A5088448473- Neuroinflammation and Neurodegeneration Mechanisms
- RNA modifications and cancer
- Cancer-related molecular mechanisms research
- Neurological Disease Mechanisms and Treatments
- Genomics and Chromatin Dynamics
- Adipose Tissue and Metabolism
- RNA Research and Splicing
- Immune cells in cancer
- Regulation of Appetite and Obesity
- Epigenetics and DNA Methylation
- Mycobacterium research and diagnosis
- Pancreatic function and diabetes
- Genomics and Phylogenetic Studies
- Diet and metabolism studies
- CRISPR and Genetic Engineering
- Immune Cell Function and Interaction
- Adipokines, Inflammation, and Metabolic Diseases
- Chromosomal and Genetic Variations
- T-cell and B-cell Immunology
- interferon and immune responses
- Error Correcting Code Techniques
- Single-cell and spatial transcriptomics
- Cardiovascular Disease and Adiposity
- MicroRNA in disease regulation
- Cancer Immunotherapy and Biomarkers
Van Andel Institute
2022-2025
Max Planck Institute of Immunobiology and Epigenetics
2018-2025
Istituto Nazionale Genetica Molecolare
2013-2016
University of Milan
2016
Ospedale Maggiore
2015
Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico
2015
The mechanisms that specify and stabilize cell subtypes remain poorly understood. Here, we identify two major of pancreatic β cells based on histone mark heterogeneity (β
Studies in genetically 'identical' individuals indicate that as much 50% of complex trait variation cannot be traced to genetics or the environment. The mechanisms generate this 'unexplained' phenotypic (UPV) remain largely unknown. Here, we identify neuronatin (NNAT) a conserved factor buffers against UPV. We find Nnat deficiency isogenic mice triggers emergence bi-stable polyphenism, where littermates emerge into adulthood either 'normal' 'overgrown'. Mechanistically, is mediated by an...
To help better understand the role of long noncoding RNAs in human immune system, we recently generated a comprehensive RNA-seq data set using 63 RNA samples from 13 subsets T (CD4(+) naive, CD4(+) TH1, TH2, TH17, Treg, TCM, TEM, CD8(+) naive) and B (B memory, CD5(+)) lymphocytes. There were five biological replicates for each subset except TCM CD5(+) populations that included 4 replicates. RNA-Seq by an Illumina HiScanSQ sequencer TruSeq v3 Cluster kit. 2.192 billion paired-ends reads,...
Chromatin immunoprecipitation followed by deep sequencing (ChIP-seq) is an invaluable tool for mapping chromatin-associated proteins. Current barcoding strategies aim to improve assay throughput and scalability but intense sample handling lack of standardization over cell types, numbers epitopes hinder wide-spread use in the field. Here, we present a method enable high-throughput ChIP-seq using common molecular biology techniques. The method, called RELACS (restriction enzyme-based labeling...
Chronic high-fat feeding triggers chronic metabolic dysfunction including obesity, insulin resistance, and diabetes. How intake first these pathophysiological states remains unknown. Here, we identify an acute microglial response that rapidly translates of diet (HFD) to a surprisingly beneficial effect on metabolism spatial / learning memory. High-fat increases palmitate levels in cerebrospinal fluid wave activation characterized by mitochondrial membrane fission as well skewing towards...
Chronic high-fat feeding triggers metabolic dysfunction including obesity, insulin resistance, and diabetes. How intake first these pathophysiological states remains unknown. Here, we identify an acute microglial response that rapidly translates of diet (HFD) to a surprisingly beneficial effect on metabolism spatial/learning memory. High-fat increases palmitate levels in cerebrospinal fluid wave activation characterized by mitochondrial membrane fission as well skewing toward aerobic...
Chronic high-fat feeding triggers widespread metabolic dysfunction including obesity, insulin resistance, and diabetes. While these ultimate pathological states are relatively well understood, we have a limited understanding of how intake first physiological changes. Here, identify an acute microglial response that rapidly translates diet (HFD) to surprisingly beneficial effect on spatial learning memory. Acute increases palmitate levels in cerebrospinal fluid wave activation characterized...
SUMMARY DNA mutations are necessary drivers of cancer, yet only a small subset mutated cells go on to cause the disease. To date, mechanisms that determine which rare transform and initiate tumorigenesis remain unclear. Here, we take advantage unique model intrinsic developmental heterogeneity ( Trim28 +/D9 ) demonstrate stochastic early life epigenetic variation can trigger distinct cancer-susceptibility ‘states’ in adulthood. We show these developmentally primed states characterized by...
Abstract Obesity is a complex chronic disease characterized by excessive adiposity and associations with numerous co-morbidities, including cancer. Despite extensive research, we have limited understanding of the mechanisms coupling obesity to cancer risk, and, contexts in which does or not exacerbate disease. Here, show that high-fat diet (HFD)-induced has no significant effect on Tp53 R270H/+ mouse, model human Li-Fraumeni multi-cancer syndrome. Surprisingly, despite inducing rapid highly...
Chronic high-fat feeding triggers chronic metabolic dysfunction including obesity, insulin resistance, and diabetes. How intake first these pathophysiological states remains unknown. Here, we identify an acute microglial response that rapidly translates of diet (HFD) to a surprisingly beneficial effect on metabolism spatial / learning memory. High-fat increases palmitate levels in cerebrospinal fluid wave activation characterized by mitochondrial membrane fission as well skewing towards...
Chronic high-fat feeding triggers metabolic dysfunction including obesity, insulin resistance, and diabetes. How intake first these pathophysiological states remains unknown. Here, we identify an acute microglial response that rapidly translates of diet (HFD) to a surprisingly beneficial effect on metabolism spatial/learning memory. High-fat increases palmitate levels in cerebrospinal fluid wave activation characterized by mitochondrial membrane fission as well skewing toward aerobic...