Search results for "PROTEIN KINASE"

showing 10 items of 1188 documents

Fungal Deoxynivalenol-Induced Enterocyte Distress Is Attenuated by Adulterated Adlay: In Vitro Evidences for Mucoactive Counteraction

2018

Adlay is a cereal crop that has long been used as traditional herbal medicine and as a highly nourishing food. However, deoxynivalenol (DON), the most prevalent trichothecene mycotoxin worldwide, frequently spoils grains, including adlay, via fungal infection. On the basis of an assumption that the actions of DON in the gut could be modified by adlay consumption, we simulated the impacts of co-exposure in enterocytes and investigated the effectiveness of treatment with adlay for reducing the risk of DON-induced inflammation and epithelia barrier injury. In particular, adlay suppressed DON-induced pro-inflammatory signals such as mitogen-activated kinase transduction and the epidermal growth…

0301 basic medicinelcsh:Immunologic diseases. AllergyEnterocytewoundImmunologyTrichothecenedeoxynivalenolInflammationPharmacologyBiologyadlay03 medical and health sciences0302 clinical medicineEpidermal growth factormedicineImmunology and AllergyProtein kinase Cgut barrierKinasefood and beveragesIn vitroCytosol030104 developmental biologymedicine.anatomical_structureinflammation030220 oncology & carcinogenesismedicine.symptomlcsh:RC581-607Frontiers in Immunology
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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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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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TSH/IGF-1 Receptor Cross-Talk Rapidly Activates Extracellular Signal-Regulated Kinases in Multiple Cell Types

2017

We previously showed that thyrotropin (TSH)/insulinlike growth factor (IGF)-1 receptor cross-talk appears to be involved in Graves’ orbitopathy (GO) pathogenesis and upregulation of thyroid-specific genes in human thyrocytes. In orbital fibroblasts from GO patients, coadministration of TSH and IGF-1 induces synergistic increases in hyaluronan secretion. In human thyrocytes, TSH plus IGF-1 synergistically increased expression of the sodium-iodide symporter that appeared to involve ERK1/2 activation. However, the details of ERK1/2 activation were not known, nor was whether ERK1/2 was involved in this synergism in other cell types. Using primary cultures of GO fibroblasts (GOFs) and human thyr…

0301 basic medicinemedicine.medical_specialtyCell typeendocrine systemendocrine system diseasesMAP Kinase Signaling SystemThyrotropinPertussis toxinReceptor IGF Type 103 medical and health sciencesEndocrinologyDownregulation and upregulationInternal medicinemedicineHumansSecretionHyaluronic AcidInsulin-Like Growth Factor IPhosphorylationReceptorResearch ArticlesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3SymportersChemistryHEK 293 cellsReceptors ThyrotropinReceptor Cross-TalkFibroblastsSignalingGraves Ophthalmopathy030104 developmental biologyEndocrinologyHEK293 CellsThyroid Epithelial CellsSymporterPhosphorylationhormones hormone substitutes and hormone antagonistsEndocrinology
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Biomarker analysis of the MITO2 phase III trial of first-line treatment in ovarian cancer: Predictive value of DNA-PK and phosphorylated ACC

2016

// Francesco Perrone 1,* , Gustavo Baldassarre 2,* , Stefano Indraccolo 3,* , Simona Signoriello 4 , Gennaro Chiappetta 1 , Franca Esposito 5 , Gabriella Ferrandina 6 , Renato Franco 1,15 , Delia Mezzanzanica 7 , Maura Sonego 2 , Elisabetta Zulato 3 , Gian F. Zannoni 6 , Vincenzo Canzonieri 2 , Giovanni Scambia 6 , Roberto Sorio 2 , Antonella Savarese 8 , Enrico Breda 9 , Paolo Scollo 10 , Antonella Ferro 11 , Stefano Tamberi 12 , Antonio Febbraro 13 , Donato Natale 14 , Massimo Di Maio 1,16 , Daniela Califano 1 , Giosue  Scognamiglio 1 , Domenica Lorusso 7 , Silvana Canevari 7 , Simona Losito 1 , Ciro Gallo 4,** and Sandro Pignata 1,** 1 Istituto Nazionale per lo Studio e la Cura dei Tumor…

0301 basic medicinemedicine.medical_specialtyLiposomal Doxorubicinovarian cancer; phase 3 clinical trial; predictive factors; pACC; DNA-PKDNA-Activated Protein KinaseDisease-Free Survivalpredictive factorDNA-PK03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOvarian cancerPhase 3 clinical trialAntineoplastic Combined Chemotherapy ProtocolsOverall survivalMedicineHumansDNA-PK; ovarian cancer; pACC; phase 3 clinical trial; predictive factorsGynecologyOvarian NeoplasmsAdvanced ovarian cancerphase 3 clinical trialbusiness.industrySignificant differenceDNA-PK; Ovarian cancer; PACC; Phase 3 clinical trial; Predictive factors; Antineoplastic Combined Chemotherapy Protocols; DNA-Activated Protein Kinase; Disease-Free Survival; Female; Humans; Ovarian Neoplasms; Prognosismedicine.diseasePrognosisPredictive valuePACCCarboplatinhumanitiesFirst line treatmentovarian cancer030104 developmental biologyOncologychemistry030220 oncology & carcinogenesisFemalebusinessOvarian cancerPredictive factorsResearch PaperpACC
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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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Therapeutic Potential of AntagomiR-23b for Treating Myotonic Dystrophy

2020

Myotonic dystrophy type 1 (DM1) is a chronically debilitating, rare genetic disease that originates from an expansion of a noncoding CTG repeat in the dystrophia myotonica protein kinase (DMPK) gene. The expansion becomes pathogenic when DMPK transcripts contain 50 or more repetitions due to the sequestration of the muscleblind-like (MBNL) family of proteins. Depletion of MBNLs causes alterations in splicing patterns in transcripts that contribute to clinical symptoms such as myotonia and muscle weakness and wasting. We previously found that microRNA (miR)-23b directly regulates MBNL1 in DM1 myoblasts and mice and that antisense technology (“antagomiRs”) blocking this microRNA (miRNA) boost…

0301 basic medicinemusculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesMyotonic dystrophyArticleantagomiR03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDrug DiscoverymicroRNAMedicineMBNL1AntagomirProtein kinase AmiRNAmyotonic dystrophybusiness.industrylcsh:RM1-950Muscle weaknessmedicine.diseaseMyotoniaMbnl1030104 developmental biologylcsh:Therapeutics. Pharmacologychemistry030220 oncology & carcinogenesisRNA splicingCancer researchHSALR miceMolecular Medicinemedicine.symptomDM1antisense oligonucleotidesbusinessMolecular Therapy: Nucleic Acids
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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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