A5054142721- Pluripotent Stem Cells Research
- NF-κB Signaling Pathways
- CRISPR and Genetic Engineering
- T-cell and B-cell Immunology
- CAR-T cell therapy research
- Zebrafish Biomedical Research Applications
- Genomics and Chromatin Dynamics
- RNA Interference and Gene Delivery
- Immunotherapy and Immune Responses
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Renal and related cancers
- Genetics, Aging, and Longevity in Model Organisms
- interferon and immune responses
- Cytokine Signaling Pathways and Interactions
- Phytochemical Studies and Bioactivities
- Retinoids in leukemia and cellular processes
- Immune Response and Inflammation
- Ubiquitin and proteasome pathways
- Epigenetics and DNA Methylation
- Protein Degradation and Inhibitors
Josep Carreras Leukaemia Research Institute
2022-2025
Centro de Investigación Biomédica en Red de Cáncer
2021-2025
Hospital del Mar Research Institute
2020-2024
Hospital Del Mar
2020-2024
University of Coimbra
2017-2018
Ectopic expression of transcription factors PU.1, IRF8, and BATF3 reprograms fibroblasts to dendritic cells.
Maintenance of pluripotency is a multifactorial process in which NF-κB negative regulator. Our previous work identified chromatin role for IκBα, the master regulator signaling, that critical proper regulation various tissue stem cells. Here, we found IκBα accumulates specifically fraction pluripotent embryonic depletion does not affect NF-kB-dependent transcription, but causes profound epigenetic rewiring cells, including alterations H3K27me3, histone mark catalyzed by Polycomb repression...
Maintenance of pluripotency is a multifactorial process in which NF-κB negative regulator. Our previous work identified chromatin role for IκBα, the master regulator signaling, that critical proper regulation various tissue stem cells. Here, we found IκBα accumulates specifically fraction pluripotent embryonic depletion does not affect NF-kB-dependent transcription, but causes profound epigenetic rewiring cells, including alterations H3K27me3, histone mark catalyzed by Polycomb repression...
Abstract We previously demonstrated that the NF-κB inhibitor IκBα binds chromatin together with PRC2 to regulate a subset of developmental- and stem cell-related genes. This alternative function has been elusive in both physiological disease conditions because predominant role as negative regulator NF-κB. here uniquely characterize specific residues allow generation separation-of-function (SOF) mutants are defective for either NF-κB-related (SOF ΔNF-κB ) or chromatin-related ΔH2A,H4...
Creating hematopoietic stem cells (HSCs) capable of multilineage engraft while possessing the ability to self-renew stands as a pivotal achievement within field regenerative medicine. However, achieving generation these without transgene expression or teratoma formation has not been fully accomplished. In recent publication featured in
Reprogramming somatic cells into induced pluripotent stem (iPSCs) requires activation of the pluripotency network and resetting epigenome by erasing epigenetic memory state. In female mouse cells, a critical reprogramming step is reactivation inactive X chromosome. Despite its importance, systematic understanding regulatory networks linking X-reactivation missing. Here, we reveal important pathways for acquisition using genome-wide CRISPR screen during neural precursor to iPSC reprogramming....
Summary Maintenance of pluripotency is a multifactorial process in which NF-κB negative regulator. Our previous work identified chromatin role for IκBα, the master regulator signaling, that critical proper regulation various tissue stem cells. Here, we found IκBα accumulates specifically fraction pluripotent embryonic depletion does not affect NF-kB-dependent transcription, but causes profound epigenetic rewiring cells, including alterations H3K27me3, histone mark catalyzed by Polycomb...
Abstract Reprogramming somatic cells into induced pluripotent stem (iPSCs) requires activation of the pluripotency network and resetting epigenome by erasing epigenetic memory state. In female mouse cells, a critical reprogramming step is reactivation inactive X chromosome. Despite its importance, systematic understanding regulatory networks linking X-reactivation missing. Here we reveal pathways important for iPSC using genome-wide CRISPR screen. particular, discover that interferon γ...