2020
Glucocorticoids and serum- and glucocorticoid-inducible kinase 1 are potent regulators of CFTR in the native intestine: implications for stress-induced diarrhea
Ahsan MK, Figueroa-Hall L, Baratta V, Garcia-Milian R, Lam TT, Hoque K, Salas PJ, Ameen NA. Glucocorticoids and serum- and glucocorticoid-inducible kinase 1 are potent regulators of CFTR in the native intestine: implications for stress-induced diarrhea. AJP Gastrointestinal And Liver Physiology 2020, 319: g121-g132. PMID: 32567324, PMCID: PMC7500270, DOI: 10.1152/ajpgi.00076.2020.Peer-Reviewed Original Research14-3-3 ProteinsAnimalsBacterial ToxinsCystic Fibrosis Transmembrane Conductance RegulatorDexamethasoneDiarrheaDimethyl SulfoxideEnterotoxinsEscherichia coli ProteinsGene Expression RegulationImmediate-Early ProteinsMaleNedd4 Ubiquitin Protein LigasesPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProtein TransportProto-Oncogene Proteins c-aktPyruvate Dehydrogenase Acetyl-Transferring KinaseRatsRats, Sprague-DawleySodium-Hydrogen Exchanger 3
2017
Reciprocal regulation of ARPP-16 by PKA and MAST3 kinases provides a cAMP-regulated switch in protein phosphatase 2A inhibition
Musante V, Li L, Kanyo J, Lam TT, Colangelo CM, Cheng SK, Brody AH, Greengard P, Le Novère N, Nairn AC. Reciprocal regulation of ARPP-16 by PKA and MAST3 kinases provides a cAMP-regulated switch in protein phosphatase 2A inhibition. ELife 2017, 6: e24998. PMID: 28613156, PMCID: PMC5515580, DOI: 10.7554/elife.24998.Peer-Reviewed Original ResearchConceptsARPP-16ARPP-19Protein phosphatase 2A inhibitionProtein phosphatase PP2A.Inhibition of PP2ASwitch-like responseKinase inhibitsPhosphatase PP2A.Regulatory interactionsPKA phosphorylationAntagonistic interplayReciprocal regulationBasal phosphorylationPhosphorylationMAST3PP2APKAENSAKinaseStriatal signalingPP2A.Multiple sitesInhibitionMitosisSignaling
2016
MKK3 influences mitophagy and is involved in cigarette smoke-induced inflammation
Mannam P, Rauniyar N, Lam TT, Luo R, Lee PJ, Srivastava A. MKK3 influences mitophagy and is involved in cigarette smoke-induced inflammation. Free Radical Biology And Medicine 2016, 101: 102-115. PMID: 27717867, DOI: 10.1016/j.freeradbiomed.2016.10.001.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsCigarette SmokingGene Expression ProfilingGene Expression RegulationHumansInflammationInterleukin-1betaInterleukin-6MacrophagesMAP Kinase Kinase 3MiceMice, Inbred C57BLMice, KnockoutMitochondriaMitophagyNF-kappa BOxidative PhosphorylationPlant ExtractsPrimary Cell CulturePulmonary Disease, Chronic ObstructiveReactive Oxygen SpeciesTobaccoTumor Necrosis Factor-alphaConceptsCigarette smoke extractCigarette smokeCSE treatmentInflammatory responseLung tissueCigarette smoke-induced inflammationWild typeSerum pro-inflammatory cytokinesSmoke-induced inflammationProgression of COPDMitochondrial dysfunctionReactive oxygen speciesPro-inflammatory cytokinesInflammatory cytokine productionPrimary risk factorAssociated inflammatory responsePatient's lung tissueMouse lung tissueMitochondrial functionDual-specificity protein kinaseRespiratory capacitySpare respiratory capacityAirflow obstructionProtein kinase kinase 3CSE exposure