Search results for "kinases"

showing 10 items of 929 documents

Cryptotanshinone deregulates unfolded protein response and eukaryotic initiation factor signaling in acute lymphoblastic leukemia cells.

2015

Abstract Background: Unfolded protein responses (UPR) determine cell fate and are recognized as anticancer targets. In a previous research, we reported that cryptotanshinone (CPT) exerted cytotoxic effects toward acute lymphoblastic leukemia cells through mitochondria-mediated apoptosis. Purpose: In the present study, we further investigated the role of UPR in CPT-induced cytotoxicity on acute lymphoblastic leukemia cells by applying tools of pharmacogenomics and bioinformatics. Methods: Gene expression profiling was performed by mRNA microarray hybridization. Potential transcription factor binding motifs were identified in the promoter regions of the deregulated genes by Cistrome software.…

0301 basic medicineendocrine systemXBP1Eukaryotic Initiation Factor-2Pharmaceutical ScienceApoptosisBiology03 medical and health sciencesPhosphatidylinositol 3-KinasesEukaryotic initiation factorCell Line TumorDrug DiscoveryHumansheterocyclic compoundsRNA MessengerEukaryotic Initiation FactorsTranscription factorPharmacologyeIF2ATF4Computational BiologyPromoterPhenanthrenesPrecursor Cell Lymphoblastic Leukemia-LymphomaMolecular Docking Simulation030104 developmental biologyComplementary and alternative medicineCistromePharmacogeneticsEukaryotic Initiation Factor-4AUnfolded protein responseCancer researchUnfolded Protein ResponseMolecular MedicineTranscription Factor CHOPSignal TransductionTranscription FactorsPhytomedicine : international journal of phytotherapy and phytopharmacology
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Tyro3 Contributes to Retinal Ganglion Cell Function, Survival and Dendritic Density in the Mouse Retina

2020

Retinal ganglion cells (RGCs) are the only output neurons of the vertebrate retina, integrating signals from other retinal neurons and transmitting information to the visual centers of the brain. The death of RGCs is a common outcome in many optic neuropathies, such as glaucoma, demyelinating optic neuritis and ischemic optic neuropathy, resulting in visual defects and blindness. There are currently no therapies in clinical use which can prevent RGC death in optic neuropathies; therefore, the identification of new targets for supporting RGC survival is crucial in the development of novel treatments for eye diseases. In this study we identify that the receptor tyrosine kinase, Tyro3, is crit…

0301 basic medicineinner plexiform layergenetic structuresdendritesNerve fiber layerTAM receptorelectroretinogramBiologyRetinal ganglionlcsh:RC321-57103 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineOptic neuritislcsh:Neurosciences. Biological psychiatry. NeuropsychiatryOriginal ResearchRetinaoptical coherence tomographymedicine.diagnostic_testreceptor tyrosine kinasesGeneral NeuroscienceRetinalInner plexiform layermedicine.diseaseeye diseases030104 developmental biologymedicine.anatomical_structurechemistryRetinal ganglion cellsense organsNeuroscience030217 neurology & neurosurgeryNeuroscienceElectroretinographyFrontiers in Neuroscience
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The Unfolded Protein Response Plays a Predominant Homeostatic Role in Response to Mitochondrial Stress in Pancreatic Stellate Cells.

2016

Activated pancreatic stellate cells (PaSC) are key participants in the stroma of pancreatic cancer, secreting extracellular matrix proteins and inflammatory mediators. Tumors are poorly vascularized, creating metabolic stress conditions in cancer and stromal cells that necessitate adaptive homeostatic cellular programs. Activation of autophagy and the endoplasmic reticulum unfolded protein response (UPR) have been described in hepatic stellate cells, but the role of these processes in PaSC responses to metabolic stress is unknown. We reported that the PI3K/mTOR pathway, which AMPK can regulate through multiple inputs, modulates PaSC activation and fibrogenic potential. Here, using primary a…

0301 basic medicinelcsh:MedicineApoptosisMitochondrionAMP-Activated Protein KinasesEndoplasmic ReticulumBiochemistrychemistry.chemical_compoundMiceeIF-2 KinasePhosphatidylinositol 3-Kinases0302 clinical medicineFluorescence MicroscopyCell SignalingTumor Microenvironment2.1 Biological and endogenous factorsSmall interfering RNAsAetiologylcsh:ScienceEnergy-Producing OrganellesCancerMice KnockoutMicroscopyMultidisciplinarySecretory PathwayCell DeathTOR Serine-Threonine KinasesLight MicroscopySignaling CascadesCell biologyMitochondriaNeoplasm ProteinsUp-RegulationNucleic acidsCell Processes030220 oncology & carcinogenesisCellular Structures and OrganellesResearch ArticleSignal TransductionProgrammed cell deathCell PhysiologyGeneral Science & TechnologyAutophagic Cell DeathKnockoutBiologyBioenergeticsResearch and Analysis MethodsStress Signaling Cascade03 medical and health sciencesGeneticsAutophagyAnimalsNon-coding RNAPancreasPI3K/AKT/mTOR pathwaylcsh:RAutophagyAMPKBiology and Life SciencesCell BiologyCell MetabolismGene regulationPancreatic NeoplasmsEnzyme Activation030104 developmental biologychemistryHepatic stellate cellUnfolded protein responseUnfolded Protein ResponseRNAlcsh:QGene expressionInterleukin-4Digestive DiseasesRottlerinTranscription Factor CHOP
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PFN1 and integrin‐β1/mTOR axis involvement in cornea differentiation of fibroblast limbal stem cells

2019

Abstract Ex vivo limbal stem cell transplantation is the main therapeutic approach to address a complete and functional re‐epithelialization in corneal blindness, the second most common eye disorder. Although important key points were defined, the molecular mechanisms involved in the epithelial phenotype determination are unclear. Our previous studies have demonstrated the pluripotency and immune‐modulatory of fibroblast limbal stem cells (f‐LSCs), isolated from the corneal limbus. We defined a proteomic profile especially enriched in wound healing and cytoskeleton‐remodelling proteins, including Profilin‐1 (PFN1). In this study we postulate that pfn‐1 knock down promotes epithelial lineage…

0301 basic medicinelimbal stem cellApoptosisintegrin-β1Settore MED/13 - EndocrinologiaProfilins0302 clinical medicinesignallingCells CulturedCorneal epitheliumIntegrin beta1TOR Serine-Threonine KinasesEpithelium CornealCell DifferentiationCell biologymedicine.anatomical_structuremTOR pathway030220 oncology & carcinogenesisMolecular MedicineOriginal ArticleStem cellHomeobox protein NANOGintegrin‐β1regenerative medicineBiologyLimbus CorneaeCorneal limbus03 medical and health sciencesstem cellsmedicineHumansprofilinFibroblastlimbal stem cellsPI3K/AKT/mTOR pathwayCell ProliferationWound HealingSettore MED/30 - Malattie Apparato VisivoCell BiologyOriginal ArticlesFibroblastseye diseasesepithelial differentiation030104 developmental biologyGene Expression RegulationEye disordersense organscorneal regenerationWound healingBiomarkersJournal of Cellular and Molecular Medicine
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Protein kinase inhibitor-based cancer therapies: Considering the potential of nitric oxide (NO) to improve cancer treatment.

2020

The deregulation of a wide variety of protein kinases is associated with cancer cell initiation and tumor progression. Owing to their indispensable function in signaling pathways driving malignant cell features, protein kinases constitute major therapeutic targets in cancer. Over the past two decades, intense efforts in drug development have been dedicated to this field. The development of protein kinase inhibitors (PKIs) have been a real breakthrough in targeted cancer therapy. Despite obvious successes across patients with different types of cancer, the development of PKI resistance still prevails. Combination therapies are part of a comprehensive approach to address the problem of drug r…

0301 basic medicinemedicine.drug_class[SDV]Life Sciences [q-bio]Nitric OxideBiochemistry03 medical and health sciences0302 clinical medicineNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsMedicineHumansNitric Oxide DonorsMolecular Targeted TherapyProtein kinase AProtein Kinase InhibitorsPharmacologybusiness.industryKinaseCancerProtein kinase inhibitormedicine.disease3. Good health030104 developmental biologyDrug developmentTumor progressionDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellCancer researchSignal transductionbusinessProtein KinasesSignal TransductionBiochemical pharmacology
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Expert opinion on the metabolic complications of mTOR inhibitors

2018

Abstract Using mTOR inhibitors (mTORi) as anticancer drugs led to hyperglycemia (12–50%) and hyperlipidemia (7–73%) in phase-III trials. These high rates require adapted treatment in cancer patients. Before initiating mTORi treatment, lipid profile screening should be systematic, with fasting glucose assay in non-diabetic patients and HbA1C in diabetic patients. After initiation, lipid profile monitoring should be systematic, with fasting glucose assay in non-diabetic patients, every 2 weeks for the first month and then monthly. The HbA1C target is ≤ 8%, before and after treatment initiation in known diabetic patients and in case of onset of diabetes under mTORi. LDL-cholesterol targets sho…

0301 basic medicinemedicine.medical_specialtyConsensusEndocrinology Diabetes and MetabolismAtorvastatinAntineoplastic Agents03 medical and health sciences0302 clinical medicineEndocrinologyMetabolic DiseasesNeoplasmsInternal medicineDiabetes mellitusHyperlipidemiamedicineHumansDyslipidemiasFenofibratemedicine.diagnostic_testbusiness.industryTOR Serine-Threonine KinasesHypertriglyceridemianutritional and metabolic diseasesGeneral Medicinemedicine.diseaseHypoglycemia030104 developmental biologySimvastatin030220 oncology & carcinogenesislipids (amino acids peptides and proteins)Lipid profilebusinessPravastatinmedicine.drugAnnales d'Endocrinologie
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Prolonged Fasting Reduces IGF-1/PKA to Promote Hematopoietic-Stem-Cell-Based Regeneration and Reverse Immunosuppression

2016

SummaryImmune system defects are at the center of aging and a range of diseases. Here, we show that prolonged fasting reduces circulating IGF-1 levels and PKA activity in various cell populations, leading to signal transduction changes in long-term hematopoietic stem cells (LT-HSCs) and niche cells that promote stress resistance, self-renewal, and lineage-balanced regeneration. Multiple cycles of fasting abated the immunosuppression and mortality caused by chemotherapy and reversed age-dependent myeloid-bias in mice, in agreement with preliminary data on the protection of lymphocytes from chemotoxicity in fasting patients. The proregenerative effects of fasting on stem cells were recapitula…

0301 basic medicinemedicine.medical_specialtyhematopoietic regenerationfastingmedicine.medical_treatmentCellBiologyMice03 medical and health sciences0302 clinical medicineImmune systemSettore BIO/13 - Biologia ApplicataInternal medicinemedicineGeneticsAnimalsRegenerationInsulin-Like Growth Factor I030304 developmental biologyImmunosuppression Therapy0303 health sciencesstem cells; fasting; nutrition; hematopoietic regenerationRegeneration (biology)Hematopoietic stem cellImmunosuppressionCell BiologyHematopoietic Stem CellsCyclic AMP-Dependent Protein Kinases3. Good healthCell biologyMice Inbred C57BLstem cellHaematopoiesisEndocrinologynutrition030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisMolecular MedicineSignal transductionStem cellCell Stem Cell
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HSP60 activity on human bronchial epithelial cells

2017

HSP60 has been implicated in chronic inflammatory disease pathogenesis, including chronic obstructive pulmonary disease (COPD), but the mechanisms by which this chaperonin would act are poorly understood. A number of studies suggest a role for extracellular HSP60, since it can be secreted from cells and bind Toll-like receptors; however, the effects of this stimulation have never been extensively studied. We investigated the effects (pro- or anti-inflammatory) of HSP60 in human bronchial epithelial cells (16-HBE) alone and in comparison with oxidative, inflammatory, or bacterial challenges. 16-HBE cells were cultured for 1–4 h in the absence or presence of HSP60, H2O2, lipopolysaccharide (…

0301 basic medicinep38αSettore BIO/17 - IstologiaLipopolysaccharidep38 mitogen-activated protein kinasesImmunologyStimulationBronchip38 Mitogen-Activated Protein KinasesERK1Cell LinePathogenesisMitochondrial Proteins03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOriginal Research ArticlesHumansImmunology and AllergyCOPDInterleukin 8Protein kinase AReceptor16-HBE; COPD; CREB1; ERK1; HSP60; IL-10; IL-8; JNK1; MyD88; NF-κB p65 subunit; TLR-4; p38αPharmacologyIL-8Settore BIO/16 - Anatomia UmanaInterleukin-8JNK1NF-κB p65 subunitEpithelial CellsTLR-4Chaperonin 60MyD88Interleukin-1016-HBEToll-Like Receptor 416-HBE; COPD; CREB1; ERK1; HSP60; IL-10; IL-8; JNK1; MyD88; NF-κB p65 subunit; p38α; TLR-4; Immunology and Allergy; Immunology; PharmacologyInterleukin 10030104 developmental biologychemistry030220 oncology & carcinogenesisIL-10Cancer researchCREB1NF-κB p65 subunitHSP60p38α
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Wip1 phosphatase: between p53 and MAPK kinases pathways.

2016

IF 5.008; International audience; Cells undergoing oncogenic transformation frequently inactivate tumor suppressor pathways that could prevent their uncontrolled growth. Among those pathways p53 and p38MAPK pathways play a critical role in regulation of cell cycle, senescence and cell death in response to activation of oncogenes, stress and DNA damage. Consequently, these two pathways are important in determining the sensitivity of tumor cells to anti-cancer treatment. Wild type p53-induced phosphatase, Wip1, is involved in governance of both pathways. Recently, strategies directed to manipulation with Wip1 activity proposed to advance current day anticancer treatment and novel chemical com…

0301 basic medicinep53Programmed cell deathDNA damagetumor suppressorPhosphatase[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyReviewPyruvate dehydrogenase phosphataseBiologyBioinformaticsmedicine.disease_causechemotherapyp38 Mitogen-Activated Protein Kinases[ SDV.CAN ] Life Sciences [q-bio]/Cancerphosphatase03 medical and health sciencesmedicineAnimalsHumansGenetically modified animal[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyCell CycleCell cycleCell biologyProtein Phosphatase 2C030104 developmental biologyCell Transformation NeoplasticOncologyMutationSignal transductionTumor Suppressor Protein p53CarcinogenesisDNA DamageSignal TransductionOncotarget
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Multifaceted Mechanisms of WY-14643 to Stabilize the Blood-Brain Barrier in a Model of Traumatic Brain Injury

2017

The blood-brain barrier (BBB) is damaged during ischemic insults such as traumatic brain injury or stroke. This contributes to vasogenic edema formation and deteriorate disease outcomes. Enormous efforts are pursued to understand underlying mechanisms of ischemic insults and develop novel therapeutic strategies. In the present study the effects of PPARα agonist WY-14643 were investigated to prevent BBB breakdown and reduce edema formation. WY-14643 inhibited barrier damage in a mouse BBB in vitro model of traumatic brain injury based on oxygen/glucose deprivation in a concentration dependent manner. This was linked to changes of the localization of tight junction proteins. Furthermore, WY-1…

0301 basic medicinepirinixic acidTraumatic brain injuryp38 mitogen-activated protein kinasesIschemiaischemiaPharmacologyBlood–brain barrierPPARαlcsh:RC321-57103 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineDownregulation and upregulationmedicinelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologyOriginal ResearchTight junctionbusiness.industryKinasetraumatic brain injuryblood-brain barriermedicine.diseasestroke030104 developmental biologymedicine.anatomical_structureKnockout mousebusinessNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Molecular Neuroscience
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