2016
Targeting KIT on innate immune cells to enhance the antitumor activity of checkpoint inhibitors
Stahl M, Gedrich R, Peck R, LaVallee T, Eder JP. Targeting KIT on innate immune cells to enhance the antitumor activity of checkpoint inhibitors. Immunotherapy 2016, 8: 767-774. PMID: 27349976, DOI: 10.2217/imt-2016-0040.Peer-Reviewed Original ResearchConceptsMyeloid-derived suppressor cellsInnate immune cellsCheckpoint inhibitorsSuppressor cellsImmune cellsMast cellsImmune checkpoint inhibitorsAntitumor immune responseImmune cell numbersReceptor tyrosine kinase KITDurable responsesMelanoma patientsClinical benefitTyrosine kinase KITCancer patientsPreclinical dataPoor survivalImmune responseSuppressive componentsImmune systemKIT inhibitorsTumor microenvironmentAntitumor activityKinase KITRecent evidenceLost in translation? Ten years of development of histone deacetylase inhibitors in acute myeloid leukemia and myelodysplastic syndromes
Stahl M, Gore SD, Vey N, Prebet T. Lost in translation? Ten years of development of histone deacetylase inhibitors in acute myeloid leukemia and myelodysplastic syndromes. Expert Opinion On Investigational Drugs 2016, 25: 307-317. PMID: 26807602, DOI: 10.1517/13543784.2016.1146251.BooksConceptsHistone deacetylase inhibitorsAcute myeloid leukemiaMyeloid malignanciesMyelodysplastic syndromeMyeloid leukemiaDeacetylase inhibitorsSelection of patientsFuture clinical developmentClinical resultsDNA methyltransferase inhibitorClinical developmentSingle agentHDAC inhibitorsRobust biomarkersPleiotropic activitiesMalignancyPotential targetCancer therapyMethyltransferase inhibitorSyndromeLeukemiaInhibitorsEpigenetic modifiersEpigenetic changesMyeloma
2015
ANP and CNP activate CFTR expressed in Xenopus laevis oocytes by direct activation of PKA
Stahl K, Stahl M, de Jonge HR, Forrest JN. ANP and CNP activate CFTR expressed in Xenopus laevis oocytes by direct activation of PKA. Journal Of Receptors And Signal Transduction 2015, 35: 493-504. PMID: 26016495, DOI: 10.3109/10799893.2015.1015738.Peer-Reviewed Original Researchactive and inactive
2011
Divergent CFTR orthologs respond differently to the channel inhibitors CFTRinh-172, glibenclamide, and GlyH-101
Stahl M, Stahl K, Brubacher MB, Forrest JN. Divergent CFTR orthologs respond differently to the channel inhibitors CFTRinh-172, glibenclamide, and GlyH-101. American Journal Of Physiology - Cell Physiology 2011, 302: c67-c76. PMID: 21940661, PMCID: PMC3328903, DOI: 10.1152/ajpcell.00225.2011.Peer-Reviewed Original ResearchConceptsCystic fibrosis transmembrane conductance regulatorGlyH-101Expression studiesChannel proteinsCFTR chloride channel proteinFibrosis transmembrane conductance regulatorChloride channel proteinSite-directed mutagenesisShark rectal glandAmino acid residuesTransmembrane conductance regulatorDifferent orthologsSingle amino acidPrevious site-directed mutagenesisOocyte expression studiesThree-dimensional structureRegulatory regionsXenopus laevis oocytesCFTR proteinAdditional residuesConductance regulatorOrthologsAcid residuesRectal glandSpecific inhibitor
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