2023
Computational Random Mutagenesis to Investigate RAS Mutant Signaling
Stites E. Computational Random Mutagenesis to Investigate RAS Mutant Signaling. Methods In Molecular Biology 2023, 2634: 329-335. PMID: 37074586, PMCID: PMC10530643, DOI: 10.1007/978-1-0716-3008-2_15.Peer-Reviewed Original Research
2021
Identification of RAS mutant biomarkers for EGFR inhibitor sensitivity using a systems biochemical approach
McFall T, Stites E. Identification of RAS mutant biomarkers for EGFR inhibitor sensitivity using a systems biochemical approach. Cell Reports 2021, 37: 110096. PMID: 34910921, PMCID: PMC8867612, DOI: 10.1016/j.celrep.2021.110096.Peer-Reviewed Original ResearchConceptsSensitivity to EGFR inhibitionSubsets of mutationsRAS mutationsKRAS G13DCancer cell biologyEGFR inhibitionEpidermal growth factor receptor (EGFR)-targeted therapyTumor suppressor neurofibrominGene-basedBiophysical biomarkersInhibitor sensitivityCell biologyMutationsPersonalized medicineBiomarker strategiesKRAS mutantRasCancer treatmentKRASNF1BiomarkersBiophysical characteristicsG13DMutantsInhibitionMathematical Modeling to Study KRAS Mutant-Specific Responses to Pathway Inhibition
Stites E. Mathematical Modeling to Study KRAS Mutant-Specific Responses to Pathway Inhibition. Methods In Molecular Biology 2021, 2262: 311-321. PMID: 33977486, PMCID: PMC8639139, DOI: 10.1007/978-1-0716-1190-6_19.Peer-Reviewed Original ResearchConceptsRegulates Ras signalingMutant Ras proteinsKRAS G13D mutationRas proteinsRAS communityRas mutantsRas signalingRas pathwayBiochemical reactionsWild-typeRasMutationsPathway inhibitionG13D mutationDose-response experimentsMutantsKnowledge of reaction mechanismsInhibitionEGFR inhibitionKRAS mutationsProteinKRAS
2020
Abstract 37: Computational analysis of the KRAS G13D colorectal cancer response to EGFR inhibition with an alternatively parameterized model
McFall T, Stites E. Abstract 37: Computational analysis of the KRAS G13D colorectal cancer response to EGFR inhibition with an alternatively parameterized model. Clinical Cancer Research 2020, 26: 37-37. DOI: 10.1158/1557-3265.advprecmed20-37.Peer-Reviewed Original ResearchColon cancer cellsMultiple colon cancer cell linesBiochemical rate constantsCancer cellsColon cancer cell linesCell linesResponse to EGFR inhibitionKRAS mutantRAS biologyCancer cell linesRas signalingEGFR inhibitionMedicinal drug developmentSignaling regulationComputational analysisPersonalized cancer medicineMutantsG13D mutantWild-typeCombination of computational modelingEGFR inhibitor cetuximabColorectal cancer patientsDrug developmentCellsCancer medicine
2018
Quantitative Systems Pharmacology Analysis of KRAS G12C Covalent Inhibitors
Stites E, Shaw A. Quantitative Systems Pharmacology Analysis of KRAS G12C Covalent Inhibitors. CPT Pharmacometrics & Systems Pharmacology 2018, 7: 342-351. PMID: 29484842, PMCID: PMC5980551, DOI: 10.1002/psp4.12291.Peer-Reviewed Original ResearchConceptsRegulates Ras activitySystems biology approachBiology approachRas activationProtein turnoverKRAS-G12C covalent inhibitorsKRAS G12C inhibitorsSystems pharmacology analysisRasKRAS mutantDrug developmentG12C inhibitorsCovalent inhibitorsInhibitorsKRASMutantsPharmacological analysisMutationsKRAS G12C
2015
Cooperation between Noncanonical Ras Network Mutations
Stites E, Trampont P, Haney L, Walk S, Ravichandran K. Cooperation between Noncanonical Ras Network Mutations. Cell Reports 2015, 10: 307-316. PMID: 25600866, PMCID: PMC4503519, DOI: 10.1016/j.celrep.2014.12.035.Peer-Reviewed Original ResearchCollection of mutationsRAS pathway mutationsRas signaling networkGenomic data setsPathway mutationsTumor suppressor gene NF1Combinations of mutationsRandom mutagenesisRas mutantsNetwork genesSignaling networksGene NF1Genomic instabilityCancer phenotypeNF1 mutationsMutationsPromote cancerRasMutated cancersIncreased co-occurrenceMutantsMutagenesisGenesPhenotypeNF1
2013
Allosteric Activation of Functionally Asymmetric RAF Kinase Dimers
Hu J, Stites E, Yu H, Germino E, Meharena H, Stork P, Kornev A, Taylor S, Shaw A. Allosteric Activation of Functionally Asymmetric RAF Kinase Dimers. Cell 2013, 154: 1036-1046. PMID: 23993095, PMCID: PMC3844432, DOI: 10.1016/j.cell.2013.07.046.Peer-Reviewed Original ResearchMeSH KeywordsAllosteric RegulationAmino Acid MotifsAmino Acid SequenceAnimalsCell LineDimerizationEnzyme ActivationHumansMiceModels, MolecularMolecular Sequence DataMutationPhosphorylationProtein ConformationProtein KinasesProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-rafRaf KinasesSequence AlignmentTryptophanConceptsN-terminal phosphorylationReceiver kinaseRaf kinaseActivation-loop phosphorylationPhosphorylation of CRAFConstitutively active mutantCis-autophosphorylationRaf activationActive mutantActivated CRAFActive kinaseMechanism of activationKinase activityActive conformationKinasePhosphorylationControl cellsRafCRAFDimerMutantsRasActivityMEKBRAF
2012
Mathematical Investigation of How Oncogenic Ras Mutants Promote Ras Signaling
Stites E, Ravichandran K. Mathematical Investigation of How Oncogenic Ras Mutants Promote Ras Signaling. Methods In Molecular Biology 2012, 880: 69-85. PMID: 23361982, DOI: 10.1007/978-1-61779-833-7_5.Peer-Reviewed Original Research
2010
Modeling Membrane Localization: Case Study of a Ras Signaling Model
Stites E. Modeling Membrane Localization: Case Study of a Ras Signaling Model. Advances In Experimental Medicine And Biology 2010, 680: 661-667. PMID: 20865552, DOI: 10.1007/978-1-4419-5913-3_73.Peer-Reviewed Original Research