Helmholtz Munich

molecule body concept of the human DNA vector chemistry science illustration

Immunosensing and genomic integrity in diseases

Our research aims to understand the maladaptive crosstalks between metabolism and the genomic integrity of the cells to develop novel approaches for the timely diagnosis and treatment of pulmonary and vascular disease, diabetes, and cancer.

Life depends on energy flux, which constantly challenges the integrity of our genome. Once the finely tuned balance between metabolism, DNA damage, and DNA repair capacity has been tilted, several chronic diseases may develop. Increased DNA damage and impaired DNA repair initiate a pathological cascade marked by the persistent DNA damage signaling, senescence, and senescence-associated secretory phenotype (SASP), leading to compromised organ function and/or oncogenesis. This cascade has been described in metabolic diseases such as diabetes, obesity, COPD, and the onset of neuroendocrine cancers.

Thus, the three hallmarks of perturbed DNA Double-strand break (DNA-DSB) repair, DNA interstrand crosslink (DNA-ICL) repair, and DNA replication stress (DNA-RS) response are intermittently linked to these pathological conditions. We intend to understand how their malfunction leads to various pathological disorders. Recently, we have characterized a central orchestrator of the repair process nuclear RAGE (nRAGE) which in conjunction with ATM, FANCD2, and DNA replication helicase (Mcm) complex, play a critical role in maintaining the integrity of our genome under basal as well as perturbed metabolic situations. Hence, we will utilize the advanced tools to translate this knowledge into clinical applications for early diagnosis and treatment of DNA repair-related diseases.

Picture right: Schematic depiction of crosstalks between metabolism and the DNA damage responses

To study maladaptive crosstalks of metabolism with the DNA repair potential of cells, we use advanced laser and molecular cell biology tools complemented with genetic engineering methods and transgenic lines (at both in vitro and in vivo levels), representing metabolic perturbation, disease, or cancer. In addition, we have developed tools to study markers of these events in clinical cohorts.

right: Recruitment of indicated factors to the site of DNA damage or DNA replication perturbations (Laser irradiation, APH Aphidicolin)

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