ChIP-MS proteomics in BLM depletable cells
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In this study we can investigate the ability to pull down BLM in BLM-AID cells with its inserted GFP tag and use the BLM-depleted cell line as a control. The ChIP-MS analysis of BLM in synchronized cells can reveal new interaction partners invovled in the resolution of UFBs. On the other hand pulling down other UFB binding proteins in BLM depleted cells can help to understand the impact of cell-cycle specific BLM depletion on UFB resolution.
SEEK ID: https://seek-for2800.de/studies/13
Identification of factors involved in UFB resolution
Projects: SP-6: Proteomics of mitotic inter sister chromatid junctions
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Created: 7th Feb 2022 at 16:26
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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/
Replication stress is a key driver of genomic instability giving rise to human disease, for instance cancer or developmental disorders. It is caused by a variety of defects such as lesions blocking replication (e.g. DNA interstrand crosslinks) or processes that lead to the exhaustion of DNA precursors. This generates under-replicated DNA and replication intermediates that can be rescued by repair processes requiring homologous recombination between sister chromatids. Often, cells exposed to ...
Programme: FOR2800
Public web page: https://for2800.de/cases/sub-project-6-proteomics-of-mitotic-inter-sister-chromatid-junctions/
Replication stress is one of the major causes for chromosomal instability which is a hallmark of cancer. Incomplete repair can lead to severe mitotic defects and ultra-fine anaphase bridges (UFBs) are a typical consequence. So far, five different classes of UFBs have been discribed: fragile sites-UFBs, centromeric-UFBs, telomeric-UFBs, homologous recombination-UFBs and rDNA-UFBs, which can be distinguished by their location and the way how they arise. Although previous studies have already proposed ...
