A5021017705- Telomeres, Telomerase, and Senescence
- Single-cell and spatial transcriptomics
- DNA Repair Mechanisms
- 3D Printing in Biomedical Research
- Genomics and Chromatin Dynamics
- Biosimilars and Bioanalytical Methods
- Cell Image Analysis Techniques
- interferon and immune responses
- Extracellular vesicles in disease
- CRISPR and Genetic Engineering
- Renal cell carcinoma treatment
- T-cell and B-cell Immunology
- Erythropoietin and Anemia Treatment
Linköping University
2019-2025
Karolinska Institutet
2017
Genomic medicine has paved the way for identifying biomarkers and therapeutically actionable targets complex diseases, but is complicated by involvement of thousands variably expressed genes across multiple cell types. Single-cell RNA-sequencing study (scRNA-seq) allows characterization such changes in whole organs. The based on applying network tools to organize analyze scRNA-seq data from a mouse model arthritis human rheumatoid arthritis, order find diagnostic therapeutic targets....
The complex formed by Ku70/80 and DNA-PKcs (DNA-PK) promotes the synapsis joining of double strand breaks (DSBs) during canonical non-homologous end (c-NHEJ). In c-NHEJ V(D)J recombination, DNA-PK processing ends opening DNA hairpins recruiting and/or activating nuclease Artemis/DCLRE1C/SNM1C. Paradoxically, is also required to prevent fusions newly replicated leading-end telomeres. Here, we describe role for in controlling Apollo/DCLRE1B/SNM1B, that resects We show telomeric function Apollo...
Abstract During classical non-homologous end joining (cNHEJ), DNA-dependent protein kinase (DNA-PK) encapsulates free DNA ends, forming a recruitment platform for downstream end-joining factors including ligase 4 (LIG4) 1 . DNA-PK can also bind telomeres and regulate their resection 2–4 , but does not initiate cNHEJ at this position. How the process is regulated in context-specific manner currently unclear. Here we show that shelterin components TRF2 RAP1 form complex with directly represses...
Significance Understanding the molecular mechanisms underlying drug resistance of antiangiogenic therapy is crucial to improvement therapeutic efficacy in cancer patients. Our data uncover a mechanism by which off-tumor targets compromise anti-VEGF sensitivity. The implication our findings poses concept that blocking drugs are for efficacy. Based on findings, modest inhibition excessive EPO production recommended therapy. work will result significant paradigm shift and conceptual advances as...
During classical non-homologous end joining (cNHEJ), DNA-dependent protein kinase (DNA-PK) encapsulates free DNA ends, forming a recruitment platform for downstream end-joining factors including Ligase 4 (LIG4) 1 . DNA-PK can also bind telomeres and regulate their resection 2–4 , but does not initiate cNHEJ at this position. How the process is regulated in context-specific manner currently unclear. Here we show that shelterin components TRF2 RAP1 form complex with directly represses its...