Search results for "ATR"

showing 10 items of 21758 documents

Oxidative Stress-Induced Axon Fragmentation Is a Consequence of Reduced Axonal Transport in Hereditary Spastic Paraplegia SPAST Patient Neurons

2020

Hereditary spastic paraplegia (HSP) is a group of inherited disorders characterized by progressive spasticity and paralysis of the lower limbs. Autosomal dominant mutations in SPAST gene account for ∼40% of adult-onset patients. We have previously shown that SPAST patient cells have reduced organelle transport and are therefore more sensitive to oxidative stress. To test whether these effects are present in neuronal cells, we first generated 11 induced pluripotent stem (iPS) cell lines from fibroblasts of three healthy controls and three HSP patients with different SPAST mutations. These cells were differentiated into FOXG1-positive forebrain neurons and then evaluated for multiple aspects …

0301 basic medicineHereditary spastic paraplegiaOxidative phosphorylationSpastinmedicine.disease_causelcsh:RC321-57103 medical and health sciences0302 clinical medicinemedicineSPASTAxonFragmentation (cell biology)hereditary spastic paraplegialcsh:Neurosciences. Biological psychiatry. NeuropsychiatryGeneral Neuroscienceperoxisomesaxon transportmedicine.diseaseepothilone Daxon degenerationCell biology030104 developmental biologymedicine.anatomical_structurenervous systemForebrainAxoplasmic transport030217 neurology & neurosurgeryOxidative stressFrontiers in Neuroscience
researchProduct

Mitochondrial Function in Hereditary Spastic Paraplegia: Deficits in SPG7 but Not SPAST Patient-Derived Stem Cells

2020

Mutations in SPG7 and SPAST are common causes of hereditary spastic paraplegia (HSP). While some SPG7 mutations cause paraplegin deficiency, other SPG7 mutations cause increased paraplegin expression. Mitochondrial function has been studied in models that are paraplegin-deficient (human, mouse, and Drosophila models with large exonic deletions, null mutations, or knockout models) but not in models of mutations that express paraplegin. Here, we evaluated mitochondrial function in olfactory neurosphere-derived cells, derived from patients with a variety of SPG7 mutations that express paraplegin and compared them to cells derived from healthy controls and HSP patients with SPAST mutations, as …

0301 basic medicineHereditary spastic paraplegiaoxidative phosphorylationOxidative phosphorylationMitochondrionmedicine.disease_causeSpastinSPG7lcsh:RC321-57103 medical and health sciences0302 clinical medicinemedicineSPASThereditary spastic paraplegialcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMutationparapleginParapleginGeneral NeuroscienceBrief Research Reportspastinmedicine.diseasePhenotypeCell biologymitochondria030104 developmental biology030217 neurology & neurosurgeryOxidative stressNeuroscienceFrontiers in Neuroscience
researchProduct

Neonatal hyperinsulinemic hypoglycemia: case report of kabuki syndrome due to a novel KMT2D splicing-site mutation

2020

Abstract Background Persistent neonatal hypoglycemia, owing to the possibility of severe neurodevelopmental consequences, is a leading cause of neonatal care admission. Hyperinsulinemic hypoglycemia is often resistant to dextrose infusion and needs rapid diagnosis and treatment. Several congenital conditions, from single gene defects to genetic syndromes should be considered in the diagnostic approach. Kabuki syndrome type 1 (MIM# 147920) and Kabuki syndrome type 2 (MIM# 300867), can be associated with neonatal hyperinsulinemic hypoglycemia. Patient presentation We report a female Italian (Sicilian) child, born preterm at 35 weeks gestation, with persistent hypoglycemia. Peculiar facial dys…

0301 basic medicineHeterozygotePediatricsmedicine.medical_specialtyFacial dysmorphismNeonatal hypotoniaCase ReportHypoglycemiamedicine.disease_causeDiagnosis DifferentialNervous system malformation03 medical and health sciences0302 clinical medicineHyperinsulinismmedicineHumansAbnormalities MultipleHyperinsulinemic hypoglycemiaPathologicalbusiness.industryNeonatal hypoglycemiaInfant Newbornlcsh:RJ1-570lcsh:Pediatricsmedicine.diseaseHematologic DiseasesNeoplasm ProteinsDNA-Binding ProteinsPhenotype030104 developmental biologyNeonatal hypotoniaItalyVestibular DiseasesFaceMutationGestationFemalebusinessHyperinsulinismKabuki syndromeInfant PrematureNeonatal hypoglycemia030217 neurology & neurosurgeryItalian Journal of Pediatrics
researchProduct

Shank3 Mice Carrying the Human Q321R Mutation Display Enhanced Self-Grooming, Abnormal Electroencephalogram Patterns, and Suppressed Neuronal Excitab…

2019

Shank3, a postsynaptic scaffolding protein involved in regulating excitatory synapse assembly and function, has been implicated in several brain disorders, including autism spectrum disorders (ASD), Phelan-McDermid syndrome, schizophrenia, intellectual disability, and mania. Here we generated and characterized a Shank3 knock-in mouse line carrying the Q321R mutation (Shank3Q321R mice) identified in a human individual with ASD that affects the ankyrin repeat region (ARR) domain of the Shank3 protein. Homozygous Shank3Q321R/Q321R mice show a selective decrease in the level of Shank3a, an ARR-containing protein variant, but not other variants. CA1 pyramidal neurons in the Shank3Q321R/Q321R hip…

0301 basic medicineHippocampusautism spectrum disorderBiologyNeurotransmissionElectroencephalographyInhibitory postsynaptic potentiallcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceExcitatory synapse assembly0302 clinical medicinePostsynaptic potentialexcitabilitymedicineself-groomingEEGMolecular Biologylcsh:Neurosciences. Biological psychiatry. Neuropsychiatrypatient mutationsOriginal Researchmedicine.diagnostic_testanxiety-like behaviorseizure susceptibilitymedicine.disease030104 developmental biologyShank3SchizophreniaExcitatory postsynaptic potentialNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Molecular Neuroscience
researchProduct

Deciphering Alzheimer’s Disease Pathogenic Pathway: Role of Chronic Brain Hypoperfusion on p-Tau and mTOR

2021

This review examines new biomolecular findings that lend support to the hemodynamic role played by chronic brain hypoperfusion (CBH) in driving a pathway to Alzheimer’s disease (AD). CBH is a common clinical feature of AD and the current topic of intense investigation in AD models. CBH is also the basis for the vascular hypothesis of AD which we originally proposed in 1993. New biomolecular findings reveal the interplay of CBH in increasing tau phosphorylation (p-Tau) in the hippocampus and cortex of AD mice, damaging fast axonal transport, increasing signaling of mammalian target of rapamycin (mTOR), impairing learning-memory function, and promoting the formation of neurofibrillary tangles…

0301 basic medicineHippocampustau ProteinsDisease03 medical and health sciences0302 clinical medicineAlzheimer DiseasemedicineAnimalsHumansCognitive declinePI3K/AKT/mTOR pathwayCerebral hypoperfusionbusiness.industryTOR Serine-Threonine KinasesGeneral NeuroscienceNeurodegenerationBrainGeneral Medicinemedicine.diseaseCortex (botany)Psychiatry and Mental healthClinical Psychology030104 developmental biologyCerebrovascular CirculationAxoplasmic transportGeriatrics and GerontologybusinessNeuroscience030217 neurology & neurosurgeryJournal of Alzheimer's Disease
researchProduct

Childhood cancer predisposition syndromes-A concise review and recommendations by the Cancer Predisposition Working Group of the Society for Pediatri…

2017

Heritable predisposition is an important cause of cancer in children and adolescents. Although a large number of cancer predisposition genes and their associated syndromes and malignancies have already been described, it appears likely that there are more pediatric cancer patients in whom heritable cancer predisposition syndromes have yet to be recognized. In a consensus meeting in the beginning of 2016, we convened experts in Human Genetics and Pediatric Hematology/Oncology to review the available data, to categorize the large amount of information, and to develop recommendations regarding when a cancer predisposition syndrome should be suspected in a young oncology patient. This review su…

0301 basic medicineHistoryMedizinGene Expression0302 clinical medicineNeoplasm Proteins/geneticsNeoplasmsChildGenetics (clinical)Societies Medicalddc:618HematologyJuvenile myelomonocytic leukemiaCancer predispositionSyndromeFocus Groups21st Century3. Good healthNeoplasm Proteins030220 oncology & carcinogenesisHematologic NeoplasmsGenetic Testing/methodsmedicine.medical_specialtyAdolescentGenetics MedicalGenetic CounselingHistory 21st CenturyMedical/history/instrumentation/methodsFamilial adenomatous polyposis03 medical and health sciencesInternal medicineGeneticsmedicineHumansFocus Groups/methodsGenetic Predisposition to DiseaseGenetic TestingIntensive care medicineGenetic Counseling/ethicsbusiness.industryHematologic Neoplasms/diagnosis/genetics/pathologyCancermedicine.diseasePediatric cancerHuman genetics030104 developmental biologyLi–Fraumeni syndromeNeoplasms/diagnosis/genetics/pathologyMutationMedical/historySocietiesbusinessAmerican journal of medical genetics. Part A
researchProduct

Efficient Delivery of Human Cytomegalovirus T Cell Antigens by Attenuated Sendai Virus Vectors.

2018

ABSTRACT Human cytomegalovirus (HCMV) represents a major cause of clinical complications during pregnancy as well as immunosuppression, and the licensing of a protective HCMV vaccine remains an unmet global need. Here, we designed and validated novel Sendai virus (SeV) vectors delivering the T cell immunogens IE-1 and pp65. To enhance vector safety, we used a replication-deficient strain (rdSeV) that infects target cells in a nonproductive manner while retaining viral gene expression. In this study, we explored the impact that transduction with rdSeV has on human dendritic cells (DCs) by comparing it to the parental, replication-competent Sendai virus strain (rcSeV) as well as the poxvirus …

0301 basic medicineHuman cytomegalovirusModified vaccinia AnkaraT cellmedicine.medical_treatmentvirusesImmunologyGenetic VectorsAlpha interferonCytomegalovirusMice TransgenicMicrobiologySendai virusViral Matrix Proteins03 medical and health sciencesCytomegalovirus VaccinesMiceTransduction GeneticVirologyCricetinaeChlorocebus aethiopsVaccines and Antiviral AgentsmedicineCytotoxic T cellAnimalsHumansAntigens ViralVero Cellsbiologyvirus diseasesImmunotherapymedicine.diseasebiology.organism_classificationPhosphoproteinsVirologySendai virus030104 developmental biologymedicine.anatomical_structureViral replicationInsect ScienceJournal of virology
researchProduct

Regulatory Interaction between the Cellular Restriction Factor IFI16 and Viral pp65 (pUL83) Modulates Viral Gene Expression and IFI16 Protein Stabili…

2016

ABSTRACT A key player in the intrinsic resistance against human cytomegalovirus (HCMV) is the interferon-γ-inducible protein 16 (IFI16), which behaves as a viral DNA sensor in the first hours postinfection and as a repressor of viral gene transcription in the later stages. Previous studies on HCMV replication demonstrated that IFI16 binds to the viral protein kinase pUL97, undergoes phosphorylation, and relocalizes to the cytoplasm of infected cells. In this study, we demonstrate that the tegument protein pp65 (pUL83) recruits IFI16 to the promoter of the UL54 gene and downregulates viral replication, as shown by use of the HCMV mutant v65Stop, which lacks pp65 expression. Interestingly, at…

0301 basic medicineHuman cytomegalovirusViral proteinviruses030106 microbiologyImmunologyCytomegalovirusDNA-Directed DNA PolymeraseBiologymedicine.disease_causeVirus ReplicationMicrobiologyViral Matrix Proteins03 medical and health sciencesViral ProteinsVirologymedicineHumansNuclear proteinPromoter Regions GeneticGeneCells CulturedViral matrix proteinIFI16Protein Stabilityvirus diseasesNuclear ProteinsViral tegumentmedicine.diseasePhosphoproteinsMolecular biologyVirus-Cell Interactions030104 developmental biologyViral replicationInsect ScienceDNA ViralHost-Pathogen InteractionsProtein BindingJournal of virology
researchProduct

Dynamic regulatory interaction between cytomegalovirus major tegument protein pp65 and protein kinase pUL97 in intracellular compartments, dense bodi…

2017

Human cytomegalovirus (HCMV) is a ubiquitous pathogen of considerable clinical importance. Understanding the processes that are important for viral replication is essential for the development of therapeutic strategies against HCMV infection. The HCMV-encoded protein kinase pUL97 is an important multifunctional regulator of viral replication. Several viral and cellular proteins are phosphorylated by pUL97. The phosphoprotein pp65 is one important substrate of pUL97. It is the most abundant tegument protein of HCMV virions, mediating the upload of other virion constituents and contributing to particle integrity. Further to that, it interferes with host innate immune defences, thereby enablin…

0301 basic medicineHuman cytomegalovirusvirusesDNA Mutational AnalysisMutantCytomegalovirusBiologyVirus ReplicationViral Matrix ProteinsViral Proteins03 medical and health sciencesViral entryVirologyProtein Interaction MappingViral structural proteinmedicineHumansProtein kinase Avirus diseasesViral tegumentbiochemical phenomena metabolism and nutritionPhosphoproteinsmedicine.diseaseVirologyCell biology030104 developmental biologyViral replicationPhosphoproteinJournal of General Virology
researchProduct

The Role of the Multifunctional BAG3 Protein in Cellular Protein Quality Control and in Disease

2017

In neurons, but also in all other cells the complex proteostasis network is monitored and tightly regulated by the cellular protein quality control (PQC) system. Beyond folding of newly synthesized polypeptides and their refolding upon misfolding the PQC also manages the disposal of aberrant proteins either by the ubiquitin-proteasome machinery or by the autophagic-lysosomal system. Aggregated proteins are primarily degraded by a process termed selective macroautophagy (or aggrephagy). One such recently discovered selective macroautophagy pathway is mediated by the multifunctional HSP70 co-chaperone BAG3 (BCL-2-associated athanogene 3). Under acute stress and during cellular aging, BAG3 in …

0301 basic medicineHuntingtinSOD1AggrephagyReviewBAG3lcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceUbiquitinselective macroautophagymedicineprotein quality controllcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologyproteostasisbiologyBAG3NeurodegenerationAutophagymedicine.diseaseCell biology030104 developmental biologyProteostasisneurodegenerative disordersbiology.proteinNeuroscienceFrontiers in Molecular Neuroscience
researchProduct