0000000001098125

AUTHOR

Francesco Spallotta

0000-0002-0466-6286

showing 3 related works from this author

Enhancement of lysine acetylation accelerates wound repair

2013

In physiopathological conditions, such as diabetes, wound healing is significantly compromised and chronic complications, including ulcers, may occur. In a mouse model of skin repair, we recently reported that wound treatment with Sirtuin activators and class I HDAC inhibitors induced keratinocyte proliferation and enhanced healing via a nitric oxide (NO) dependent mechanism. We observed an increase in total protein acetylation in the wound area, as determined by acetylation of α-tubulin and histone H3 Lysine 9. We reasoned that this process activated cell function as well as regulated gene expression to foster tissue repair. We report here that the direct activation of P300/CBP-associated …

Skin repairWound HealingepigeneticsActivator (genetics)Short CommunicationkeratinocyteBiologyNitric OxideCell biologyHistone H3medicine.anatomical_structureepigenetics; pathology Wound Healing; lysine acetylation; PCAF; keratinocyte; Nitric OxideBiochemistryPCAFAcetylationPCAFSirtuinmedicinebiology.proteinpathologyGeneral Agricultural and Biological SciencesKeratinocyteWound healinglysine acetylationCommunicative & Integrative Biology
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A point mutation in the Ncr1 signal peptide impairs the development of innate lymphoid cell subsets.

2018

International audience; NKp46 (CD335) is a surface receptor shared by both human and mouse natural killer (NK) cells and innate lymphoid cells (ILCs) that transduces activating signals necessary to eliminate virus-infected cells and tumors. Here, we describe a spontaneous point mutation of cysteine to arginine (C14R) in the signal peptide of the NKp46 protein in congenic Ly5.1 mice and the newly generated NCR(B6C14R) strain. Ly5.1(C14R) NK cells expressed similar levels of Ncr1 mRNA as C57BL/6, but showed impaired surface NKp46 and reduced ability to control melanoma tumors in vivo. Expression of the mutant NKp46(C14R) in 293T cells showed that NKp46 protein trafficking to the cell surface …

lcsh:Immunologic diseases. Allergy0301 basic medicineSignal peptideintracellular traffickingImmunologyCellCongenicinnate lymphoid cellsBiologymedicine.disease_causelcsh:RC254-28203 medical and health sciences0302 clinical medicinemedicineImmunology and Allergyddc:610congenic miceReceptorOriginal ResearchMutationEndoplasmic reticulumInnate lymphoid cellHEK 293 cellslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensCell biology030104 developmental biologymedicine.anatomical_structureOncologyactivation receptors[SDV.IMM]Life Sciences [q-bio]/Immunologylcsh:RC581-607030215 immunology
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Stable Oxidative Cytosine Modifications Accumulate in Cardiac Mesenchymal Cells From Type2 Diabetes Patients

2018

Rationale: Human cardiac mesenchymal cells (CMSCs) are a therapeutically relevant primary cell population. Diabetes mellitus compromises CMSC function as consequence of metabolic alterations and incorporation of stable epigenetic changes. Objective: To investigate the role of α-ketoglutarate (αKG) in the epimetabolic control of DNA demethylation in CMSCs. Methods and Results: Quantitative global analysis, methylated and hydroxymethylated DNA sequencing, and gene-specific GC methylation detection revealed an accumulation of 5-methylcytosine, 5-hydroxymethylcytosine, and 5-formylcytosine in the genomic DNA of human CMSCs isolated from diabetic donors. Whole heart genomic DNA analysis reveale…

Male0301 basic medicinePhysiologyPopulationheartBiologyMixed Function OxygenasesCytosineMice03 medical and health sciencesProto-Oncogene ProteinsfibroblastsHuman Umbilical Vein Endothelial CellsAnimalsHumansMyocytes CardiacEpigeneticsEnzyme InhibitorseducationCells CulturedEpigenomicsDemethylationeducation.field_of_studyDNA methylationDNA methylation; epigenomics; fibroblasts; heart; hyperglycemia; metabolism; physiology; cardiology and cardiovascular medicineMesenchymal Stem CellsSettore MED/13 - ENDOCRINOLOGIABase excision repairMolecular biologyThymine DNA GlycosylaseMice Inbred C57BLHEK293 Cells030104 developmental biologyDNA demethylationDiabetes Mellitus Type 2epigenomicsDNA methylationKetoglutaric AcidshyperglycemiaThymine-DNA glycosylaseCardiology and Cardiovascular MedicineOxidation-ReductionmetabolismCirculation Research
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