Matteo M. Guerrini

ORCID: 0000-0003-1481-4104
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About
Contact & Profiles
Research Areas
  • Bone Metabolism and Diseases
  • Bone health and treatments
  • NF-κB Signaling Pathways
  • RNA Research and Splicing
  • Immune Cell Function and Interaction
  • Cell Adhesion Molecules Research
  • Cytokine Signaling Pathways and Interactions
  • Virus-based gene therapy research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Cancer-related molecular mechanisms research
  • Immune Response and Inflammation
  • Diabetes and associated disorders
  • RNA Interference and Gene Delivery
  • Tryptophan and brain disorders
  • Dermatology and Skin Diseases
  • Effects of Environmental Stressors on Livestock
  • Cytomegalovirus and herpesvirus research
  • Viral gastroenteritis research and epidemiology
  • Genomics and Rare Diseases
  • Genomics and Chromatin Dynamics
  • Single-cell and spatial transcriptomics
  • RNA modifications and cancer
  • Gut microbiota and health
  • Digestive system and related health
  • Mass Spectrometry Techniques and Applications

RIKEN Center for Integrative Medical Sciences
2017-2021

The University of Tokyo
2014-2015

Japan Science and Technology Agency
2014-2015

Institute of Genetic and Biomedical Research
2011-2012

Humanitas University
2012

National Research Council
2007-2011

IRCCS Humanitas Research Hospital
2008-2011

Institute of Biomedical Technologies
2007-2009

Fondazione Humanitas per la Ricerca
2007

Vita-Salute San Raffaele University
2006

Objective RANKL is mainly expressed by synovial fibroblasts and T cells within the joints of rheumatoid arthritis patients. The relative importance expression these cell types for formation bone erosions unclear. We therefore aimed to quantify contribution each type osteoclast differentiation destruction during inflammatory arthritis. Methods was specifically deleted in ( Tnfsf11 flox/Δ Lck -Cre), collagen VI expressing including Col6a1 -Cre) II articular chondrocytes Col2a1 -Cre). Erosive...

10.1136/annrheumdis-2014-207137 article EN Annals of the Rheumatic Diseases 2015-05-29

Abstract Autosomal recessive osteopetrosis (ARO) is a genetically heterogeneous disorder attributed to reduced bone resorption by osteoclasts. Most human AROs are classified as osteoclast rich, but recently two subsets of osteoclast-poor ARO have been recognized caused defects in either TNFSF11 or TNFRSF11A genes, coding the RANKL and RANK proteins, respectively. The RANKL/RANK axis drives differentiation also plays role immune system. In fact, we reported that mutations gene lead associated...

10.1002/jbmr.559 article EN other-oa Journal of Bone and Mineral Research 2011-11-09

Abstract In the last decades molecular basis of monogenic diseases has been largely unraveled, although their treatment often remained unsatisfactory. Autosomal recessive osteopetrosis (ARO) belongs to small group genetic that are usually treated with hematopoietic stem cell transplantation (HSCT). However, this approach is not effective in recently identified form carrying mutations receptor activator NF-κB ligand (RANKL) gene. subset, therapy replacement based on RANKL delivery a strong...

10.1002/jbmr.1712 article EN Journal of Bone and Mineral Research 2012-07-26

Borna disease virus 1 (BoDV1) is a disease-causing agent in some livestock and, as has recently been shown, humans. What constitutes protective immune response to BoDV1 unclear. Previous studies found that endogenous bornavirus-like nucleoprotein elements (EBLNs) present mammalian genomes produce piRNAs antisense mRNAs. As known function of restrict transposons via RNA interference, it hypothesized EBLN-derived may BoDV1. Here we used EBLN knockout (KO) and other KO mice test genetic factors...

10.1371/journal.ppat.1013165 article EN cc-by PLoS Pathogens 2025-05-09

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10.1017/s0029665108006198 article EN Proceedings of The Nutrition Society 2008-05-01
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