2025
Neuronal ALKAL2 and its ALK receptor contribute to the development of colitis-associated colorectal cancer
Delanne-Cuménal M, Defaye M, Delanne-Cuménal A, Ahmed M, Ho V, Abdullah N, Alhassoun M, Svendsen K, Mager L, Schlessinger J, Hirota S, Altier C. Neuronal ALKAL2 and its ALK receptor contribute to the development of colitis-associated colorectal cancer. Proceedings Of The National Academy Of Sciences Of The United States Of America 2025, 122: e2500632122. PMID: 40493183, PMCID: PMC12184428, DOI: 10.1073/pnas.2500632122.Peer-Reviewed Original ResearchConceptsColitis-associated colorectal cancerAnaplastic lymphoma kinaseColorectal cancerAnaplastic lymphoma kinase activityColitis-associated colorectal cancer progressionAnaplastic lymphoma kinase receptorTRPV1+ nociceptorsDevelopment of colitis-associated colorectal cancerMouse colonic organoidsALK signalingInflammatory painTumor burdenTreatment resistanceSensory neuronsTumor growthColonic organoidsALKAL2Colonic mucosaOverall inflammationCancer progressionCancerIn vivoTRPV1NeuronsInflammationEvidence of secondary Notch signaling within the rat small intestine.
Zagoren E, Dias N, Santos A, Smith Z, Ameen N, Sumigray K. Evidence of secondary Notch signaling within the rat small intestine. Development 2025, 152 PMID: 40371707, PMCID: PMC12188240, DOI: 10.1242/dev.204277.Peer-Reviewed Original ResearchConceptsSecretory lineageRegulate luminal pHSecretory cellsNotch signalingSecretory cell typesSmall intestinal epithelial cellsRNA sequencing dataIntestinal epithelial cellsIntestinal stem cellsSmall intestineFate in vivoFibrosis pathophysiologyRat small intestineCrypt progenitorsTranscription factorsEpithelial cellsRat jejunumStem cellsPseudotime trajectory analysisRare populationLuminal pHRatsHigher expressionIntestinal functionIn vitroMetabolic switches in cell death regulation
Galluzzi L. Metabolic switches in cell death regulation. Cell Metabolism 2025, 37: 1252-1254. PMID: 40466623, DOI: 10.1016/j.cmet.2025.04.017.Peer-Reviewed Original ResearchLatent EBV enhances the efficacy of anti-CD3 mAb in Type 1 diabetes
Lledó-Delgado A, Preston-Hurlburt P, Higdon L, Hu A, James E, Lim N, Long S, McNamara J, Nguyen H, Serti E, Sumida T, Herold K. Latent EBV enhances the efficacy of anti-CD3 mAb in Type 1 diabetes. Nature Communications 2025, 16: 5033. PMID: 40447640, PMCID: PMC12125364, DOI: 10.1038/s41467-025-60276-5.Peer-Reviewed Original ResearchConceptsCD8+ T cellsEBV-seropositive individualsType 1 diabetesT cellsImmune cellsAntigen-specific CD8+ T cellsDiagnosis of type 1 diabetesEBV-seronegative patientsEBV-seropositive patientsT cell activation pathwaysRegulatory T cellsAnti-CD3 mAbInnate immune cellsPeripheral blood cellsT cell receptorProgression of diseaseContext of type 1 diabetesImpaired signaling pathwaysTeplizumabClinical trialsLatent EBVBlood cellsSingle cell transcriptomicsModulate progressionMTOR signalingIdentification of F-box proteins in ABA- and GA-regulated seed germination: interaction of GASA1 signalling peptide and ABA-induced ubiquitination
Kasera M, Ceciliato P, Lopez B, Hauser F, Gendron J, Schroeder J. Identification of F-box proteins in ABA- and GA-regulated seed germination: interaction of GASA1 signalling peptide and ABA-induced ubiquitination. Philosophical Transactions Of The Royal Society B Biological Sciences 2025, 380: 20240233. PMID: 40439299, PMCID: PMC12121378, DOI: 10.1098/rstb.2024.0233.Peer-Reviewed Original ResearchConceptsSeed germinationSignal peptideGenetic screeningF-box proteinsForward genetic screensHomology-based gene silencingInhibition of seed germinationABA-insensitiveHomologous genesFunctional genomicsGene familyTriple mutantF-boxABA inhibitionProteasome pathwayAmiRNA linesGene silencingInteraction partnersGerminating seedsArtificial microRNAGenesABAGerminationMutantsUbiquitinIntermediate Signaling Mechanisms Regulating Human Fetal Membrane Responses to Gram‐Positive Bacterial Peptidoglycan
Georges H, Fischer A, Abrahams V. Intermediate Signaling Mechanisms Regulating Human Fetal Membrane Responses to Gram‐Positive Bacterial Peptidoglycan. American Journal Of Reproductive Immunology 2025, 93: e70090. PMID: 40435036, PMCID: PMC12124414, DOI: 10.1111/aji.70090.Peer-Reviewed Original ResearchConceptsToll-like receptorsPro-inflammatory cytokines IL-1bFetal membrane explantsHuman FM explantsPathogenesis of chorioamnionitisP65-NFkBResponse to Gram-positive bacteriaP38 MAPKElevated levelsTLR2 agonist peptidoglycanCytokines IL-1bChemokine IL-8FM explantsNeonatal morbidityPreterm birthStimulation of TLR4Fetal membranesMembrane weakeningIL-1BIL-8TLR7/8 activationMembrane explantsSecreted factorsERK signalingLipopolysaccharide stimulationIL‐6 signaling regulates the inflammatory response without impacting pathogen burden during influenza‐associated pulmonary aspergillosis
Sharma L, Singh R, Tolman N, Ngeow C, Duray A, Naghshtabrizi N, Ahmad A, Bain W, Robinson K. IL‐6 signaling regulates the inflammatory response without impacting pathogen burden during influenza‐associated pulmonary aspergillosis. Physiological Reports 2025, 13: e70372. PMID: 40420617, PMCID: PMC12106949, DOI: 10.14814/phy2.70372.Peer-Reviewed Original ResearchConceptsAF infectionAspergillus fumigatusInterleukin-6IL-6 signalingLung inflammationInfluenza-associated pulmonary aspergillosisInterleukin-6 knockout miceNeutrophilic lung inflammationBronchoalveolar lavage fluidEpithelial cell damageLung capillary permeabilitySusceptibility to opportunistic pathogensPulmonary aspergillosisClinical courseLavage fluidKnockout miceOpportunistic pathogenRAGE levelsEpithelial integrityMouse modelIL-6Pathological inflammationTissue injuryInflammatory responseViral infectionYAP controls cell migration and invasion through a Rho GTPase switch
Shah S, Ren C, Tippens N, Park J, Mohyeldin A, Wang S, Vela G, Martinez-Gutierrez J, Margolis S, Schmidt S, Quiñones-Hinojosa A, Levchenko A. YAP controls cell migration and invasion through a Rho GTPase switch. Science Signaling 2025, 18: eadu3794. PMID: 40424361, DOI: 10.1126/scisignal.adu3794.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsBrain NeoplasmsCell Line, TumorCell MovementFemaleGlioblastomaGuanine Nucleotide Exchange FactorsHumansMiceNeoplasm InvasivenessPhosphoproteinsProtein Serine-Threonine Kinasesrac1 GTP-Binding ProteinrhoA GTP-Binding ProteinSignal TransductionSTAT3 Transcription FactorTranscription FactorsYAP-Signaling ProteinsConceptsCell migrationGuanine nucleotide exchange factor TrioRegulation of cytoskeletal dynamicsRho family guanosine triphosphatasesInvasive cell spreadTranscriptional coactivator YAPActivation of Rac1Inhibition of RhoAHyperactivation of YAPHuman breast epithelial cellsIncreased cell migrationBreast epithelial cellsGTPase switchAssociated with cancer metastasisMovement of cellsCytoskeletal dynamicsGuanosine triphosphataseSignaling networksInvasion in vitroIntronic enhancerTranscription factorsCell spreadingRac1Invasive behaviorPathological contextsFapR regulates HssRS-mediated heme homeostasis in Bacillus anthracis
Pi H, Burroughs O, Carlin S, Beavers W, Hillebrand G, Krystofiak E, Stauff D, Skaar E. FapR regulates HssRS-mediated heme homeostasis in Bacillus anthracis. MBio 2025, 16: e02057-24. PMID: 40407322, PMCID: PMC12153329, DOI: 10.1128/mbio.02057-24.Peer-Reviewed Original ResearchMeSH KeywordsBacillus anthracisBacterial ProteinsGene Expression Regulation, BacterialHemeHistidine KinaseHomeostasisSignal TransductionTranscription FactorsConceptsHeme homeostasisKnowledge of bacterial physiologyTwo-component signaling systemRegulation of fatty acid biosynthesisMembrane integrityFatty acid biosynthesisHeme toxicityCausative agent of anthraxHeme stressGram-positive pathogensAgent of anthraxGram-positive bacteriaBacterial physiologyHeme sensingTranscriptional regulationAcid biosynthesisTranscription factorsFapRFacultative anaerobesHeme biosynthesisRegulatory pathwaysHssRSVertebrate bloodMolecular adaptationsMolecular mechanismsp53-inducible lncRNA LOC644656 causes genotoxic stress-induced stem cell maldifferentiation and cancer chemoresistance
Tamura A, Yamagata K, Kono T, Fujimoto M, Fuchigami T, Nishimura M, Yokoyama M, Nakayama A, Hashimoto N, Sakuma I, Mitsukawa N, Kawashima Y, Ohara O, Motohashi S, Kawakami E, Miki T, Onodera A, Tanaka T. p53-inducible lncRNA LOC644656 causes genotoxic stress-induced stem cell maldifferentiation and cancer chemoresistance. Nature Communications 2025, 16: 4818. PMID: 40410129, PMCID: PMC12102190, DOI: 10.1038/s41467-025-59886-w.Peer-Reviewed Original ResearchConceptsDNA damage responseDamage responseDNA damageDNA damage signalingResistance to genotoxic stressTGF-b signalingGenotoxic stressDamage signalingDNA-PKcsLineage-specific differentiationLoss of stemnessPoor patient survivalStem cell biologyEmbryonic stem cellsMolecular mechanismsDNACell biologyEnhanced chemoresistanceCancer chemoresistancePotential therapeutic targetDifferentiation pathwayCell propagationHuman embryonic stem cellsStem cell propagationChemoresistanceRottlerin inhibits macropinocytosis of Porcine Reproductive and Respiratory Syndrome Virus through the PKCδ-Cofilin signaling pathway
Kang Y, Choi J, Lee J, Park S, Oh C. Rottlerin inhibits macropinocytosis of Porcine Reproductive and Respiratory Syndrome Virus through the PKCδ-Cofilin signaling pathway. PLOS ONE 2025, 20: e0324500. PMID: 40392868, PMCID: PMC12091787, DOI: 10.1371/journal.pone.0324500.Peer-Reviewed Original ResearchConceptsRespiratory syndrome virusPorcine ReproductiveLIM domain kinase 1Actin dynamicsPRRSV replicationPRRSV entryPRRSVSignaling pathwayDecreased actin polymerizationActin polymerizationCofilin activityEffects of rottlerinHost cellsKinase 1Enveloped virusesRottlerin treatmentInhibit viral replicationAntiviral moleculesReplicationRottlerinVirusMacropinocytosisEntry pathwayViral replicationPathwayUsing TCR-CAR dual signaling for precise cancer targeting
Shahbazy M, Leo I, Faridi P, Caron E. Using TCR-CAR dual signaling for precise cancer targeting. Trends In Immunology 2025, 46: 435-437. PMID: 40368698, DOI: 10.1016/j.it.2025.04.007.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsHumansImmunotherapy, AdoptiveNeoplasmsReceptors, Antigen, T-CellReceptors, Chimeric AntigenSignal TransductionT-LymphocytesMitochondrial gene SLC25A24 regulated anti-tumor immunity and inhibited the proliferation and metastasis of colorectal cancer by PKG1-dependent cGMP/PKG1 pathway
Gao Y, Peng Y, Zhou Y, Zhu J, Fu S, Chen Y, Cai C, Han Y, Shen H, Zeng S, Mao L, Xiao Z. Mitochondrial gene SLC25A24 regulated anti-tumor immunity and inhibited the proliferation and metastasis of colorectal cancer by PKG1-dependent cGMP/PKG1 pathway. International Immunopharmacology 2025, 157: 114664. PMID: 40334626, DOI: 10.1016/j.intimp.2025.114664.Peer-Reviewed Original ResearchConceptsImmune checkpoint inhibitorsAnti-tumor immunityColorectal cancerResponse to immune checkpoint inhibitorsAssociated with worse overall survivalKaplan-Meier survival analysisProgression-free survivalTumor immune regulationMetastasis of colorectal cancerMitochondrial solute carriersMicrosatellite instabilityColorectal cancer cell linesColorectal cancer patientsCancer-related mortalityProliferation-related markersCheckpoint inhibitorsColorectal cancer progressionOverall survivalImmune infiltrationPotential therapeutic targetPrognostic markerUnfavorable prognosisColorectal cancer tissuesImmune regulationClinical cohortCardiomyocyte-specific NHE1 overexpression confers protection against myocardial infarction during hyperglycemia
Jiang K, Su F, Deng R, Xu Y, Qin A, Yuan X, Xing D, Chen Y, Wang D, Shen L, Hwa J, Hou L, Xiang Y. Cardiomyocyte-specific NHE1 overexpression confers protection against myocardial infarction during hyperglycemia. Cardiovascular Diabetology 2025, 24: 184. PMID: 40287728, PMCID: PMC12034198, DOI: 10.1186/s12933-025-02743-3.Peer-Reviewed Original ResearchConceptsNa+/H+ exchanger 1Na+/H+ exchanger 1 activationAcute hyperglycemiaMyocardial infarctionNHE1 overexpressionNHE1 activityTherapeutic strategiesCardiomyocyte necroptosisHistory of diabetes mellitusReduced extracellular Na+Worsened cardiac dysfunctionRetrospective cohort studyDouble knockout miceIschemia-reperfusion modelNon-diabetic individualsPost-MI patientsReduced infarct sizePathophysiology of MIBackgroundAcute hyperglycemiaElevated BNPMLKL knockoutReduced cardiomyocyte deathAcute myocardial infarctionExtracellular Na+Intracellular Na+Pancreatic β-cell apoptosis caused by apolipoprotein C3-rich low-density lipoprotein is attenuated by kansuinine A through oxidative stress inhibition
Lulji Taraqaz B, Hsu Y, Tsai P, Li Y, Chen F, Yang W, Shen M. Pancreatic β-cell apoptosis caused by apolipoprotein C3-rich low-density lipoprotein is attenuated by kansuinine A through oxidative stress inhibition. Biomedicine & Pharmacotherapy 2025, 187: 118066. PMID: 40262236, DOI: 10.1016/j.biopha.2025.118066.Peer-Reviewed Original ResearchConceptsB cell apoptosisRat pancreatic B-cellsLow-density lipoproteinPathway analysisSignaling pathwayOxidative stressApoptosisImproved cell viabilityRIN-m5FB cellsLectin-like oxidized low-density lipoprotein receptor-1Pancreatic B-cellsHigh-fat dietCell viabilityInsulin toleranceAntiapoptotic propertiesKansuinine AMitigated apoptosisMechanism of actionMolecular dockingStress inhibitionPathwayLow-density lipoprotein receptor-1Improved glucoseHigh-fatCrystal structure of Isthmin-1 and reassessment of its functional role in pre-adipocyte signaling
Li T, Stayrook S, Li W, Wang Y, Li H, Zhang J, Liu Y, Klein D. Crystal structure of Isthmin-1 and reassessment of its functional role in pre-adipocyte signaling. Nature Communications 2025, 16: 3580. PMID: 40234450, PMCID: PMC12000326, DOI: 10.1038/s41467-025-58828-w.Peer-Reviewed Original ResearchMeSH Keywords3T3-L1 CellsAdipocytesAnimalsCrystallography, X-RayHumansMiceModels, MolecularProtein DomainsProto-Oncogene Proteins c-aktSignal TransductionConceptsThrombospondin type I repeatsIsthmin-1Pre-adipocytesType I repeatsBacterial streptavidinSurface helicesI repeatsMolecular detailsDiverse functionsFunctional studiesAkt phosphorylationFunctional roleStructural plasticityInsulin-like propertiesCrystal structureAMOPGrowth factorDomainPhosphorylationApoptosisLiver steatosisProteinHelixAktStreptavidin4-Anilinoquinolinylchalcone derivatives mediate antifibrotic effects through ERK/MRTF—a signaling pathway crosstalk
Selvam P, Tseng C, Wang C, Sun Y, Chen Y, Kao Y, Dahms H, Cheng C. 4-Anilinoquinolinylchalcone derivatives mediate antifibrotic effects through ERK/MRTF—a signaling pathway crosstalk. Environmental Science And Pollution Research 2025, 32: 11685-11696. PMID: 40234319, DOI: 10.1007/s11356-025-36382-8.Peer-Reviewed Original ResearchConceptsSide effectsAbnormal liver functionAnti-fibrosisSevere side effectsGroup of drugsAnti-inflammatory responseHuman immune systemSkin rashGenitourinary cancersMechanism of actionAntifibrotic effectsBreast cancerScreened 6Immunomodulatory qualitiesLiver functionPharmacological profileImmune systemSignaling pathwaySignaling pathway crosstalkQuinolone analoguesCancerAnti-cancerDerivativesBleedingRashTSC-mTORC1 Pathway in Postnatal V-SVZ Neurodevelopment
Feliciano D, Bordey A. TSC-mTORC1 Pathway in Postnatal V-SVZ Neurodevelopment. Biomolecules 2025, 15: 573. PMID: 40305300, PMCID: PMC12024678, DOI: 10.3390/biom15040573.Peer-Reviewed Original ResearchConceptsMTOR pathwayNeural stem cellsVentricular-subventricular zoneTranscriptional programsMTOR pathway signalingPathway signalingSignaling pathwayNutrient sufficiencyPathwayOlfactory bulb circuitryMTORNeurodevelopmental disordersFunctional cellsGrowth factorNeurogenesisCellsRodent brainStem cellsNarrative reviewTranslational genomics of osteoarthritis in 1,962,069 individuals
Hatzikotoulas K, Southam L, Stefansdottir L, Boer C, McDonald M, Pett J, Park Y, Tuerlings M, Mulders R, Barysenka A, Arruda A, Tragante V, Rocco A, Bittner N, Chen S, Horn S, Srinivasasainagendra V, To K, Katsoula G, Kreitmaier P, Tenghe A, Gilly A, Arbeeva L, Chen L, de Pins A, Dochtermann D, Henkel C, Höijer J, Ito S, Lind P, Lukusa-Sawalena B, Minn A, Mola-Caminal M, Narita A, Nguyen C, Reimann E, Silberstein M, Skogholt A, Tiwari H, Yau M, Yue M, Zhao W, Zhou J, Alexiadis G, Banasik K, Brunak S, Campbell A, Cheung J, Dowsett J, Faquih T, Faul J, Fei L, Fenstad A, Funayama T, Gabrielsen M, Gocho C, Gromov K, Hansen T, Hudjashov G, Ingvarsson T, Johnson J, Jonsson H, Kakehi S, Karjalainen J, Kasbohm E, Lemmelä S, Lin K, Liu X, Loef M, Mangino M, McCartney D, Millwood I, Richman J, Roberts M, Ryan K, Samartzis D, Shivakumar M, Skou S, Sugimoto S, Suzuki K, Takuwa H, Teder-Laving M, Thomas L, Tomizuka K, Turman C, Weiss S, Wu T, Zengini E, Zhang Y, Ferreira M, Babis G, Baras A, Barker T, Carey D, Cheah K, Chen Z, Cheung J, Daly M, de Mutsert R, Eaton C, Erikstrup C, Furnes O, Golightly Y, Gudbjartsson D, Hailer N, Hayward C, Hochberg M, Homuth G, Huckins L, Hveem K, Ikegawa S, Ishijima M, Isomura M, Jones M, Kang J, Kardia S, Kloppenburg M, Kraft P, Kumahashi N, Kuwata S, Lee M, Lee P, Lerner R, Li L, Lietman S, Lotta L, Lupton M, Mägi R, Martin N, McAlindon T, Medland S, Michaëlsson K, Mitchell B, Mook-Kanamori D, Morris A, Nabika T, Nagami F, Nelson A, Ostrowski S, Palotie A, Pedersen O, Rosendaal F, Sakurai-Yageta M, Schmidt C, Sham P, Singh J, Smelser D, Smith J, Song Y, Sørensen E, Tamiya G, Tamura Y, Terao C, Thorleifsson G, Troelsen A, Tsezou A, Uchio Y, Uitterlinden A, Ullum H, Valdes A, van Heel D, Walters R, Weir D, Wilkinson J, Winsvold B, Yamamoto M, Zwart J, Stefansson K, Meulenbelt I, Teichmann S, van Meurs J, Styrkarsdottir U, Zeggini E. Translational genomics of osteoarthritis in 1,962,069 individuals. Nature 2025, 641: 1217-1224. PMID: 40205036, PMCID: PMC12119359, DOI: 10.1038/s41586-025-08771-z.Peer-Reviewed Original ResearchConceptsEffector genesGenome-wide association study meta-analysesTargets of approved drugsVariant associationsTranslational genomicsEpigenomic profilingStudy meta-analysesCircadian clockBiological processesLines of evidenceConditions associated with disabilityRepurposing opportunitiesSignal enrichmentGenesEffectorPathwayIndependent associationsMeta-analysesEffect sizeAccelerated translationEpigenomeTranscriptomeProteomicsDisease-modifying treatmentsOsteoarthritisPhospholipid scramblase 1: a frontline defense against viral infections
Yang A, Norbrun C, Sorkhdini P, Zhou Y. Phospholipid scramblase 1: a frontline defense against viral infections. Frontiers In Cellular And Infection Microbiology 2025, 15: 1573373. PMID: 40248364, PMCID: PMC12003403, DOI: 10.3389/fcimb.2025.1573373.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntiviral AgentsHumansInterferonsPhospholipid Transfer ProteinsSARS-CoV-2Signal TransductionVirus DiseasesVirus ReplicationVirusesConceptsPhospholipid scramblase 1Human immunodeficiency virusInfluenza A virusToll-like receptor 9Human T-cell leukemia virus type 1Epstein-Barr virusHepatitis B virusInterferon-stimulated genesViral infectionHuman cytomegalovirusVirus type 1Antiviral activityTranslocation of phospholipidsFrontline defenseTransactivation of human immunodeficiency virusImmunodeficiency virusActivation of JAK/STAT pathwayImmune cellsSevere acute respiratory syndrome coronavirus 2Acute respiratory syndrome coronavirus 2A virusB virusReceptor 9Respiratory syndrome coronavirus 2Entry of severe acute respiratory syndrome coronavirus 2
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