A5027589460- Parathyroid Disorders and Treatments
- Glioma Diagnosis and Treatment
- Neuroinflammation and Neurodegeneration Mechanisms
- Nutrition and Health in Aging
- Genetics and Neurodevelopmental Disorders
- Muscle Physiology and Disorders
- Ubiquitin and proteasome pathways
- Genetic Syndromes and Imprinting
- Immune cells in cancer
- Microtubule and mitosis dynamics
- Hair Growth and Disorders
- interferon and immune responses
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Melanoma and MAPK Pathways
- Nerve injury and regeneration
- Cytokine Signaling Pathways and Interactions
- Ocular Oncology and Treatments
- Cancer-related Molecular Pathways
- Protein Kinase Regulation and GTPase Signaling
- Genomics and Chromatin Dynamics
- Pancreatic function and diabetes
- Cancer Cells and Metastasis
- Ferroptosis and cancer prognosis
- Diabetes and associated disorders
- RNA Research and Splicing
Boehringer Ingelheim (United Kingdom)
2020-2021
Stem Cell Institute
2021
Boehringer Ingelheim (Germany)
2021
Boehringer Ingelheim (United States)
2019-2020
The Francis Crick Institute
2017-2019
Molecular Oncology (United States)
2017-2019
Cancer Research UK
2010
Aging is accompanied by disrupted information flow, resulting from accumulation of molecular mistakes. These mistakes ultimately give rise to debilitating disorders including skeletal muscle wasting, or sarcopenia. To derive a global metric growing ‘disorderliness’ aging muscle, we employed statistical physics approach estimate the state parameter, entropy, as function genes associated with hallmarks aging. Escalating network entropy reached an inflection point at old age, while structural...
The AP-1 transcription factor c-Jun is required for Ras-driven tumorigenesis in many tissues and considered as a classical proto-oncogene. To determine the requirement mouse model of K-RasG12D–induced lung adenocarcinoma, we inducibly deleted adult lung. Surprisingly, found that inactivation c-Jun, or mutation its JNK phosphorylation sites, actually increased tumor burden. Mechanistically, protein levels Jun family member JunD were absence c-Jun. In c-Jun–deficient cells, was increased,...
The streptozotocin (STZ) model is widely used in diabetes research. However, the cellular and molecular states of pancreatic endocrine cells this remain unclear. This study explored characteristics islet treated with STZ re-evaluated β-cell dysfunction regeneration model. We performed single-cell RNA sequencing from STZ-treated mice. High-quality data 2,999 were to identify clusters via Louvain clustering analysis. Principal component analysis (PCA), t-distributed stochastic neighbor...
Mutations of WD repeat domain 62 (WDR62) lead to autosomal recessive primary microcephaly (MCPH), and down-regulation WDR62 expression causes the loss neural progenitor cells (NPCs). However, how is regulated hence controls neurogenesis brain size remains elusive. Here, we demonstrate that mitogen-activated protein kinase 3 (MEKK3) forms a complex with promote c-Jun N-terminal (JNK) signaling synergistically in control neurogenesis. The deletion Mekk3, Wdr62, or Jnk1 resulted phenocopied...
Squamous cell carcinomas (SCCs) account for the majority of cancer mortalities. Although TP63 is an established lineage-survival oncogene in SCCs, therapeutic strategies have not been developed to target or it's downstream effectors. In this study we demonstrate that directly regulates NRG1 expression human SCC lines and a critical component transcriptional program. Notably, show squamous tumors are dependent signaling vivo, both genetically engineered mouse models xenograft models,...
Choroid plexus tumours (CPTs) account for 2–5% of brain in children. They can spread along the neuraxis and recur after treatment. Little is known about molecular mechanisms underlying their formation only few high fidelity mouse models p53-deficient malignant CPTs are available. We show here that c-MYC overexpression choroid epithelium induces T-cell inflammation-dependent papillomas a model. demonstrate expressed substantial proportion human this subgroup characterised by an inflammatory...
Choroid plexus tumours (CPTs) account for up to 20% of brain in children under 2 years age. They can spread along the neuraxis and recur after treatment. Little is known about molecular mechanisms underlying their formation only one high fidelity mouse model p53-deficient CPTs available. c-Myc a proto-oncogene deregulated various malignancies, including paediatric tumours. Here, we conditionally overexpressed neural progenitor cells assess its role tumour pathogenesis. We show that...
Abstract Choroid plexus tumours (CPT) account for up to 20% of brain in children under 2 years age. Histologically CPTs are classified into three categories - Plexus Papilloma (CPP), Atypical (ACPP) and Carcinoma (CPC). Recent literature demonstrates that CPP ACPP molecularly distinct from CPC. Initial management CPT include surgery followed by adjuvant therapy selected patients. Currently there no disease-specific chemotherapeutic agents available, possibly because their rarity paucity...
In the original version of this article [1], there was 1 error in affiliation European Institute Oncology (affiliation 3). correction updated is shown for clarification.
ABSTRACT Aging is accompanied by a disrupted information flow, which results from accumulation of molecular mistakes. These mistakes ultimately give rise to debilitating disorders such as skeletal muscle wasting, or sarcopenia. To estimate the growing “disorderliness” aging system, we employed statistical physics approach state parameter, entropy, function genes associated with hallmarks aging. Although most prominent structural and functional alterations were observed in oldest old mice...