2024
Nuclear-penetrating scleroderma autoantibody inhibits topoisomerase 1 cleavage complex formation
May C, Noble P, Herzog E, Meffre E, Hansen J. Nuclear-penetrating scleroderma autoantibody inhibits topoisomerase 1 cleavage complex formation. Biochemical And Biophysical Research Communications 2024, 720: 150123. PMID: 38759301, DOI: 10.1016/j.bbrc.2024.150123.Peer-Reviewed Original ResearchDiffuse cutaneous systemic sclerosisCutaneous systemic sclerosisAnti-topoisomerase 1Systemic lupus erythematosusDiscovery of autoantibodiesMechanisms of autoimmunityInhibit DNA repairScleroderma autoantibodiesScleroderma subtypeSystemic sclerosisLupus erythematosusAutoantibodiesCancer therapyPathophysiologyReagent resourcesCellular dysfunctionAntibodiesCell nucleiDNA repair
2022
Advanced Glycation End Products-Mediated Oxidative Stress and Regulated Cell Death Signaling in Cancer
Pathak C, Vaidya F, Waghela B, Chhipa A, Tiwari B, Ranjan K. Advanced Glycation End Products-Mediated Oxidative Stress and Regulated Cell Death Signaling in Cancer. 2022, 535-550. DOI: 10.1007/978-981-15-9411-3_44.ChaptersRegulated cell deathCell deathDanger-associated molecular patternsOxidative stressTranscription factorsMolecular mechanismsCancer progressionCellular dysfunctionMolecular patternsRedox imbalanceCancer cellsPathological consequencesTypes of cancerROS generationCurrent understandingAGEs/RAGENucleic acidsAdvanced glycation end productsEnd productsGlycation of proteinsRAGE interactionAccumulationPathophysiological effectsGenesGlycation end products
2018
A review of micronutrients in sepsis: the role of thiamine, l-carnitine, vitamin C, selenium and vitamin D
Belsky JB, Wira CR, Jacob V, Sather JE, Lee PJ. A review of micronutrients in sepsis: the role of thiamine, l-carnitine, vitamin C, selenium and vitamin D. Nutrition Research Reviews 2018, 31: 281-290. PMID: 29984680, DOI: 10.1017/s0954422418000124.Peer-Reviewed Original ResearchConceptsVitamin CLife-threatening organ dysfunctionRole of micronutrientsCurrent available dataSeptic patientsOrgan dysfunctionSeptic shockVitamin DVitamin D.Clinical trialsRole of thiamineThiamine deficiencySepsisHuman studiesHost responseConclusion statementsCellular dysfunctionNormal physiologyMetabolic demandsCarnitinePotential roleDysfunctionPresent reviewCellular turnoverPivotal role
2013
Myocardial Loss of IRS1 and IRS2 Causes Heart Failure and Is Controlled by p38α MAPK During Insulin Resistance
Qi Y, Xu Z, Zhu Q, Thomas C, Kumar R, Feng H, Dostal D, White M, Baker K, Guo S. Myocardial Loss of IRS1 and IRS2 Causes Heart Failure and Is Controlled by p38α MAPK During Insulin Resistance. Diabetes 2013, 62: 3887-3900. PMID: 24159000, PMCID: PMC3806607, DOI: 10.2337/db13-0095.Peer-Reviewed Original ResearchConceptsIRS2 proteinGene expressionType 2 diabetesEnergy metabolism gene expressionInsulin resistanceMetabolic gene expressionBox class ODouble knockout miceHeart failureActivation of p38Chronic insulin exposureActivation of p38αMetabolism gene expressionProtein kinaseRole of IRS1Cellular metabolismMolecular mechanismsInsulin receptorNeonatal rat ventricular cardiomyocytesP38α MAPKCause heart failureCellular dysfunctionIRS1Myocardial insulin resistanceClass O
2010
A conceptual framework for the molecular pathogenesis of progressive kidney disease
Schnaper HW, Hubchak SC, Runyan CE, Browne JA, Finer G, Liu X, Hayashida T. A conceptual framework for the molecular pathogenesis of progressive kidney disease. Pediatric Nephrology 2010, 25: 2223-2230. PMID: 20352456, PMCID: PMC5558437, DOI: 10.1007/s00467-010-1503-4.Peer-Reviewed Original ResearchConceptsKidney diseaseProgressive nephron lossChronic kidney diseaseProgressive kidney diseaseRole of cytokinesProgressive glomerular diseaseNephron lossGlomerular diseaseClinical conditionsCytokine effectsClinical practiceMolecular pathogenesisDiseasePathogenesisCellular dysfunctionAdaptive physiological responsesPhysiological factorsCellular responsesRepairSubsequent cyclesPhysiological responsesTissue-specific cellular responsesProteinuriaDysfunctionCytokines
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