Dr. med. Aplaslan Tasdogan

Dr. med. Alpaslan Tasdogan is a postdoctoral fellow at the Institute for Immunology (PI: Prof. Hans Jörg Fehling) and is also a participant of the Dermatology Residency Programme at the University Hospital Ulm. Recently, he has received an Else-Kröner Fresenius fellowship for clinician scientist. Dr. Tasdogan is partially responsible for the Flow Cytometry Core and developing novel flow cytometric techniques at his institute.

His current interest is dissecting hematopoietic defects in Mixed-lineage-Leukemia-5-deficient mice and cell lines. Mixed-Lineage-Leukemia-5 (MLL5) is a distant and understudied member of the MLL/Trithorax gene family of epigenetic regulators. Classical members of this family (MLL1 – MLL4) are known to exhibit histone H3K4 methyltransferase activity and to be critically involved in normal hematopoiesis as well as hematopoietic malignancies. Along this line, human MLL5 is located in a genomic region (chromosome 7q22) recurrently deleted in leukemic cells from patients with aggressive forms of acute myeloid leukemia (AML). This initial observation has given rise to the view that MLL5 might exhibit tumor suppressor activities. However, no direct role of MLL5 in leukemogenesis has been documented so far, and also physiological roles of MLL5 are still poorly understood. The analysis of adult Mll5-deficient mice, generated in our own and two other laboratories, has revealed a variety of phenotypic abnormalities, including infertility, retarded growth and severe defects in hematopoiesis – a combination of traits often found in mouse mutants with defective DNA double strand break repair. Moreover, hematopoietic stem/progenitor cell compartments were functionally severely compromised.

With over 5 years of research experience in stem cell biology, gene targeting, hematopoiesis, and immunology, my current research goal is to develop and translate efficient stem cell based therapies for the treatment of cancer and genetic diseases that effect the hematopoietic system.

My main research philosophy relies on the idea that creative thinking and collaboration are the basis of scientific innovation that leads to new successful therapies for disease.



Jun. Prof. Dr. Karin Danzer

Jun. Prof. Dr. Karin Danzer, is a group leader in the Department of Neurology (Head: Prof. Albert Ludolph). Her research interest is elucidating the underlying mechanisms of different neurodegenerative disorders with a special focus in Parkinson's disease. Aggregation of alpha-synuclein and related toxicities play a central role in the development of Parkinson's disease. Recently, oligomeric and pre-fibrillar forms of alpha-synuclein have been identified as the toxic species in Parkinson's disease. Until recently, alpha-synuclein was thought to exert its toxic effects intracellularly. However, new data support an alternative possibility: that some forms of alpha-synuclein are secreted from, and taken up by neurons, and that this extracellular alpha-synuclein may be a toxic species. The goal of Dr. Danzer's research is to understand the underlying mechanisms of secretion, uptake of alpha-synuclein oligomers into neighboring neurons and propagation of alpha-synuclein pathology. Her special interest is not only the exosomal secretion of alpha-synuclein oligomers but also additional key proteins in neurodegenerative disorders like amyloid beta, Tau und SOD1. Using a wealth of biochemical, cell biological and molecular approaches, as well as analysis of patient samples and establishing new animal models Dr. Danzer hopes to understand underlying disease mechanisms and to identify not only new biomarkers but also additional and new factors contributing to neurodegeneration.



Dr. Verena Gaidzik

Dr. Verena I. Gaidzik works in the department of internal medicine III (Head Prof. H. Döhner) as clinical fellow. Her research projects take place in the research group of Prof. K. Döhner (Head of the molecular and cytogenetic laboratory). Dr. Gaidzik is mainly responsible for the molecular diagnostics in the laboratory. Major focus of Dr. Gaidzik's research interest is elucidating the underlying mechanisms of acute myeloid leukemia (AML) by the identification of new genetic aberrations as well as their evaluation of their prognostic and predictive relevance in AML patients. Most of the scientific projects of Dr. Gaidzik are embedded in the framework of prospective clinical AML trials of the German-Austrian AML Study Group (AMLSG). Thus, she was able to analyze molecular markers like WT1, RUNX1, TET2, DNMT3A in large patient cohorts with regard to their mutation incidence and found out their associations with specific clinical and genetic characteristics. Furthermore, these studies aim to optimize the classification systems of AML patients and therefore also guide new and more specific treatment options. Another task is to improve the survival of AML patients by prediction and identification of patients with high risk of relapse. This is possible due to investigation of minimal residual disease (MRD) during therapy and follow-up. Currently, she works on the establishment and integration of DNMT3A mutations as a new MRD marker. In the SFB 1074 "Experimental Models and Clinical Translation in leukemia" she serves as a project leader. In this project Dr. Gaidzik is investigating a novel recurrent micro-deletion in the chromosomal band 3p14.1-p13 recently identified in cytogenetically-normal AML patients by single nucleotide polymorphism-array analyses. The commonly deleted region contains 8 protein-coding genes and one microRNA and will further be characterized by functional and (epi)-genetic analyses. The detected (epi)-genetic findings will be correlated with clinical characteristics and survival.


Dr. Susanne Kühl

Wnt signaling is required for kidney development and misregulation of Wnt contributes to congenital kidney disease. We investigated the potential role of non-canonical Wnt target genes such as Pes1 and Ppan during Xenopus renal development (Tecza et al., 2011). In our recent study, we analyzed Alcam during embryonic kidney development (Cizelsky et al., 2014). Expression analysis showed that alcam expression in the kidney is conserved across species (Gessert et al., 2008). Moreover, several studies demonstrated that alcam is regulated by non-canonical Wnt signaling (Gessert et al., 2008). Loss of function approaches demonstrated that Alcam is required for tubule formation. Additionally, we showed a similar expression pattern of alcam and the potential non-canonical Wnt receptor fzd3 in the pronephros and that Fzd3 acts upstream of alcam. Importantly, we also demonstrated that alcam is a direct target gene of non-canonical Wnt signaling. Our data set up a novel mechanism demonstrating a Fzd3/JNK/Alcam branch regulating tubular development in the embryonic kidney. In cooperation with Seppo Vainio, Oulu, Finland, we furthermore examined the regulation of wnt4 by Wt1 and Sox11 on a transcriptional level (Murugan et al., 2012).

Dr. Diana Lieber

Herpesviruses are widespread pathogens whose prevalence can reach far beyond 90%. There are eight human herpesviruses known which cause a great number of diseases including herpes labialis (cold sores), varicella (chickenpox), infectious mononucleosis (kissing disease) and different kinds of cancer. Although herpesviruses strongly vary in their pathogenesis, they all share the ability to remain life-long persistent in the host after primary infection. In a quiescent state, the so-called latent phase, only few of the by far more than 100 viral genes are active. Their main function is to maintain latency and to suppress the host’s immune reaction. However, a repeated reactivation with active virus replication is possible. This is mostly caused by distinct factors such as immune deficiency, hormones, stress or UV-irradiation. Antiviral therapeutics act usually on the replication of the viral genome and frequently select resistant viruses. Complete removal of herpesviruses from the host organism is currently not possible. Thus, virus carriers hold a life-long risk of reactivation and disease.

Our research addresses virus-host interactions in different human herpesviruses. A special focus lies on the function of cellular genes in human cytomegalovirus (HCMV) infection. We apply virological, genetic, cell biological and biochemical procedures. A key technology of the group is the so-called RNA interference which is used to silence single genes individually. This technology is adopted in one-by-one approaches as well as in systematic screenings. In addition, existing cell culture systems are tested with regard to their applicability in research on HCMV and other herpesviruses and new tailored transgenic cell lines are generated in order to improve the conditions for state-of-the-art experimental approaches and high-throughput screens.

Our aim is to better understand the molecular mechanisms underlying herpesvirus infections and to eventually find targets for innovative antiviral therapies.

Dr. Astrid Pfister

Wnt signaling regulates cell growth, proliferation and differentiation and thus plays a crucial role in development and disease (MacDonald, 2009). Canonical Wnt ligands activate the Wnt/b-catenin pathway and drive the expression of Wnt target genes regulating e.g. cell proliferation and apoptosis (MacDonald, 2009). Consistently, it has already been demonstrated that several anti-apoptotic Wnt targets are up-regulated in tumors with constitutively active Wnt signaling, for instance in colon cancer and leukemia (Sansom, 2007). Thus, we study the cellular and molecular mechanisms underlying Wnt-mediated tumorgenesis. In particular, we focus on anti-apoptotic Wnt target genes by molecular biology methods and in vitro cell-culture assays on primary, cancer and acute myeloic leukemia (AML) cell lines. We will  investigate the Wnt target nucleophosmin (NPM) in more detail, which is commonly mutated (35%) or mis-expressed in AML patients (Colombo, 2011) and will screen for novel candidates that are relevant for tumor biology.



Dr. Christoph Schmidt

My group is based at the Institute of Pharmacology of Natural Products & Clinical Pharmacology. We are interested in innate immunology with a special focus on the protein defence network of the complement system. We study the complement cascade’s instructor roles for the entire immune system and general body physiology. To achieve this we employ a wide range of research techniques ranging from recombinant protein technology, biochemical, biophysical and diverse immunological assays. We collaborate to test promising hypotheses in suitable animal studies and have established successful collaborations with groups in Philadelphia, Melbourne, Edinburgh, Ulm and Munich. We also are very keen to utilise our basic research to develop new immunological application that one day, may aid patients. One example is the modelling, production and characterisation of the innate immune modulator miniFH (Schmidt CQ et al. , Rational engineering of a minimized immune inhibitor with unique triple-targeting properties. J Immunol. 2013, 1;190(11):5712-21).

One particular interest of our group is the process of opsonisation by the innate immune system. This is an immunological process of marking molecules and particles in our body with complement effector molecules to promote immune surveillance and body homeostasis. Such process occurs in all tissues at all time. While invasion by pathogens necessitates robust complement activation for safe clearance and alarming of the entire immune system, a more subtle measure is required for controlled disposal of common, “everyday” cellular by-products.  A fine-tuned complement opsonisation profile is of central importance, since too much or too little complement activation is the underlying cause or secondary exacerbating factor in many rare as well as common human disease conditions. We investigate how this delicate balance is maintained or destabilised. Key objectives within this project are the understanding of the transition between normal- and disease-associated opsonisation (marking) of living cells, and the identification of measures allowing normalisation of excessive disease-associated marking and its resultant damage.

Other interests within the lab are to (i) characterise the inflammatory complement activation on bio- and nanomaterials, (ii) learn more about complement's influence on shaping an inflammatory or a tolerogenic immune response and (iii) study the innate immune evasion mechanisms of the malaria parasite Plasmodium falciparum, which manipulates several complement proteins to avoid destruction or to aid entry into new erythrocytes.