Search results for "Hom"

showing 10 items of 8335 documents

Next stop: Language : the ?FOXP2? gene?s journey through time

2016

How did humans evolve language? The fossil record does not yield enough evidence to reconstruct its evolution and animals do not talk. But as the neural and molecular substrates of language are uncovered, their genesis and function can be addressed comparatively in other species. FOXP2 is such a case – a gene with a strong link to language that is also essential for learning in mice, birds and even flies. Comparing the role FOXP2 plays in humans and other animals is starting to reveal common principles that may have provided building blocks for language evolution.

0301 basic medicineCognitive scienceMultidisciplinaryFOXP2 GeneFossil Recordlanguagedeep homologymedia_common.quotation_subjectspeechevo-devoFOXP2Biology57603 medical and health sciences030104 developmental biologyHistory and Philosophy of ScienceLanguage evolutionFunction (engineering)sensory-motor learningmedia_common
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Data mining approaches to identify biomineralization related sequences.

2015

Proteomics is an efficient high throughput technique developed to identify proteins from a crude extract using sequence homology. Advances in Next Generation Sequencing (NGS) have led to increase knowledge of several non-model species. In the field of calcium carbonate biomineralization, the paucity of available sequences (such as the ones of mollusc shells) is still a bottleneck in most proteomic studies. Indeed, this technique needs proteins databases to find homology. The aim of this study was to perform different data mining approaches in order to identify novel shell proteins. To this end, we disposed of several publicly non-model molluscs databases. Previously identified molluscan she…

0301 basic medicineComputer scienceMechanical EngineeringProteomicscomputer.software_genre[ SDV.IB.BIO ] Life Sciences [q-bio]/Bioengineering/BiomaterialsBottleneckDNA sequencing[SDV.IB.BIO] Life Sciences [q-bio]/Bioengineering/Biomaterials03 medical and health sciencesAnnotation030104 developmental biologySequence homologyMechanics of Materials[ SDV.BBM.GTP ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]Shell matrix[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]General Materials ScienceData miningKEGGcomputerComputingMilieux_MISCELLANEOUSBiomineralization
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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 Binding Mechanism of Epolactaene to Hsp60 Unveiled by in Silico Modelling

2016

Molecular Dynamics (MD) simulations and DFT/MM calculations were performed in order to rationalize available experimental results and to provide structural details on the binding mechanism of Epolactaene (EPO) to the 60 KDa Heat Shock Protein (Hsp60). The available crystal structure of Hsp60 represents the last step of the chaperone folding cycle, while the Hsp60-EPO complex was obtained by using a homology model of Hsp60, in order to simulate a state related to the beginning of the folding cycle (Rs1). The results of MD simulations point out that EPO shows the highest binding affinity for the empty ATP binding site. The presence of ATP opens a channel that allows the entrance of both EPO d…

0301 basic medicineConformational changeanimal structuresStereochemistryProteins · Molecular Dynamics · Density Functional Theory · Heat Shock Proteins · Epolactaene010402 general chemistry01 natural sciences03 medical and health sciencesMolecular dynamicschemistry.chemical_compoundHeat shock proteinHomology modelingBinding siteEpolactaenebiologyChemistrySettore BIO/16 - Anatomia UmanafungiGeneral ChemistrySettore CHIM/06 - Chimica Organica0104 chemical sciencesCrystallography030104 developmental biologyCovalent bondSettore CHIM/03 - Chimica Generale E InorganicaChaperone (protein)biology.protein
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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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Mitochondrial BAX Determines the Predisposition to Apoptosis in Human AML

2017

Abstract Purpose: Cell-to-cell variability in apoptosis signaling contributes to heterogenic responses to cytotoxic stress in clinically heterogeneous neoplasia, such as acute myeloid leukemia (AML). The BCL-2 proteins BAX and BAK can commit mammalian cells to apoptosis and are inhibited by retrotranslocation from the mitochondria into the cytosol. The subcellular localization of BAX and BAK could determine the cellular predisposition to apoptotic death. Experimental Design: The relative localization of BAX and BAK was determined by fractionation of AML cell lines and patient samples of a test cohort and a validation cohort. Results: This study shows that relative BAX localization determine…

0301 basic medicineCytoplasmCancer ResearchApoptosisKaplan-Meier EstimateBiologyMitochondrionMitochondrial Proteins03 medical and health sciencesCell Line Tumorhemic and lymphatic diseasesmedicineHumansCytotoxic T cellLeukocytosisRetrospective Studiesbcl-2-Associated X ProteinMyeloid leukemiaCancerRetrospective cohort studymedicine.diseaseMitochondriaProtein TransportLeukemiabcl-2 Homologous Antagonist-Killer Protein030104 developmental biologyOncologyLeukemia MyeloidApoptosisAcute DiseaseImmunologyCancer researchmedicine.symptomHeLa CellsClinical Cancer Research
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STAT1 Isoforms Differentially Regulate NK Cell Maturation and Anti-tumor Activity

2020

Natural killer (NK) cells are important components of the innate immune defense against infections and cancers. Signal transducer and activator of transcription 1 (STAT1) is a transcription factor that is essential for NK cell maturation and NK cell-dependent tumor surveillance. Two alternatively spliced isoforms of STAT1 exist: a full-length STAT1α and a C-terminally truncated STAT1β isoform. Aberrant splicing is frequently observed in cancer cells and several anti-cancer drugs interfere with the cellular splicing machinery. To investigate whether NK cell-mediated tumor surveillance is affected by a switch in STAT1 splicing, we made use of knock-in mice expressing either only the STAT1α (S…

0301 basic medicineCytotoxicity ImmunologicLymphomaNK cellsCell MaturationMice0302 clinical medicineInterferonImmunology and AllergyProtein IsoformsSTAT1Immunologic SurveillanceOriginal ResearchBone Marrow TransplantationReceptors InterferonInterleukin-15Mice KnockoutLymphopoiesisinterferonInterferon-Stimulated Gene Factor 3Cell biologySpecific Pathogen-Free OrganismsKiller Cells NaturalSTAT1 Transcription FactorOrgan SpecificityMHC class ISignal transductionsignal transductionmedicine.druglcsh:Immunologic diseases. AllergyLymphoid TissueImmunologyBiologyLymphocyte Depletion03 medical and health sciencesInterleukin-15 Receptor alpha SubunitCell Line TumormedicineAnimalsTranscription factorInnate immune systemisoformsMice Inbred C57BL030104 developmental biologyCancer cellSTAT proteinbiology.proteinlcsh:RC581-607IL-15RαSpleen030215 immunologyFrontiers in Immunology
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A Comparison of Techniques to Evaluate the Effectiveness of Genome Editing

2018

Genome editing using engineered nucleases (meganucleases, zinc finger nucleases, transcription activator-like effector nucleases) has created many recent breakthroughs. Prescreening for efficiency and specificity is a critical step prior to using any newly designed genome editing tool for experimental purposes. The current standard screening methods of evaluation are based on DNA sequencing or use mismatch-sensitive endonucleases. They can be time-consuming and costly or lack reproducibility. Here, we review and critically compare standard techniques with those more recently developed in terms of reliability, time, cost, and ease of use.

0301 basic medicineDNA End-Joining Repair[SDV.BIO]Life Sciences [q-bio]/BiotechnologyBioengineeringComputational biologyBiologyDNA sequencing03 medical and health sciencesGenome editingScreening methodAnimalsHumansDNA Breaks Double-StrandedHomologous RecombinationComputingMilieux_MISCELLANEOUSGeneticsGene EditingHigh-Throughput Nucleotide SequencingPlantsEndonucleasesZinc finger nuclease030104 developmental biologyCRISPR-Cas SystemsGenetic EngineeringBiotechnologyRNA Guide Kinetoplastida
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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 MRN complex is transcriptionally regulated by MYCN during neural cell proliferation to control replication stress

2015

The MRE11/RAD50/NBS1 (MRN) complex is a major sensor of DNA double strand breaks, whose role in controlling faithful DNA replication and preventing replication stress is also emerging. Inactivation of the MRN complex invariably leads to developmental and/or degenerative neuronal defects, the pathogenesis of which still remains poorly understood. In particular, NBS1 gene mutations are associated with microcephaly and strongly impaired cerebellar development, both in humans and in the mouse model. These phenotypes strikingly overlap those induced by inactivation of MYCN, an essential promoter of the expansion of neuronal stem and progenitor cells, suggesting that MYCN and the MRN complex migh…

0301 basic medicineDNA ReplicationTranscription GeneticDNA damageDNA repairDNA-Binding ProteinCell Cycle ProteinsBiology03 medical and health sciencesMRE11 Homologue ProteinCell Cycle ProteinStrand-Break Repair; N-Myc; Dna-Replication; Human Neuroblastoma; Feingold-Syndrome; C-Myc; Mre11-Rad50-Nbs1 Complex; Targeted Disruption; Genomic Instability; Embryonic LethalityHumansProgenitor cellMolecular BiologyneoplasmsCells CulturedNuclear ProteinCell ProliferationGeneticsNeuronsOncogene ProteinsOriginal PaperMRE11 Homologue ProteinN-Myc Proto-Oncogene ProteinCell growthDNA Repair EnzymeDNA replicationOncogene ProteinNuclear ProteinsCell BiologyNeuronCell biologyAcid Anhydride HydrolasesDNA-Binding Proteins030104 developmental biologyDNA Repair EnzymesMRN complexGene Expression RegulationRad50HumanCell Death and Differentiation
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