Effects of clinically relevant MPL mutations in the transmembrane domain revealed at the atomic level through computational modeling

Mutations in the thrombopoietin receptor (MPL) may activate relevant pathways and lead to chronic myeloproliferative neoplasms (MPNs). The mechanisms of MPL activation remain elusive because of a lack of experimental structures. Modern computational biology techniques were utilized to explore the me...

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Veröffentlicht in:	PloS one 2011-08, Vol.6 (8), p.e23396
Hauptverfasser:	Lee, Tai-Sung, Kantarjian, Hagop, Ma, Wanlong, Yeh, Chen-Hsiung, Giles, Francis, Albitar, Maher
Format:	Artikel
Sprache:	eng
Schlagworte:	Activation Amino Acid Substitution Analysis Atomic structure Biology Computation Computational Biology - methods Computer applications Computer simulation Cytokine receptors Cytokines Dynamic models Genetic aspects Homology Humans Intracellular Janus kinase 2 Janus Kinase 2 - chemistry Janus Kinase 2 - metabolism Kinases Medicine Models, Biological Models, Molecular Molecular Conformation Molecular dynamics Molecular Dynamics Simulation Molecular modelling Molecular structure Mpl protein Mutagenesis Mutants Mutation Myeloproliferative Disorders - genetics Myeloproliferative Disorders - metabolism Myeloproliferative Disorders - pathology Neoplasms Poly-ADP-Ribose Binding Proteins Protein Inhibitors of Activated STAT Protein structure Protein structure prediction Protein Structure, Tertiary Proteins Receptors Receptors, Thrombopoietin - chemistry Receptors, Thrombopoietin - genetics Receptors, Thrombopoietin - metabolism Signal Transduction Signaling STAT Transcription Factors - chemistry STAT Transcription Factors - metabolism Stem cells Thrombopoietin Transmembrane domains
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