Search results for "Homeostasis"

showing 10 items of 630 documents

Mg2+ homeostasis and transport in cyanobacteria – at the crossroads of bacterial and chloroplast Mg2+ import

2018

Abstract Magnesium cation (Mg2+) is the most abundant divalent cation in living cells, where it is required for various intracellular functions. In chloroplasts and cyanobacteria, established photosynthetic model systems, Mg2+ is the central ion in chlorophylls, and Mg2+ flux across the thylakoid membrane is required for counterbalancing the light-induced generation of a ΔpH across the thylakoid membrane. Yet, not much is known about Mg2+ homoeostasis, transport and distribution within cyanobacteria. However, Mg2+ transport across membranes has been studied in non-photosynthetic bacteria, and first observations and findings are reported for chloroplasts. Cyanobacterial cytoplasmic membranes…

0301 basic medicineChloroplastsClinical BiochemistryCyanobacteriaPhotosynthesisBiochemistry03 medical and health sciencesHomeostasisMagnesiumElectrochemical gradientMolecular BiologyIon TransportBacteria030102 biochemistry & molecular biologybiologyChemistrySynechocystisMembrane Transport ProteinsMembrane transportbiology.organism_classificationTransmembrane proteinChloroplast030104 developmental biologyMembraneThylakoidBiophysicsBiological Chemistry
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Enhanced autophagic-lysosomal activity and increased BAG3-mediated selective macroautophagy as adaptive response of neuronal cells to chronic oxidati…

2019

Oxidative stress and a disturbed cellular protein homeostasis (proteostasis) belong to the most important hallmarks of aging and of neurodegenerative disorders. The proteasomal and autophagic-lysosomal degradation pathways are key measures to maintain proteostasis. Here, we report that hippocampal cells selected for full adaptation and resistance to oxidative stress induced by hydrogen peroxide (oxidative stress-resistant cells, OxSR cells) showed a massive increase in the expression of components of the cellular autophagic-lysosomal network and a significantly higher overall autophagic activity. A comparative expression analysis revealed that distinct key regulators of autophagy are upregu…

0301 basic medicineClinical BiochemistryLFQ Label-free quantificationLETM Leucine zipper and EF-hand containing transmembrane proteinmedicine.disease_causeBiochemistryCHX Cycloheximide0302 clinical medicineBNIP3 Bcl-2 interacting protein 3RAPA RapamycinPIK3C3 Class III PI3‐kinasePhosphorylationlcsh:QH301-705.5Neuronslcsh:R5-920PolyUB PolyubiquitinChemistryBAG3OPA1 Optic atrophy 1TOR Serine-Threonine KinasesWIPI1 WD repeat domain phosphoinositide-interacting protein 1ATG Autophagy relatedTFEB Transcription factor EBCell biologyMitochondriasiRNA Small interfering RNADLP1 Dynamin-like protein 1LAMP1 Lysosomal‐associated membrane protein 1PURO Puromycinlcsh:Medicine (General)Protein homeostasisResearch PaperBafA1 Bafilomycin A1LAMP2 Lysosomal‐associated membrane protein 2Proteasome Endopeptidase ComplexRAB18 Member RAS oncogeneTUB TubulinLC3 Light chain 3 proteinOxidative phosphorylationBAG3CTSD Cathepsin DModels BiologicalCell Line03 medical and health sciencesDownregulation and upregulationMacroautophagymedicineAutophagyHumansAdaptationBAG1 Bcl-2-associated athanogene 1BECN1 Beclin1PI3K/AKT/mTOR pathwayAdaptor Proteins Signal TransducingTEM Transmission electron microscopyHsp70 Heat shock protein 70Organic ChemistryAutophagyAutophagosomesmTOR Mammalian target of rapamycinHsp70Oxidative Stress030104 developmental biologyProteostasislcsh:Biology (General)CV CanavanineBAG3 Bcl-2-associated athanogene 3MTT (3-(45-Dimethylthiazol-2-yl)-25-Diphenyltetrazolium Bromide)Apoptosis Regulatory ProteinsLysosomes030217 neurology & neurosurgeryOxidative stressRedox Biology
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Harnessing mechanosensation in next generation cardiovascular tissue engineering

2020

The ability of the cells to sense mechanical cues is an integral component of ”social” cell behavior inside tissues with a complex architecture. Through ”mechanosensation” cells are in fact able to decrypt motion, geometries and physical information of surrounding cells and extracellular matrices by activating intracellular pathways converging onto gene expression circuitries controlling cell and tissue homeostasis. Additionally, only recently cell mechanosensation has been integrated systematically as a crucial element in tissue pathophysiology. In the present review, we highlight some of the current efforts to assess the relevance of mechanical sensing into pathology modeling and manufact…

0301 basic medicineComputer sciencelcsh:QR1-502Review030204 cardiovascular system & hematologyBiochemistryCardiovascular SystemMechanotransduction Cellularlcsh:MicrobiologyCardiac regeneration03 medical and health sciences0302 clinical medicineTissue engineeringMechanosensingExtracellularAnimalsHumansMolecular BiologyTissue homeostasisMechanosensationTissue EngineeringExtracellular Matrix030104 developmental biologyCardiac regenerationNeuroscienceIntracellular
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The good and bad of targeting cancer-associated extracellular matrix

2017

The maintenance of tissue homeostasis requires extracellular matrix (ECM) remodeling. Immune cells actively participate in regenerating damaged tissues contributing to ECM deposition and shaping. Dysregulated ECM deposition characterizes fibrotic diseases and cancer stromatogenesis, where a chronic inflammatory state sustains the ECM increase. In cancer, the ECM fosters several steps of tumor progression, providing pro-survival and proliferative signals, promoting tumor cell dissemination via collagen fibers or acting as a barrier to impede drug diffusion. Interfering with processes leading to chronic ECM deposition, as occurring in cancer, might allow the simultaneous targeting of both pri…

0301 basic medicineContext (language use)BiologyExtracellular matrix03 medical and health sciencesImmune systemNeoplasmsDrug DiscoverymedicineTumor MicroenvironmentAnimalsHumansPharmacology; Drug Discovery3003 Pharmaceutical ScienceMyeloid CellsReceptorTissue homeostasisPharmacologyTumor microenvironmentDrug Discovery3003 Pharmaceutical ScienceCancermedicine.diseaseCell biologyExtracellular Matrix030104 developmental biologyTumor progressionImmunology
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DNA Damage and Repair in Degenerative Diseases 2016

2016

Given the great importance of the integrity of DNA for the correct transmission of the genetic message, repairing the induced lesions to its molecular structure by different endogenous or exogenous origin is crucial for the maintenance of homeostasis and biological functions of living organisms.[...]

0301 basic medicineDNA RepairDNA damageEndogenyBiologyCatalysisEpigenesis GeneticInorganic Chemistrylcsh:Chemistry03 medical and health scienceschemistry.chemical_compoundAnimalsHumansDiseasePhysical and Theoretical ChemistryMolecular Biologylcsh:QH301-705.5SpectroscopyOrganic ChemistryGeneral MedicineComputer Science ApplicationsCell biologyDietOxidative Stress030104 developmental biologyEditorialn/achemistrylcsh:Biology (General)lcsh:QD1-999DNAHomeostasisDNA DamageInternational Journal of Molecular Sciences
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The Transcription Factor MAZR/PATZ1 Regulates the Development of FOXP3+ Regulatory T Cells

2019

Summary: Forkhead box protein P3+ (FOXP3+) regulatory T cells (Treg cells) play a key role in maintaining tolerance and immune homeostasis. Here, we report that a T cell-specific deletion of the transcription factor MAZR (also known as PATZ1) leads to an increased frequency of Treg cells, while enforced MAZR expression impairs Treg cell differentiation. Further, MAZR expression levels are progressively downregulated during thymic Treg cell development and during in-vitro-induced human Treg cell differentiation, suggesting that MAZR protein levels are critical for controlling Treg cell development. However, MAZR-deficient Treg cells show only minor transcriptional changes ex vivo, indicating…

0301 basic medicineFOXP3PATZ1chemical and pharmacologic phenomenaBiologyTreg cellGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineIntestinal inflammationmedicineForkhead Box Protein P3Immune homeostasisColitisTranscription factorlcsh:QH301-705.5DSS-induced colitisMAZRT(reg)FOXP3hemic and immune systemsmedicine.diseaseCell biology030104 developmental biologyregulatory T cellslcsh:Biology (General)030217 neurology & neurosurgeryCell Reports
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Causes and consequences of DNA damage-induced autophagy.

2021

Abstract Autophagy is a quality control pathway that maintains cellular homeostasis by recycling surplus and dysregulated cell organelles. Identification of selective autophagy receptors demonstrated the existence of pathways that selectively degrade organelles, protein aggregates or pathogens. Interestingly, different types of DNA damage can induce autophagy and autophagy-deficiency leads to genomic instability. Recent studies provided first insights into the pathways that connect autophagy with the DNA damage response. However, the physiological role of autophagy and the identity of its targets after DNA damage remain enigmatic. In this review, we summarize recent literature on the target…

0301 basic medicineGenome instabilityDNA RepairDNA damageAutophagyCellular homeostasisProtein aggregationBiologyGenomic InstabilityCell biology03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicinechemistry030220 oncology & carcinogenesisOrganelleAutophagyHumansReceptorMolecular BiologyDNADNA DamageMatrix biology : journal of the International Society for Matrix Biology
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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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Classic Models for New Perspectives: Delving into Helminth–Microbiota–Immune System Interactions

2018

Whilst a wealth of data indicate that infections by gastrointestinal helminths are accompanied by significant alterations in the composition of the vertebrate gut flora, little is known of the immune-molecular mechanisms that regulate host-parasite-microbiota interactions. 'Traditional' experimental models of gastrointestinal helminthiases, in which the role(s) of each of the components of this triad can be tested, provide an opportunity to advance research in this area. In this article, we propose the Echinostoma caproni-mouse system as a potentially useful tool for studies of the role of the host gut microbiota in preventing pathology and inducing parasite clearance via interleukin (IL)-2…

0301 basic medicineHelminthiasisHelminthiasisInterleukinBiologyGut floramedicine.diseasebiology.organism_classificationModels BiologicalHost-Parasite Interactions03 medical and health sciences030104 developmental biologyInfectious DiseasesImmune systemImmunological FactorsImmunityImmunologymedicineAnimalsHumansHelminthsParasitologyGut homeostasisTrends in Parasitology
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Tetrahydrocarbazoles decrease elevated SOCE in medium spiny neurons from transgenic YAC128 mice, a model of Huntington's disease

2017

AbstractHuntington's disease (HD) is a hereditary neurodegenerative disease caused by a polyglutamine expansion within the huntingtin (HTT) gene. One of the cellular functions that is dysregulated in HD is store-operated calcium entry (SOCE), a process in which the depletion of Ca2+ from the endoplasmic reticulum (ER) induces Ca2+ influx from the extracellular space. We detected an enhanced activity of SOC channels in medium spiny neurons (MSNs) from YAC128 mice, a transgenic model of HD, and investigated whether this could be reverted by tetrahydrocarbazoles. The compound 6-bromo-N-(2-phenylethyl)-2,3,4,9-tetrahydro-1H-carbazol-1-amine hydrochloride was indeed able to restore the disturbed…

0301 basic medicineHuntingtinTransgeneCarbazolesBiophysicsMice TransgenicBiologyEndoplasmic ReticulumMedium spiny neuronYAC128BiochemistryMice03 medical and health sciences0302 clinical medicineHuntington's diseaseTetrahydrocarbazolesmedicineAnimalsHomeostasisHuntingtinMolecular BiologyCells CulturedMembrane Potential MitochondrialNeuronsSOC channelsMedium spiny neuronsIon TransportEndoplasmic reticulumHuntington's diseaseStore-operated calcium entryCell Biologymedicine.diseaseStore-operated calcium entryCulture MediaCell biology030104 developmental biologyBiochemistryCalcium030217 neurology & neurosurgeryHomeostasisBiochemical and Biophysical Research Communications
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