Institute of Molecular Biology (IMB)
Department: Not specified
ROR ID: Not specified
Web page: https://www.imb.de/
Country: 
Germany
City: Mainz
Address:
Ackermannweg 4, 55128 Mainz
Related items
Our Research Unit addresses an important question on the origin of chromosome instability (CIN), which causes structural as well as numerical chromosome aberrations. Importantly, CIN and increased levels of chromosome aberrations are closely associated with many human diseases including cancer, neurodegenerative diseases and age-related syndromes and can act as key drivers for disease development and progression. An important condition that causes structural chromosome instability (S-CIN) leading ...
Projects: SP-3: A statistical modeling approach to identify common triggers for replication stress and mitotic chromosome missegregation, SP-1: Deciphering signaling pathways that promote accurate chromosome segregation after replication stress, SP-2: Molecular mechanisms of replication stress-induced mitotic chromosome missegregation, SP-4: Centrosome integrity as a determinant of replication stress and mitotic dysfunction, SP-5: Impaired chromosome integrity caused by mutations in members of the BTR complex, SP-6: Proteomics of mitotic inter sister chromatid junctions, SP-8: The causes of replication stress in response to whole chromosomal aneuploidy, SP-Z: NGS-based approaches for systematic analysis of genomic and chromosome instability Bernd Wollnik, Göttingen, SP9: Mutual impact of replication origin firing regulation and mitotic chromosome segregation
Web page: https://for2800.de/
To maintain genome stability, human cells depend on accurate DNA replication in S-phase and chromosome segregation in mitosis. Replication stress refers to slowing down or stalling of replication forks that occurs due to DNA lesions, R-loops or oncogene activation. One consequence of replication stress is entry of cells into mitosis with incompletely replicated DNA and thus aberrant mitosis. Phosphorylation of proteins by kinase ATR and its downstream effector CHK1 protects stalled replication ...
