Search results for "BP"

showing 10 items of 672 documents

Mechanisms of action of metformin in type 2 diabetes: Effects on mitochondria and leukocyte-endothelium interactions.

2020

Type 2 diabetes (T2D) is a very prevalent, multisystemic, chronic metabolic disorder closely related to atherosclerosis and cardiovascular diseases. It is characterised by mitochondrial dysfunction and the presence of oxidative stress. Metformin is one of the safest and most effective anti-hyperglycaemic agents currently employed as first-line oral therapy for T2D. It has demonstrated additional beneficial effects, unrelated to its hypoglycaemic action, on weight loss and several diseases, such as cancer, cardiovascular disorders and metabolic diseases, including thyroid diseases. Despite the vast clinical experience gained over several decades of use, the mechanism of action of metformin i…

0301 basic medicineAdvanced glycation end product (AGE)AMP-activated protein kinase (AMPK)endocrine system diseasesglycerol 3-phosphate dehydrogenase (GPD)Clinical Biochemistrytype 1 diabetes (T1D)Type 2 diabetesmTORC1Review Articleelectron transport chain (ETC)PharmacologyMitochondrionmedicine.disease_causeBiochemistry0302 clinical medicineLeukocytesCREB-binding protein (CBP)inner mitochondrial membrane (IMM)lcsh:QH301-705.5lcsh:R5-920cAMP response element-binding (CREB)glucagon-like peptide 1 (GLP-1)type 2 diabetes (T2D)Type 2 diabetesMetforminMetforminMitochondriamedicine.anatomical_structurereactive nitrogen species (RNS)reactive oxygen species (ROS)sirtuin (SIRT)medicine.symptomlcsh:Medicine (General)cardiovascular diseases (CVD)medicine.drugEndotheliumnitric oxide synthase (NOS)polycystic ovary syndrome (PCOS)Pathophysiologyinsulin resistance (IR)superoxide dismutase (SOD)03 medical and health sciencesglycated haemoglobin (HbA1c)medicineorganic cation transporter (OCT)HumansEndotheliumintercellular adhesion molecule-1 (ICAM-1)business.industryoxidative phosphorylation (OXPHOS)Organic Chemistryperoxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)AMPKmedicine.diseaseAtherosclerosisvascular cell adhesion molecule-1 (VCAM-1)Treatment030104 developmental biologylcsh:Biology (General)Mechanism of actionDiabetes Mellitus Type 2Oxidative stressbusinessinsulin receptor substrate (IRS)030217 neurology & neurosurgeryOxidative stress
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Expression of Alpha-Enolase (ENO1), Myc Promoter-Binding Protein-1 (MBP-1) and Matrix Metalloproteinases (MMP-2 and MMP-9) Reflect the Nature and Agg…

2019

Breast cancer is a complex and heterogeneous disease: Several molecular alterations cause cell proliferation and the acquisition of an invasive phenotype. Extracellular matrix (ECM) is considered essential for sustaining tumor growth and matrix metalloproteinases (MMPs) have been identified as drivers of many aspects of the tumor phenotype. Mounting evidence indicates that both &alpha

0301 basic medicineAlpha-enolaseENO1Kaplan-Meier EstimateMatrix metalloproteinasemedicine.disease_causeMetastasisExtracellular matrixlcsh:Chemistry0302 clinical medicineSettore BIO/06 - Anatomia Comparata E Citologialcsh:QH301-705.5SpectroscopybiologyMMP-2General MedicineComputer Science ApplicationsDNA-Binding ProteinsGene Expression Regulation NeoplasticMatrix Metalloproteinase 9030220 oncology & carcinogenesisDisease ProgressionMatrix Metalloproteinase 2FemaleMMP-9Breast NeoplasmsCatalysisArticleInorganic Chemistry03 medical and health sciencesBreast cancerbreast cancerCell Line TumormedicineBiomarkers TumorHumansPhysical and Theoretical ChemistryMBP-1Molecular BiologyCell ProliferationTumor Suppressor ProteinsOrganic ChemistryCancermedicine.diseaseSettore BIO/18 - Genetica030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Phosphopyruvate HydrataseCancer cellbiology.proteinCancer researchCarcinogenesisInternational Journal of Molecular Sciences
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Spectrum of mutations in Italian patients with familial hypercholesterolemia: New results from the LIPIGEN study

2017

Abstract Background Familial hypercholesterolemia (FH) is an autosomal dominant disease characterized by elevated plasma levels of LDL-cholesterol that confers an increased risk of premature atherosclerotic cardiovascular disease. Early identification and treatment of FH patients can improve prognosis and reduce the burden of cardiovascular mortality. Aim of this study was to perform the mutational analysis of FH patients identified through a collaboration of 20 Lipid Clinics in Italy (LIPIGEN Study). Methods We recruited 1592 individuals with a clinical diagnosis of definite or probable FH according to the Dutch Lipid Clinic Network criteria. We performed a parallel sequencing of the major…

0301 basic medicineApolipoprotein ECandidate geneSettore MED/09 - Medicina InternaDatabases FactualApolipoprotein BDNA Mutational AnalysisFamilial hypercholesterolemia030204 cardiovascular system & hematologyCompound heterozygosityPCSK90302 clinical medicineRisk FactorsReceptorsGeneticsHomozygoteAutosomal dominant traitPathogenic variantsGeneral MedicinePrognosisAPOB; Familial hypercholesterolemia; LDLR; PCSK9; Pathogenic variantsCholesterolPhenotypeItalyAutosomal Recessive HypercholesterolemiaApolipoprotein B-100lipids (amino acids peptides and proteins)Proprotein Convertase 9APOBCardiology and Cardiovascular MedicinePreliminary DataGenetic MarkersFamilial hypercholesterolemiaLDLRPCSK9APOBPathogenic variantsHeterozygoteFamilial hypercholesterolemiaBiologyPathogenic variantLDLHyperlipoproteinemia Type II03 medical and health sciencesDatabasesmedicineInternal MedicineHumansAPOB; Familial hypercholesterolemia; LDLR; Pathogenic variants; PCSK9; Internal Medicine; Cardiology and Cardiovascular MedicineGenetic Predisposition to DiseaseFactualPCSK9Settore MED/13 - ENDOCRINOLOGIAAPOB; Familial hypercholesterolemia; LDLR; Pathogenic variants; PCSK9; Cardiology and Cardiovascular Medicine; Internal Medicinemedicine.diseaseAtherosclerosis030104 developmental biologyLDLRReceptors LDLMutationbiology.proteinAPOB; Familial hypercholesterolemia; LDLR; Pathogenic variants; PCSK9; Apolipoprotein B-100; Atherosclerosis; Cholesterol; DNA Mutational Analysis; Databases Factual; Genetic Markers; Genetic Predisposition to Disease; Heterozygote; Homozygote; Humans; Hyperlipoproteinemia Type II; Italy; Phenotype; Preliminary Data; Prognosis; Proprotein Convertase 9; Receptors LDL; Risk Factors; Mutation; Internal Medicine; Cardiology and Cardiovascular Medicine
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ALS-Related Mutant FUS Protein Is Mislocalized to Cytoplasm and Is Recruited into Stress Granules of Fibroblasts from Asymptomatic <b><i>…

2017

<b><i>Background:</i></b> Amyotrophic lateral sclerosis (ALS) shows a strong genetic basis, with <i>SOD1</i>, <i>FUS</i>, <i>TARDBP</i>, and <i>C9ORF72 </i>being the genes most frequently involved<i>. </i>This has allowed identification of asymptomatic mutation carriers, which may be of help in understanding the molecular changes preceding disease onset. <b><i>Objectives:</i></b> We studied the cellular expression of FUS protein and the effect of heat-shock- and dithiothreitol-induced stress in fibroblasts from <i>FUS</i> P525L mutation carriers, healthy controls, and pati…

0301 basic medicineBiologymedicine.diseaseSubcellular localizationTARDBPMolecular biology03 medical and health sciencesCell nucleus030104 developmental biology0302 clinical medicineStress granulemedicine.anatomical_structureNeurologyC9orf72CytoplasmmedicineNeurology (clinical)Amyotrophic lateral sclerosis030217 neurology & neurosurgeryRNA-Binding Protein FUSNeurodegenerative Diseases
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Temporal quantitative phosphoproteomics of ADP stimulation reveals novel central nodes in platelet activation and inhibition

2017

Adenosine diphosphate (ADP) enhances platelet activation by virtually any other stimulant to complete aggregation. It binds specifically to the G-protein-coupled membrane receptors P2Y1 and P2Y12, stimulating intracellular signaling cascades, leading to integrin aIIbb3 activation, a process antagonized by endothelial prostacyclin. P2Y12 inhibitors are among the most successful antiplatelet drugs, however, show remarkable variability in efficacy. We reasoned whether a more detailed molecular understanding of ADP-induced protein phosphorylation could identify (1) critical hubs in platelet signaling toward aggregation and (2) novel molecular targets for antiplatelet treatment strategies. We ap…

0301 basic medicineBlood PlateletsPHOSPHATASEImmunologyBlotting WesternUBIQUITINATIONBINDING PROTEIN STXBP5Biochemistry03 medical and health scienceschemistry.chemical_compoundGTP-binding protein regulatorsP2Y12HumansProtein phosphorylationPlatelet activationIloprostPHOSPHORYLATIONCOMBINATIONChemistryPhosphoproteomicsPATHWAYSCell BiologyHematologyPlatelet ActivationSIGNALING REVEALSCell biologyAdenosine DiphosphateAdenosine diphosphate030104 developmental biologyCLOPIDOGRELPhosphorylationPROTEOMICSSECRETIONSignal transductionPlatelet Aggregation InhibitorsSignal TransductionBlood
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Multiple Myeloma-Derived Extracellular Vesicles Induce Osteoclastogenesis through the Activation of the XBP1/IRE1α Axis

2020

Bone disease severely affects the quality of life of over 70% of multiple myeloma (MM) patients, which daily experience pain, pathological fractures, mobility issues and an increased mortality. Recent data have highlighted the crucial role of the endoplasmic reticulum-associated unfolded protein response (UPR) in malignant transformation and tumor progression

0301 basic medicineCancer ResearchCell signalingXBP1Cellular differentiationlcsh:RC254-282Article03 medical and health sciences0302 clinical medicineSettore BIO/13 - Biologia ApplicataTranscription factorChemistryEndoplasmic reticulumextracellular-vesiclesExtracellular vesiclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensCell biologymultiple myelomaUPR-related molecules030104 developmental biologyosteoclastsOncology030220 oncology & carcinogenesisUnfolded protein responsePhosphorylationbone diseaseCancers
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Extracellular Vesicles Shed by Melanoma Cells Contain a Modified Form of H1.0 Linker Histone and H1.0 mRNA-binding Proteins

2016

Extracellular vesicles (EVs) are shed in the extracellular environment by both prokaryotes and eukaryotes. Although produced from both normal and cancer cells, malignant cells release a much higher amount of EVs, which also contain tumor-specific proteins and RNAs. We previously found that G26/24 oligodendroglioma cells shed EVs that contain the pro-apoptotic factors FasL and TRAIL1-2. Interestingly, G26/24 release, via EVs, extracellular matrix remodelling proteases3, and H1° histone protein4, and mRNA. To shed further light on the role of EVs in discarding proteins and mRNAs otherwise able to counteract proliferative signals, we studied a melanoma cell line (A375). We found that also thes…

0301 basic medicineCancer ResearchCellular differentiationBlotting WesternFluorescent Antibody TechniqueMYEF2ApoptosisRNA-binding proteinexosomesmembrane vesiclesReal-Time Polymerase Chain ReactionChromatography AffinityHistones03 medical and health sciencesH1.0 linker histone; RNA-binding proteins (RBPs); extracellular vesicles (EVs) membrane vesicles (MVs); exosomes; MYEF2Settore BIO/10 - BiochimicaTumor Cells CulturedHumansexosomeSecretionRNA MessengerSettore BIO/06 - Anatomia Comparata E Citologiamelanoma cell line (A375) myelin expression factor-2 (MYEF2)MelanomaTranscription factorCell ProliferationH1.0 linker histonebiologyReverse Transcriptase Polymerase Chain ReactionEXTRACELLULAR VESICLESRNA-Binding ProteinsRNACell DifferentiationArticlesCell biologyBlotCell Transformation Neoplastic030104 developmental biologyHistoneOncologySpectrometry Mass Matrix-Assisted Laser Desorption-IonizationCancer cellbiology.proteinRNA-binding proteins (RBPs)extracellular vesicles (EVs) membrane vesicles (MVs)
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RBFOX1, encoding a splicing regulator, is a candidate gene for aggressive behavior

2020

The RBFOX1 gene (or A2BP1) encodes a splicing factor important for neuronal development that has been related to autism spectrum disorder and other neurodevelopmental phenotypes. Evidence from complementary sources suggests that this gene contributes to aggressive behavior. Suggestive associations with RBFOX1 have been identified in genome-wide association studies (GWAS) of anger, conduct disorder, and aggressive behavior. Nominal association signals in RBFOX1 were also found in an epigenome-wide association study (EWAS) of aggressive behavior. Also, variants in this gene affect temporal lobe volume, a brain area that is altered in several aggression-related phenotypes. In animals, this gen…

0301 basic medicineCandidate geneNeuroimagingRBFOX1Genome-wide association studyBiologyEpigenesis GeneticA2BP103 medical and health sciencesAll institutes and research themes of the Radboud University Medical Center0302 clinical medicineGeneticsmedicineAnimalsHumansPharmacology (medical)TranscriptomicsRBFOX1Genetic Association StudiesBiological PsychiatryRegulator genePharmacologyGeneticsNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]AggressionGenetic Variationmedicine.diseasePhenotypeAnimal modelsAggressionPsychiatry and Mental health030104 developmental biologyNeurologyAutism spectrum disorderEpigeneticsRBFOX1 GeneRNA Splicing FactorsNeurology (clinical)medicine.symptom030217 neurology & neurosurgeryGenome-Wide Association Study
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Opposing Effects of CREBBP Mutations Govern the Phenotype of Rubinstein-Taybi Syndrome and Adult SHH Medulloblastoma

2018

Recurrent mutations in chromatin modifiers are specifically prevalent in adolescent or adult patients with Sonic hedgehog-associated medulloblastoma (SHH MB). Here, we report that mutations in the acetyltransferase CREBBP have opposing effects during the development of the cerebellum, the primary site of origin of SHH MB. Our data reveal that loss of Crebbp in cerebellar granule neuron progenitors (GNPs) during embryonic development of mice compromises GNP development, in part by downregulation of brain-derived neurotrophic factor (Bdnf). Interestingly, concomitant cerebellar hypoplasia was also observed in patients with Rubinstein-Taybi syndrome, a congenital disorder caused by germline mu…

0301 basic medicineCerebellumCrebbp protein mousemetabolism [Cerebellar Neoplasms]acetyltransferase; cerebellum; CREBBP; development; Rubinstein-Taybi syndrome; SHH medulloblastomagenetics [Hedgehog Proteins]MiceNeurotrophic factorsmetabolism [CREB-Binding Protein]Mice KnockoutNeuronsRubinstein-Taybi Syndromepathology [Rubinstein-Taybi Syndrome]CREBBPCREB-Binding ProteinPhenotypegenetics [CREB-Binding Protein]3. Good healthpathology [Cerebellar Neoplasms]acetyltransferasePhenotypemedicine.anatomical_structuregenetics [Rubinstein-Taybi Syndrome]Femalemetabolism [Hedgehog Proteins]Signal TransductionSHH medulloblastomaAdultcerebellumBiologyGeneral Biochemistry Genetics and Molecular BiologyCREBBP; Rubinstein-Taybi syndrome; SHH medulloblastoma; acetyltransferase; cerebellum; development.03 medical and health sciencesGermline mutationAcetyltransferasesmetabolism [Medulloblastoma]medicineAnimalsHumansgenetics [Cerebellar Neoplasms]Hedgehog Proteinsddc:610Cerebellar NeoplasmsdevelopmentMolecular BiologyMedulloblastomaRubinstein–Taybi syndromegenetics [Medulloblastoma]metabolism [Rubinstein-Taybi Syndrome]pathology [Medulloblastoma]Cell Biologymedicine.disease030104 developmental biologyMutationphysiology [CREB-Binding Protein]Cancer researchSHH protein humanCerebellar hypoplasia (non-human)metabolism [Acetyltransferases]CREBBP protein humanMedulloblastomaDevelopmental BiologyCongenital disorderDevelopmental Cell
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Transmembrane signaling and cytoplasmic signal conversion by dimeric transmembrane helix 2 and a linker domain of the DcuS sensor kinase

2020

Transmembrane (TM) signaling is a key process of membrane-bound sensor kinases. The C4-dicarboxylate (fumarate) responsive sensor kinase DcuS of Escherichia coli is anchored by TM helices TM1 and TM2 in the membrane. Signal transmission across the membrane relies on the piston-type movement of the periplasmic part of TM2. To define the role of TM2 in TM signaling, we use oxidative Cys cross-linking to demonstrate that TM2 extends over the full distance of the membrane and forms a stable TM homodimer in both the inactive and fumarate-activated state of DcuS. An S186xxxGxxxG194 motif is required for the stability and function of the TM2 homodimer. The TM2 helix further extends on the periplas…

0301 basic medicineCytoplasmGpA glycophorin AC4DC C4-dicarboxylateCL cross-linkingpiston-typeMBP maltose-binding proteinBiochemistry03 medical and health sciencesProtein DomainsDcuSEscherichia coli(Gly)xxx(Gly) motifMolecular Biologysensor kinasefumarate030102 biochemistry & molecular biologyChemistryEscherichia coli ProteinsCell MembraneHistidine kinaseGene Expression Regulation BacterialCell BiologyPeriplasmic spacelinkerTransmembrane proteinoxidative Cys cross-linkingTransmembrane domain030104 developmental biologyMembrane proteinProtein kinase domainHelixBiophysicsProtein MultimerizationProtein Kinasestransmembrane signalingLinkerResearch ArticleTM transmembraneJournal of Biological Chemistry
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