhrk.uni-kl.de

Roth Robin

Tel. +49 (0)631-205-5921 (Büro 24/107)

Fax +49 (0)631-205-4090

Email: rroth[at]rhrk.uni-kl.de

Kirchner Isabell

Tel. +49 (0)631-205-5920 (Office 24/109)

Tel. +49 (0)631-205-4296 (Laboratory 24/135)

Fax +49 (0)631-205-4090

Email:  isabell.kirchner[at]bio.uni-kl.de