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Perturbation of the mutated EGFR interactome identifies vulnerabilities and resistance mechanismsStructural coupling of SH2-kinase domains links Fes and Abl substrate recognition and kinase activationThe growing arsenal of ATP-competitive and allosteric inhibitors of BCR-ABLA potent and highly specific FN3 monobody inhibitor of the Abl SH2 domainTargeting the SH2-Kinase Interface in Bcr-Abl Inhibits LeukemogenesisPharmacological targeting of the Wdr5-MLL interaction in C/EBPα N-terminal leukemia.The different functions of Stat5 and chromatin alteration through Stat5 proteinsStat5 regulates cellular iron uptake of erythroid cells via IRP-2 and TfR-1.CD14 is a coreceptor of Toll-like receptors 7 and 9.Using iTRAQ combined with tandem affinity purification to enhance low-abundance proteins associated with somatically mutated EGFR core complexes in lung cancer.Cell size control: new evidence for a general mechanism.STAT3 regulated ARF expression suppresses prostate cancer metastasis.JAK-STAT signaling in cancer: From cytokines to non-coding genome.Affinity purification strategies for proteomic analysis of transcription factor complexes.Systems-pharmacology dissection of a drug synergy in imatinib-resistant CML.Optimisation of Downscaled Tandem Affinity Purifications to Identify Core Protein Complexes.BCR-ABL uncouples canonical JAK2-STAT5 signaling in chronic myeloid leukemia.NVT: a fast and simple tool for the assessment of RNA-seq normalization strategies.Analysis of the interplay between all-trans retinoic acid and histone deacetylase inhibitors in leukemic cells.Erythroid progenitor renewal versus differentiation: genetic evidence for cell autonomous, essential functions of EpoR, Stat5 and the GR.Stat5 is indispensable for the maintenance of bcr/abl-positive leukaemia.Increased survival and cell cycle progression pathways are required for EWS/FLI1-induced malignant transformation.Stat5 activation enables erythropoiesis in the absence of EpoR and Jak2.Acceleration of Bcr-Abl+ leukemia induced by deletion of JAK2.Targeting allosteric regulatory modules in oncoproteins: "drugging the undruggable".STAT5BN642H is a driver mutation for T cell neoplasia.Nilotinib-induced vasculopathy: identification of vascular endothelial cells as a primary target site.Pharmacologic inhibition of STAT5 in acute myeloid leukemia.MLL-fusion-driven leukemia requires SETD2 to safeguard genomic integrity.Dependency on the TYK2/STAT1/MCL1 axis in anaplastic large cell lymphomaErratum: Pharmacological targeting of the Wdr5-MLL interaction in C/EBPα N-terminal leukemiaEvaluation of Stat5 as a potential drug target in bcr/abl-induced leukemiasErratum: STAT3 regulated ARF expression suppresses prostate cancer metastasisOxytocin-like signaling in ants influences metabolic gene expression and locomotor activityCorrection: Increased survival and cell cycle progression pathways are required for EWS/FLI1-induced malignant transformationThe phosphatase UBASH3B/Sts-1 is a negative regulator of Bcr-Abl kinase activity and leukemogenesisDependence on Myb expression is attenuated in myeloid leukaemia with N-terminal CEBPA mutationsRoles of SETD2 in Leukemia-Transcription, DNA-Damage, and BeyondA kinase-independent role for CDK8 in BCR-ABL1+ leukemiaCEBPA-mutated leukemia is sensitive to genetic and pharmacological targeting of the MLL1 complex
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P50
description
hulumtues
@sq
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Florian Grebien
@ast
Florian Grebien
@en
Florian Grebien
@es
Florian Grebien
@nl
Florian Grebien
@sl
type
label
Florian Grebien
@ast
Florian Grebien
@en
Florian Grebien
@es
Florian Grebien
@nl
Florian Grebien
@sl
prefLabel
Florian Grebien
@ast
Florian Grebien
@en
Florian Grebien
@es
Florian Grebien
@nl
Florian Grebien
@sl
P106
P1153
24830329800
P21
P31
P496
0000-0003-4289-2281