A5070504731- Mitochondrial Function and Pathology
- RNA modifications and cancer
- NF-κB Signaling Pathways
- Ubiquitin and proteasome pathways
- Metabolism and Genetic Disorders
- Neurogenetic and Muscular Disorders Research
- Peptidase Inhibition and Analysis
- Congenital Anomalies and Fetal Surgery
- interferon and immune responses
- Receptor Mechanisms and Signaling
- ATP Synthase and ATPases Research
- Lymphoma Diagnosis and Treatment
- RNA and protein synthesis mechanisms
- Chemokine receptors and signaling
- Hippo pathway signaling and YAP/TAZ
- Cytokine Signaling Pathways and Interactions
- Angiogenesis and VEGF in Cancer
- Cancer Mechanisms and Therapy
- Education, sociology, and vocational training
- Healthcare Systems and Practices
- Acute Myeloid Leukemia Research
- Axon Guidance and Neuronal Signaling
- Signaling Pathways in Disease
- Psychoanalysis and Psychopathology Research
- Health, Medicine and Society
Boston Children's Hospital
2021-2023
Dana-Farber Cancer Institute
2022-2023
Harvard Stem Cell Institute
2023
Harvard University
2021-2023
Hôpital de la Timone
2023
Assistance Publique Hôpitaux de Marseille
2022
Inserm
2012-2017
Centre National de la Recherche Scientifique
2014-2017
Structure et Instabilité des Génomes
2017
Institut Cochin
2015
VE-cadherin-mediated cell-cell junction weakening increases paracellular permeability in response to both angiogenic and inflammatory stimuli. Although Semaphorin 3A has emerged as one of the few known anti-angiogenic factors exhibit pro-permeability activity, little is about how it triggers vascular leakage. Here we report that induced VE-cadherin serine phosphorylation internalization, destabilization, loss barrier integrity brain endothelial cells. In addition, high-grade glioma-isolated...
The endoplasmic reticulum functions as a key subcellular gateway for NF-κB activation.
Abstract Background NF-κB is a master gene regulator involved in plethora of biological processes, including lymphocyte activation and proliferation. Reversible ubiquitinylation key adaptors required to convey the optimal NF-κB. However deubiquitinylases (DUBs), which catalyze removal these post-translational modifications participate reset system basal level following T-Cell receptor (TCR) engagement continue be elucidated. Findings Here, we performed an unbiased siRNA library screen...
The interleukin-8 chemokine (IL-8) G-protein coupled receptor CXCR2 governs pro-inflammatory and pro-angiogenic responses in leukocytes endothelial cells. At a molecular standpoint, is widely reported to operate through calcium flux, phosphoinoisitide 3 kinase (PI3K) mitogen-activated protein (MAPK). While trafficking suspected be intertwined with its signaling, the exact mechanism not fully elucidated.Here, we identified lysine 327 within C-terminal tail as key residue for ubiquitination,...
Abstract Cells experience intrinsic and extrinsic pressures that affect their proclivity to expand persist in vivo . In congenital disorders caused by loss-of-function mutations mitochondrial DNA (mtDNA), metabolic vulnerabilities may result cell-type specific phenotypes depletion of pathogenic alleles, contributing purifying selection. However, the impact mtDNA on cellular hematopoietic landscape is not well understood. Here, we establish a multi-omics approach quantify deletions alongside...
Abstract Background Spinal muscular atrophy (SMA) is a rare genetic neuromuscular disorder due to an autosomal recessive mutation in the survival motor neuron 1 gene ( SMN1 ) causing degeneration of anterior horn cells spinal cord and resulting muscle atrophy. The aim this paper report 36-month follow-up children with SMA treated nusinersen before age 3 years. Change function, nutritional ventilatory support orthopedics outcomes were evaluated at baseline 36 months after intrathecal...