Search results for "TRANSFERASE"

showing 10 items of 1030 documents

Autism and carnitine: A possible link

2019

Patients with autism spectrum disorders (ASD) present deficits in social interactions and communication, they also show limited and stereotypical patterns of behaviors and interests. The pathophysiological bases of ASD have not been defined yet. Many factors seem to be involved in the onset of this disorder. These include genetic and environmental factors, but autism is not linked to a single origin, only. Autism onset can be connected with various factors such as metabolic disorders: including carnitine deficiency. Carnitine is a derivative of two amino acid lysine and methionine. Carnitine is a cofactor for a large family of enzymes: the carnitine acyltransferases. Through their action th…

0301 basic medicineAutismMetabolic homeostasisBioinformatics03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCarnitinemental disordersmedicineDietary supplementationCarnitineMethioninebusiness.industryCarnitine AcyltransferasesMinireviewsmedicine.diseaseMetabolism disorderMetabolism030104 developmental biologychemistry030220 oncology & carcinogenesisPathophysiological basesNeurodevelopmentalAutismbusinessmedicine.drugWorld Journal of Biological Chemistry
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Cardiolipin synthesis in brown and beige fat mitochondria is essential for systemic energy homeostasis

2018

Summary Activation of energy expenditure in thermogenic fat is a promising strategy to improve metabolic health, yet the dynamic processes that evoke this response are poorly understood. Here we show that synthesis of the mitochondrial phospholipid cardiolipin is indispensable for stimulating and sustaining thermogenic fat function. Cardiolipin biosynthesis is robustly induced in brown and beige adipose upon cold exposure. Mimicking this response through overexpression of cardiolipin synthase (Crls1) enhances energy consumption in mouse and human adipocytes. Crls1 deficiency in thermogenic adipocytes diminishes inducible mitochondrial uncoupling and elicits a nuclear transcriptional respons…

0301 basic medicineBiologiaBioenergeticsChop-10 ; Crls1 ; Beige Adipose ; Brown Adipose ; Cardiolipin ; Insulin Resistance ; Lipid Metabolism ; Mitochondria ; Phospholipids ; ThermogenesisPhysiologyGlucose uptakeAdipose tissueTransferases (Other Substituted Phosphate Groups)MitochondrionEnergy homeostasischemistry.chemical_compoundMice0302 clinical medicineAdipose Tissue Browninsulin resistancelipid metabolismCardiolipinAdipocytesCells CulturedThermogenesisthermogenesisCell biologyMitochondriamitochondriaCHOP-10lipids (amino acids peptides and proteins)BioquímicaCardiolipinsbeige adiposeArticle03 medical and health sciencesInsulin resistanceCRLS1medicineAnimalsHumansMolecular Biologyphospholipidsbrown adiposeMembrane ProteinsCell BiologyAdipose Tissue Beigemedicine.diseaseMice Inbred C57BL030104 developmental biologychemistrycardiolipinEnergy MetabolismThermogenesis030217 neurology & neurosurgery
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Sphingolipids and Inositol Phosphates Regulate the Tau Protein Phosphorylation Status in Humanized Yeast

2020

Hyperphosphorylation of protein tau is a hallmark of Alzheimer’s disease (AD). Changes in energy and lipid metabolism have been correlated with the late onset of this neurological disorder. However, it is uncertain if metabolic dysregulation is a consequence of AD or one of the initiating factors of AD pathophysiology. Also, it is unclear whether variations in lipid metabolism regulate the phosphorylation state of tau. Here, we show that in humanized yeast, tau hyperphosphorylation is stimulated by glucose starvation in coincidence with the downregulation of Pho85, the yeast ortholog of CDK5. Changes in inositol phosphate (IP) signaling, which has a central role in energy metabolism, altere…

0301 basic medicineCDK5Cèl·lulesTau proteinSit42HyperphosphorylationSaccharomyces cerevisiaeSACCHAROMYCES-CEREVISIAECeramide03 medical and health scienceschemistry.chemical_compoundCell and Developmental Biology0302 clinical medicineInositolceramideYpk1Inositol phosphatelcsh:QH301-705.51-IP7Original Researchchemistry.chemical_classificationScience & TechnologybiologyChemistryKinaseNEURODEGENERATIONLipid metabolismCell BiologyProtein phosphatase 2Fpk1MICROTUBULE-BINDINGPho85SERINE PALMITOYLTRANSFERASECell biologyALZHEIMERS-DISEASE030104 developmental biologylcsh:Biology (General)030220 oncology & carcinogenesisGLYCOGEN-SYNTHASE KINASE-3-BETAbiology.proteinKINASE-ACTIVITYPhosphorylationLife Sciences & BiomedicineBETA TOXICITYProteïnesDevelopmental BiologyFrontiers in Cell and Developmental Biology
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The NSL Chromatin-Modifying Complex Subunit KANSL2 Regulates Cancer Stem-like Properties in Glioblastoma That Contribute to Tumorigenesis.

2016

KANSL2 is an integral subunit of the nonspecific lethal (NSL) chromatin-modifying complex that contributes to epigenetic programs in embryonic stem cells. In this study, we report a role for KANSL2 in regulation of stemness in glioblastoma (GBM), which is characterized by heterogeneous tumor stem-like cells associated with therapy resistance and disease relapse. KANSL2 expression is upregulated in cancer cells, mainly at perivascular regions of tumors. RNAi-mediated silencing of KANSL2 in GBM cells impairs their tumorigenic capacity in mouse xenograft models. In clinical specimens, we found that expression levels of KANSL2 correlate with stemness markers in GBM stem-like cell populations. M…

0301 basic medicineCHROMATINMaleCancer ResearchCarcinogenesisCellCell SeparationMice SCIDmedicine.disease_causeMiceCANCER STEM CELLMice Inbred NODHistone AcetyltransferasesOligonucleotide Array Sequence AnalysisBrain NeoplasmsNuclear ProteinsMiddle AgedFlow CytometryImmunohistochemistryChromatinUp-Regulationmedicine.anatomical_structureOncologyGene Knockdown TechniquesNeoplastic Stem CellsHeterograftsFemaleCIENCIAS NATURALES Y EXACTASAdultKANSLOtras Ciencias BiológicasBlotting WesternGLIOBLASTOMABiologyReal-Time Polymerase Chain ReactionArticleCiencias Biológicas03 medical and health sciencesCancer stem cellmedicineBiomarkers TumorGene silencingAnimalsHumansEpigeneticsAgedEmbryonic stem cell030104 developmental biologyCancer cellImmunologyCancer researchCarcinogenesisGlioblastomaCancer research
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Efficacy and epigenetic interactions of novel DNA hypomethylating agent guadecitabine (SGI-110) in preclinical models of hepatocellular carcinoma.

2016

ABSTRACT Hepatocellular carcinoma (HCC) is a deadly malignancy characterized at the epigenetic level by global DNA hypomethylation and focal hypermethylation on the promoter of tumor suppressor genes. In most cases it develops on a background of liver steatohepatitis, fibrosis, and cirrhosis. Guadecitabine (SGI-110) is a second-generation hypomethylating agent, which inhibits DNA methyltransferases. Guadecitabine is formulated as a dinucleotide of decitabine and deoxyguanosine that is resistant to cytidine deaminase (CDA) degradation and results in prolonged in vivo exposure to decitabine following small volume subcutaneous administration of guadecitabine. Here we found that guadecitabine i…

0301 basic medicineCancer ResearchMethyltransferasesteatohepatitisDecitabineBiologyDecitabineDNA methylation Decitabine guadecitabine hepatocellular carcinoma (HCC) histone macroH2A1 steatohepatitishepatocellular carcinoma (HCC)03 medical and health scienceschemistry.chemical_compoundCDKN2AmedicineEpigeneticsMolecular BiologyneoplasmsDNA methylationGuadecitabineguadecitabinehistone macroH2A1steatohepatitidigestive system diseases3. Good healthDemethylating agent030104 developmental biologychemistryHypomethylating agentDNA methylationCancer researchResearch Papermedicine.drug
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Nicotinamide Phosphoribosyltransferase Acts as a Metabolic Gate for Mobilization of Myeloid-Derived Suppressor Cells

2019

Abstract Cancer induces alteration of hematopoiesis to fuel disease progression. We report that in tumor-bearing mice the macrophage colony-stimulating factor elevates the myeloid cell levels of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD salvage pathway, which acts as negative regulator of the CXCR4 retention axis of hematopoietic cells in the bone marrow. NAMPT inhibits CXCR4 through a NAD/Sirtuin 1–mediated inactivation of HIF1α-driven CXCR4 gene transcription, leading to mobilization of immature myeloid-derived suppressor cells (MDSC) and enhancing their production of suppressive nitric oxide. Pharmacologic inhibition or myeloid-specific ablation …

0301 basic medicineCancer ResearchMyeloidmedicine.medical_treatmentNudeNicotinamide phosphoribosyltransferaseApoptosisColorectal NeoplasmInbred C57BLMicechemistry.chemical_compound0302 clinical medicineTumor Cells CulturedHematopoiesiNicotinamide PhosphoribosyltransferaseInbred BALB CMice Inbred BALB CCulturedbiologySarcomaTumor CellsHaematopoiesismedicine.anatomical_structureOncology030220 oncology & carcinogenesisSirtuinFemaleSarcoma ExperimentalColorectal NeoplasmsAnimals; Apoptosis; Cell Proliferation; Colorectal Neoplasms; Female; Hematopoiesis; Humans; Mammary Neoplasms Experimental; Mice; Mice Inbred BALB C; Mice Inbred C57BL; Mice Nude; Myeloid-Derived Suppressor Cells; NAD; Nicotinamide Phosphoribosyltransferase; Sarcoma Experimental; Signal Transduction; Tumor Cells Cultured; Xenograft Model Antitumor AssaysHumanSignal TransductionMice NudeExperimental03 medical and health sciencesmedicineMyeloid-Derived Suppressor CellAnimalsHumansCell ProliferationAnimalMyeloid-Derived Suppressor CellsMammary NeoplasmsApoptosiMammary Neoplasms ExperimentalImmunotherapyNADXenograft Model Antitumor AssaysHematopoiesisMice Inbred C57BL030104 developmental biologychemistrybiology.proteinCancer researchMyeloid-derived Suppressor CellNAD+ kinaseBone marrowCancer Research
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Comparative analysis of the effects of a sphingosine kinase inhibitor to temozolomide and radiation treatment on glioblastoma cell lines.

2017

ABSTRACT Glioblastoma multiforme (GBM) exhibits high resistance to the standard treatment of temozolomide (TMZ) combined with radiotherapy, due to its remarkable cell heterogeneity. Accordingly, there is a need to target alternative molecules enhancing specific GBM autocrine or paracrine mechanisms and amplifying the effect of standard treatment. Sphingosine 1-phosphate (S1P) is such a lipid target molecule with an important role in cell invasion and proliferation. Sphingosine kinase inhibitors (SKI) prevent S1P formation and induce increased production of reactive oxygen species (ROS), which may potentiate radiation cytotoxicity. We analyzed the effect of SKI singular versus combined treat…

0301 basic medicineCancer ResearchRadiation-Sensitizing AgentsCell SurvivalCellSphingosine kinaseApoptosistemozolomideBiologyRadiation Tolerancesphingosine kinase inhibition03 medical and health scienceschemistry.chemical_compoundCell Line TumorX-raysmedicineHumansGPx1oxidative stressCytotoxicityAutocrine signallingAntineoplastic Agents AlkylatingPharmacologychemistry.chemical_classificationReactive oxygen speciesTemozolomideSphingosineBrain NeoplasmsDrug SynergismChemoradiotherapyMolecular biologyDacarbazinePhosphotransferases (Alcohol Group Acceptor)030104 developmental biologymedicine.anatomical_structureOncologychemistryCell cultureradiosensitivityCancer researchMolecular MedicineDrug Screening Assays AntitumorGlioblastomamedicine.drugResearch PaperCancer biologytherapy
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Nut1/Hos1 and Sas2/Rpd3 control the H3 acetylation of two different sets of osmotic stress-induced genes

2019

Epigenetic information is able to interact with the cellular environment and could be especially useful for reprograming gene expression in response to a physiological perturbation. In fact the genes induced or repressed by osmotic stress undergo significant changes in terms of the levels of various histone modifications, especially in the acetylation levels of histone H3. Exposing yeast to high osmolarity results in the activation of stress-activated protein kinase Hog1, which plays a central role in gene expression control. We evaluated the connection between the presence of Hog1 and changes in histone H3 acetylation in stress-regulated genes. We found a parallel increase in the acetylati…

0301 basic medicineCancer ResearchSaccharomyces cerevisiae Proteinschip-on-chipSaccharomyces cerevisiaeEpigenesis GeneticHistones03 medical and health sciencesHistone H30302 clinical medicineOsmotic PressureGene Expression Regulation FungalGene expressionEpigeneticsHistone H3 acetylationMolecular BiologyHistone AcetyltransferasesRegulation of gene expressionMediator ComplexbiologyepigeneticsAcetylationCell biologyChromatinDNA-Binding ProteinsHistone Code030104 developmental biologyHistoneHistone acetylationAcetylation030220 oncology & carcinogenesisbiology.proteinchromatinhog1osmotic stressMitogen-Activated Protein Kinasesgene regulationProtein Processing Post-TranslationalTranscription FactorsResearch Paper
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Epigenetic Regulation of TRAIL Signaling: Implication for Cancer Therapy

2019

International audience; One of the main characteristics of carcinogenesis relies on genetic alterations in DNA and epigenetic changes in histone and non-histone proteins. At the chromatin level, gene expression is tightly controlled by DNA methyl transferases, histone acetyltransferases (HATs), histone deacetylases (HDACs), and acetyl-binding proteins. In particular, the expression level and function of several tumor suppressor genes, or oncogenes such as c-Myc, p53 or TRAIL, have been found to be regulated by acetylation. For example, HATs are a group of enzymes, which are responsible for the acetylation of histone proteins, resulting in chromatin relaxation and transcriptional activation,…

0301 basic medicineCancer Researchtumor necrosis factor (TNF)TRAILReviewmedicine.disease_causelcsh:RC254-282Chromatin remodelingchromatin remodeling03 medical and health sciences0302 clinical medicinemedicinetumor necrosis factor (TNF).[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular Biologycancer[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyEpigeneticsHistone Acetyltransferasesbiologyhistone deacetylase (HDAC)lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthChromatin030104 developmental biologyHistonehistone deacetylase inhibitors (HDACIs)OncologyAcetylation030220 oncology & carcinogenesissilencingCancer researchbiology.proteinHistone deacetylasemethylationCarcinogenesisCancers
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Bioenergetic Failure in Rat Oligodendrocyte Progenitor Cells Treated with Cerebrospinal Fluid Derived from Multiple Sclerosis Patients

2017

In relapsing-remitting multiple sclerosis (RRMS) subtype, the patient's brain itself is capable of repairing the damage, remyelinating the axon and recovering the neurological function. Cerebrospinal fluid (CSF) is in close proximity with brain parenchyma and contains a host of proteins and other molecules, which influence the cellular physiology, that may balance damage and repair of neurons and glial cells. The purpose of this study was to determine the pathophysiological mechanisms underpinning myelin repair in distinct clinical forms of MS and neuromyelitis optica (NMO) patients by studying the effect of diseased CSF on glucose metabolism and ATP synthesis. A cellular model with primary…

0301 basic medicineCell physiologyglucose metabolismneuromyelitis opticaTransferrin receptorBiologymultiple sclerosiscerebrospinal fluidlcsh:RC321-571myelin repair03 medical and health sciencesCellular and Molecular NeuroscienceMyelin0302 clinical medicineCerebrospinal fluidGene expressionmedicineAxonlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryOriginal ResearchMultiple sclerosisoligodendrocyte progenitor cellsmedicine.disease3. Good health030104 developmental biologymedicine.anatomical_structureHypoxanthine-guanine phosphoribosyltransferaseImmunologyCancer researchgene expression030217 neurology & neurosurgeryNeuroscienceFrontiers in Cellular Neuroscience
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