Search results for "GLYCOGEN-SYNTHASE KINASE"

showing 3 items of 3 documents

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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Transcription factor NRF2 as a therapeutic target for chronic diseases: a systems medicine approach

2018

Systems medicine has a mechanism-based rather than a symptom- or organ-based approach to disease and identifies therapeutic targets in a nonhypothesis-driven manner. In this work, we apply this to transcription factor nuclear factor (erythroid-derived 2)-like 2 (NRF2) by cross-validating its position in a protein-protein interaction network (the NRF2 interactome) functionally linked to cytoprotection in low-grade stress, chronic inflammation, metabolic alterations, and reactive oxygen species formation. Multiscale network analysis of these molecular profiles suggests alterations of NRF2 expression and activity as a common mechanism in a subnetwork of diseases (the NRF2 diseasome). This netw…

0301 basic medicineRMSystems AnalysisNF-E2-Related Factor 2MedicinaNF-KAPPA-BAnti-Inflammatory AgentsTYPE-2 DIABETES-MELLITUSGENE PROMOTER POLYMORPHISMDiseaseComputational biologyInteractomeenvironment and public healthGLYCOGEN-SYNTHASE KINASETUMOR-SUPPRESSOR PTENNRF203 medical and health sciencesDrug DiscoveryAnimalsHumansTherapeutic targetsMedicineMolecular Targeted TherapyBardoxolone methylPLACEBO-CONTROLLED PHASE-3PharmacologyMechanism (biology)Drug discoverybusiness.industryDrug RepositioningRChronic inflammationrespiratory systemHEME OXYGENASE 1PROTEIN-PROTEIN INTERACTION3. Good healthSystems medicineDrug repositioning030104 developmental biologyDrug developmentEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITISChronic DiseaseSystems medicineMolecular MedicineFUMARIC-ACID ESTERSbusiness
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The Role of Erythropoietin in Neuroprotection: Therapeutic Perspectives

2007

Nervous system diseases are very complex conditions comprising a large variety of local and systemic responses. Several therapeutic agents interfering with all or in part the biochemical steps that ultimately cause neuronal death have been demonstrated to be neuroprotective in preclinical models. However, all the agents so far investigated have inexorably failed in the phase III trials carried out. A large body of evidence suggests that the hormone erythropoietin (EPO), besides its well-known hematopoietic action, exerts beneficial effects in the central nervous system. EPO's effect has been assessed in several experimental models of brain and spinal cord injury thus becoming a serious cand…

Nervous systemEXPERIMENTAL SUBARACHNOID HEMORRHAGECentral nervous systemSIGNAL-TRANSDUCTIONPharmacologyModels BiologicalNeuroprotectionErythropoietin in neuroprotectionNEURONAL APOPTOSISCEREBROSPINAL-FLUIDAnimalsHumansMedicineIN-VIVO EVIDENCEErythropoietinSpinal cord injuryPharmacologyCEREBRAL-ISCHEMIACOMMON BETA-SUBUNITbusiness.industryRECOMBINANT-HUMAN-ERYTHROPOIETIN; GLYCOGEN-SYNTHASE KINASE-3-BETA; EXPERIMENTAL SUBARACHNOID HEMORRHAGE; COMMON BETA-SUBUNIT; IN-VIVO EVIDENCE; CEREBRAL-ISCHEMIA; SIGNAL-TRANSDUCTION; CEREBROSPINAL-FLUID; NEURONAL APOPTOSIS; CYTOKINE RECEPTORSRECOMBINANT-HUMAN-ERYTHROPOIETINmedicine.diseaseRecombinant ProteinsEnzyme ActivationStrokeClinical trialNeuroprotective AgentsTreatment Outcomemedicine.anatomical_structureErythropoietinGLYCOGEN-SYNTHASE KINASE-3-BETACYTOKINE RECEPTORSBone marrowMitogen-Activated Protein Kinasesbusinessmedicine.drugDrug News & Perspectives
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