0000000000166979

AUTHOR

Maria Eriksson

showing 3 related works from this author

Rethinking Music from and through Materiality and Fragility

2021

[SHS.MUSIQ] Humanities and Social Sciences/Musicology and performing arts[SHS.HISPHILSO] Humanities and Social Sciences/History Philosophy and Sociology of Sciences[SHS.INFO] Humanities and Social Sciences/Library and information sciences
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Neurogenin 3+ cells contribute to β-cell neogenesis and proliferation in injured adult mouse pancreas

2013

Abstract: We previously showed that injury by partial duct ligation (PDL) in adult mouse pancreas activates Neurogenin 3 (Ngn3)(+) progenitor cells that can differentiate to beta cells ex vivo. Here we evaluate the role of Ngn3(+) cells in beta cell expansion in situ. PDL not only induced doubling of the beta cell volume but also increased the total number of islets. beta cells proliferated without extended delay (the so-called 'refractory' period), their proliferation potential was highest in small islets, and 86% of the beta cell expansion was attributable to proliferation of pre-existing beta cells. At sufficiently high Ngn3 expression level, upto 14% of all beta cells and 40% of small i…

MaleCancer Researchmedicine.medical_specialtyendocrine systemCell- och molekylärbiologiImmunologyCellNerve Tissue Proteinsdigestive systemNeogenesisCellular and Molecular NeuroscienceMiceInternal medicineInsulin-Secreting CellsJournal ArticlemedicineBasic Helix-Loop-Helix Transcription FactorsAnimalsInsulinRegenerationProgenitor cellBeta (finance)PancreasCell ProliferationCell SizeMice Inbred BALB CbiologydiabetesCell growthResearch Support Non-U.S. Gov'tRegeneration (biology)Cell Biologybiology.organism_classificationCell biologytissue injurycell differentiationEndocrinologymedicine.anatomical_structureOriginal ArticleHuman medicinePancreasEx vivoCell and Molecular BiologyCell Death & Disease
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Inhibition of DNA damage response at telomeres improves the detrimental phenotypes of Hutchinson–Gilford Progeria Syndrome

2019

Hutchinson–Gilford progeria syndrome (HGPS) is a genetic disorder characterized by premature aging features. Cells from HGPS patients express progerin, a truncated form of Lamin A, which perturbs cellular homeostasis leading to nuclear shape alterations, genome instability, heterochromatin loss, telomere dysfunction and premature entry into cellular senescence. Recently, we reported that telomere dysfunction induces the transcription of telomeric non-coding RNAs (tncRNAs) which control the DNA damage response (DDR) at dysfunctional telomeres. Here we show that progerin-induced telomere dysfunction induces the transcription of tncRNAs. Their functional inhibition by sequence-specific telomer…

0301 basic medicineGenome instabilityRNA UntranslatedDNA RepairGeneral Physics and AstronomyCellular homeostasisAntisense oligonucleotide therapyMice0302 clinical medicineProgeriaHomeostasislcsh:ScienceCellular SenescenceSkinProgeriaMultidisciplinaryintegumentary systemQTelomereProgerinLamin Type A3. Good healthCell biologyTelomeresPhenotypePremature agingcongenital hereditary and neonatal diseases and abnormalitiesDNA repairScienceDouble-strand DNA breaksBiologySettore MED/08 - Anatomia PatologicaGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencesmedicineDNA damage Hutchinson-Gilford Progeria SyndromeAnimalsCell Proliferationnutritional and metabolic diseasesGeneral ChemistryOligonucleotides Antisensemedicine.diseaseTelomereDisease Models Animal030104 developmental biologyMutationlcsh:Q030217 neurology & neurosurgeryLaminDNA DamageNature Communications
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