Search results for "OXPHOS"

showing 10 items of 10 documents

Melatonin Targets Metabolism in Head and Neck Cancer Cells by Regulating Mitochondrial Structure and Function.

2021

This study was funded by grants from the Ministerio de Economia, Industria y Competitividad y por el Fondo de Desarrollo Regional FEDER, Spain nº SAF2013-49019, SAF2017-85903-P, and from the Consejería de Innovación, Ciencia y Empresa, Junta de Andalucía (P07- CTS- 03135, P10- CTS- 5784, and CTS- 101), Spain. J.F. and L.M. have FPU fellowships from the Ministerio de Educación Cultura y Deporte, Spain. C.R.S. was a schorlarship holder from the Plan Propio de Investigación of the University of Granada.

0301 basic medicine:Phenomena and Processes::Chemical Phenomena::Biochemical Phenomena::Biochemical Processes::Phosphorylation::Oxidative Phosphorylation [Medical Subject Headings]PhysiologyClinical BiochemistrymelatoninMitochondrionBiochemistryMelatonina:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings]0302 clinical medicine:Anatomy::Cells::Cells Cultured::Cell Line [Medical Subject Headings]head and neck cancer cells:Phenomena and Processes::Physiological Phenomena::Pharmacological Phenomena::Drug Resistance::Drug Resistance Neoplasm [Medical Subject Headings]MitophagyMitocondriasChemistryapoptosisglycolysisOXPHOSmitochondria030220 oncology & carcinogenesishormones hormone substitutes and hormone antagonistsmedicine.drug:Phenomena and Processes::Chemical Phenomena::Biochemical Phenomena::Biochemical Processes::Carbohydrate Metabolism::Glycolysis [Medical Subject Headings]Neoplasias de cabeza y cuello:Diseases::Neoplasms::Neoplasms by Site::Head and Neck Neoplasms [Medical Subject Headings]:Chemicals and Drugs::Inorganic Chemicals::Free Radicals::Reactive Oxygen Species [Medical Subject Headings]Mitofagiafree radicalsOxidative phosphorylationArticleMelatonin03 medical and health sciencesmedicine:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Growth Processes::Cell Proliferation [Medical Subject Headings]Molecular BiologyRadicales libresCell growth:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::DNA-Binding Proteins::Receptors Cytoplasmic and Nuclear::Receptors Melatonin [Medical Subject Headings]:Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Therapeutic Uses::Antineoplastic Agents [Medical Subject Headings]lcsh:RM1-950:Anatomy::Cells::Cellular Structures::Subcellular Fractions::Mitochondria [Medical Subject Headings]Cell Biologymedicine.diseaseHead and neck squamous-cell carcinoma:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death::Apoptosis [Medical Subject Headings]Glucólisis030104 developmental biologylcsh:Therapeutics. PharmacologymitophagyApoptosisCancer cellCancer research:Chemicals and Drugs::Hormones Hormone Substitutes and Hormone Antagonists::Hormones::Melatonin [Medical Subject Headings]
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Muscle NAD+ depletion and Serpina3n as molecular determinants of murine cancer cachexia—the effects of blocking myostatin and activins

2020

Objective Cancer cachexia and muscle loss are associated with increased morbidity and mortality. In preclinical animal models, blocking activin receptor (ACVR) ligands has improved survival and prevented muscle wasting in cancer cachexia without an effect on tumour growth. However, the underlying mechanisms are poorly understood. This study aimed to identify cancer cachexia and soluble ACVR (sACVR) administration-evoked changes in muscle proteome. Methods Healthy and C26 tumour-bearing (TB) mice were treated with recombinant sACVR. The sACVR or PBS control were administered either prior to the tumour formation or by continued administration before and after tumour formation. Muscles were an…

MaleEXPRESSIONActivin receptor; APR; C26; Cancer cachexia; Nrk2; OXPHOSlcsh:Internal medicineCachexiaREVERSALActivin ReceptorsMETABOLISMactivin receptorOxidative PhosphorylationCell Line TumorAnimalsMuscle Skeletallcsh:RC31-1245aineenvaihduntaSerpinslihassolut318 Medical biotechnologyNrk2Cancer cachexiaMyostatinNADOXPHOSMUSCULAR-DYSTROPHYActivinsMitochondriaActivin receptorDisease Models AnimalMuscular AtrophyMICESIRTUINSOriginal ArticlesyöpätauditproteiinitC26lihassurkastumasairaudetAPRAcute-Phase Proteinscancer cachexia
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Metabolic Escape Routes of Cancer Stem Cells and Therapeutic Opportunities

2020

Although improvement in early diagnosis and treatment ameliorated life expectancy of cancer patients, metastatic disease still lacks effective therapeutic approaches. Resistance to anticancer therapies stems from the refractoriness of a subpopulation of cancer cells—termed cancer stem cells (CSCs)—which is endowed with tumor initiation and metastasis formation potential. CSCs are heterogeneous and diverge by phenotypic, functional and metabolic perspectives. Intrinsic as well as extrinsic stimuli dictated by the tumor microenvironment (TME)have critical roles in determining cell metabolic reprogramming from glycolytic toward an oxidative phenotype and vice versa, allowing cancer cells to th…

cancer stem cells0301 basic medicinecancer stem cellCancer ResearchStromal cellSettore MED/50 - Scienze Tecniche Mediche ApplicateCellcancer metabolismReviewTumor initiationlcsh:RC254-282glycolysi03 medical and health sciences0302 clinical medicineCancer stem celllipid metabolismmicroRNAtumor microenvironmentmetabolic reprogrammingMedicinemetabolism-based anticancer drugsTumor microenvironmentbusiness.industryglycolysislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensOXPHOSMicrovesicles030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer cellCancer researchSettore MED/46 - Scienze Tecniche Di Medicina Di LaboratoriobusinessCancers
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Oksidatīvās fosforilēšanas sistēmas funkcionalitātes novērtēšana, izmantojot citoplazmātisko hibrīdu šūnu modeļus

2020

Mitohondriju iekšējā membrānā ir izvietoti pieci enzīmu kompleksi, kas veido oksidatīvās fosforilēšanas (OXPHOS) sistēmu. OXPHOS sistēma saražo līdz pat 90% adenozīntrifosfāta šūnās. Mitohondriālās DNS (mtDNS) mutāciju izraisīti traucējumi OXPHOS sistēmā var izraisīt smagas mitohondriālās slimības. Mitohondriālo slimību diagnosikā nav vienas konkrētas metodes. Patogēno mtDNS mutāciju ietekmi var pētīt izmantojot citoplazmatisko hibrīdu šūnu modeļus. Darba mērķis ir novērtēt OXPHOS funkcionalitāti citoplazmatisko hibrīdu šūnu līniju kontroles grupā un pacienta šūnu līnijā ar iespējami patogēnu mtDNS mutāciju. Tika izveidota šūnu līniju kontroles grupa un noteiktas OXPHOS enzīmu aktivitātes, …

OXPHOS sistēmamitohondriālās slimībasmitohondriju funkcionalitātes novērtēšanacitoplazmatiskie hibrīdišūnu dzīvotspējaBioloģija
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Mitohondriālo slimību diagnostika, izmantojot molekulārās bioloģijas metodes un citoplazmatisko hibrīdu šūnu modeļus

2017

Mitohondriju galvenā funkcija ir enerģijas ražošana šūnā. Traucējumi mitohondriju elpošanas ķēdē var izraisīt plaša spektra patoloģijas. Patogēno mtDNS mutāciju ietekmi uz šūnu fenotipu iespējams pētīt citoplazmatisko hibrīdu šūnu līnijās. Darba mērķis ir analizēt citoplazmatisko hibrīdu šūnu modeļus un noteikt to piemērotību mitohondriālo slimību raksturošanai un diagnostikai. Tika veikta kontroles grupas un pacientu citoplazmatisko hibrīdu šūnu līniju mtDNS fragmentu sekvenēšana, mtDNS kopiju skaita, ATF koncentrācijas un elpošanas ķēdes kompleksu aktivitāšu noteikšana un salīdzināšana, kā arī tika raksturota izveidoto šūnu līniju stabilitāte. Lai apstiprinātu atbilstību donoru trombocītu…

mtDNS kopiju skaitsOXPHOS kompleksimitohondriālās slimībasBioloģijaATF
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Patogēnas mtDNS mutācijas saturošu citoplazmatisko hibrīdu šūnu modeļu izveide un raksturošana

2020

Eikariotu šūnās ģenētisko materiālu DNS formā satur gan kodols, gan mitohondriji. Patogēnas mutācijas mitohondriālajā DNS (mtDNS) var izraisīt dažādas heterogēnas saslimšanas. Lai izpētītu, kā patogēnas mtDNS mutācijas ietekmē mitohondriju funkciju, var izmantot citoplazmatisko hibrīdu jeb cibrīdu šūnu modeļus. Bakalaura darba mērķis ir izveidot un raksturot patogēnas mtDNS mutācijas saturošus citoplazmatisko hibrīdu šūnu modeļus. Tika veikta pilna garuma mtDNS sekvenēšana, cibrīdu šūnu modeļu izveidošana, šūnu dzīvotspējas un OXPHOS enzīmu aktivitātes noteikšana. Pilna garuma mtDNS sekvenēšana tika veikta 20 pacientiem ar aizdomām par mitohondriālo saslimšanu. Trim pacientiem tika konstatē…

mitohondriālās saslimšanasMitohondriālā DNSšūnu dzīvotspējaBioloģijaOXPHOScitoplazmatiskās hibrīdu šūnas
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Jaunu ģenētisko variantu funkcionāla raksturošana izmantojot izolētas pacientu šūnas

2022

Mutācijas gan mitohondriālajā DNS, gan kodola DNS var izraisīt traucējumus mitohondriju oksidatīvās fosforilēšanas sistēmā, kas var būt cēlonis smagām mitohondriālajām slimībām. Mitohondriālo slimību diagnostika ir komplicēta, un tai izmanto lielu laboratorijas metožu klāstu. Darba “JAUNU ĢENĒTISKO VARIANTU FUNKCIONĀLA RAKSTUROŠANA IZMANTOJOT IZOLĒTAS PACIENTU ŠŪNAS” mērķis ir raksturot jaunus ģenētiskos variantus reto ģenētisko slimību pacientiem, izmantojot molekulārās un bioķīmiskās metodes, kā arī perifēros leikocītus un kultivētus fibroblastus. Tika veikta DNS variantu validācija ar Sangera sekvencēšanu, šūnu līniju izveidošana un kultivēšana, mitohondriju izdalīšana no šūnu kultūrām u…

Mitohondriālās slimības/Mitochondrial diseasenDNS/nDNAģenētiskais variants/genetic variantBioloģijaOXPHOSmtDNS/mtDNA
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Caracterización funcional de GTPBP3: una proteína G implicada en la modificación de tRNAs mitocondriales.

2015

Determinadas enfermedades mitocondriales, como MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes), MERRF (myoclonus epilepsy associated with ragged-red-fibers), cardiomiopatía hipertrófica y acidosis láctica dependiente de GTPBP3, cardiomiopatía hipertrófica infantil y acidosis láctica dependiente de MTO1 y fallo hepático infantil agudo dependiente de TRMU, están asociadas con una disfunción severa del sistema de fosforilación oxidativa (OXPHOS) que, se cree, podría ser resultado de defectos en la modificación postranscripcional de la uridina localizada en la posición de tambaleo (U34) de ciertos tRNAs mitocondriales (mt-tRNAs) y, por consiguiente, de u…

metabolismo mitocondrialtRNA mitocondrialUNESCO::CIENCIAS DE LA VIDAgtpbp3:CIENCIAS DE LA VIDA [UNESCO]oxphosmodificación trna
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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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Mitochondrial DNA mutations in cancer--from bench to bedside.

2009

Mitochondria are cell organelles mostly known for their production of ATP through oxidative phosphorylation. As suggested over 70 years ago by O. Warburg and recently confirmed with molecular techniques, alterations in respiratory activity and mitochondrial DNA appear to be a common feature of malignant cells. Somatic mtDNA mutations have been reported in many types of cancer cells. MtDNA mutation pattern may enhance the specificity of cancer diagnostics, detection and prediction of tumor growth rate and patients' outcome. Therefore it may be used as a molecular cancer bio-marker. Nevertheless recently published papers list a large number of mitochondrial DNA mutations in many different can…

GeneticsMutationMitochondrial DNASettore BIO/16 - Anatomia UmanaSomatic cellRespiratory chainCancerContext (language use)ApoptosisMitochondrionBiologymedicine.disease_causemedicine.diseaseDNA MitochondrialModels BiologicalTranslational Research BiomedicalCell Transformation NeoplasticNeoplasmsCancer cellMutationmedicineHumansCancer Mitochondria Molecular Marker Mutation OXPHOS ReviewReactive Oxygen SpeciesCell ProliferationFrontiers in bioscience (Landmark edition)
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