A5015394450- DNA Repair Mechanisms
- CRISPR and Genetic Engineering
- PARP inhibition in cancer therapy
- Inflammasome and immune disorders
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- DNA and Nucleic Acid Chemistry
- Adenosine and Purinergic Signaling
- RNA modifications and cancer
- RNA Research and Splicing
- Synthesis and Reactions of Organic Compounds
- interferon and immune responses
- Cancer Immunotherapy and Biomarkers
- Phagocytosis and Immune Regulation
- Telomeres, Telomerase, and Senescence
- Chronic Lymphocytic Leukemia Research
- Optics and Image Analysis
- Immune Cell Function and Interaction
- Advanced biosensing and bioanalysis techniques
University of Zurich
2018-2024
Salk Institute for Biological Studies
2022-2023
Jagiellonian University
2015
Abstract Cancers arise through the accumulation of genetic and epigenetic alterations that enable cells to evade telomere-based proliferative barriers achieve immortality. One such barrier is replicative crisis—an autophagy-dependent program eliminates checkpoint-deficient with unstable telomeres other cancer-relevant chromosomal aberrations 1,2 . However, little known about molecular events regulate onset this important tumour-suppressive barrier. Here we identified innate immune sensor...
Abstract Histone H2AX plays a key role in DNA damage signalling the surrounding regions of double-strand breaks (DSBs). In response to damage, becomes phosphorylated on serine residue 139 (known as γH2AX), resulting recruitment repair effectors 53BP1 and BRCA1. Here, by studying resistance poly(ADP-ribose) polymerase (PARP) inhibitors BRCA1/2-deficient mammary tumours, we identify function for γH2AX orchestrating drug-induced replication fork degradation. Mechanistically, γH2AX-driven...
Aging is marked by the gradual accumulation of deleterious changes that disrupt organ function, creating an altered physiological state permissive for onset prevalent human diseases. While exact mechanisms governing aging remain a subject ongoing research, there are several cellular and molecular hallmarks contribute to this biological process. This review focuses on two factors, namely telomere dysfunction inflammation, which have emerged as crucial contributors We aim discuss mechanistic...
Cancer cells display high levels of DNA damage and replication stress, vulnerabilities that could be exploited by drugs targeting repair proteins. Human CtIP promotes homology-mediated double-strand breaks (DSBs) protects stalled forks from nucleolytic degradation, thus representing an attractive candidate for targeted cancer therapy. Here, we establish a peptide mimetic the tetramerization motif inhibits activity. The hydrocarbon-stapled encompassing amino acid residues 18 to 28 (SP18-28)...
Human CtIP is best known for its role in DNA end resection to initiate double-strand break repair by homologous recombination. Recently, has also been shown protect reversed replication forks from nucleolytic degradation upon stress. However, still little about the damage response (DDR) networks that preserve genome integrity and sustain cell survival context of insufficiency. Here, reveal such potential buffering relationships, we screened a DDR siRNA library CtIP-deficient cells identify...