Matches in DBpedia 2014 for { ?s ?p Leonard (Len) R Stephens FRS (born 18 June 1960) is a molecular biologist, senior group leader and associate director at the Babraham Institute.Len Stephens has contributed much to the understanding of inositol lipids functions in eukaryotic cells, and in particular in neutrophils. Early highlights were the mapping of new pathways of inositol phosphate synthesis.Together with his long-time collaborator Phillip Thomas Hawkins, he established that PtdIns(4,5)P2 is the main substrate of receptor-controlled Type 1 phosphoinositide 3-kinases (PI3Ks), thus identifying PtdIns(3,4,5)P3 as the key output signal produced by this enzyme.They identified and isolated the GPCR-activated Type 1B PI3K (PI3KΥ) and, in a sustained body of work, defined its structure, explained its complex pattern of regulation by GβΥ and Ras, and proved its role in inflammatory events in vivo.They - in parallel with Dario Alessi - identified phosphoinositide-dependent kinase-1 as the PtdIns(3,4,5)P3-activated link between PI3K-1 activation and protein kinase B activation, a key pathway through which PtdIns(3,4,5)P3 formation regulates cell proliferation and survival.. }
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- Leonard_R._Stephens abstract "Leonard (Len) R Stephens FRS (born 18 June 1960) is a molecular biologist, senior group leader and associate director at the Babraham Institute.Len Stephens has contributed much to the understanding of inositol lipids functions in eukaryotic cells, and in particular in neutrophils. Early highlights were the mapping of new pathways of inositol phosphate synthesis.Together with his long-time collaborator Phillip Thomas Hawkins, he established that PtdIns(4,5)P2 is the main substrate of receptor-controlled Type 1 phosphoinositide 3-kinases (PI3Ks), thus identifying PtdIns(3,4,5)P3 as the key output signal produced by this enzyme.They identified and isolated the GPCR-activated Type 1B PI3K (PI3KΥ) and, in a sustained body of work, defined its structure, explained its complex pattern of regulation by GβΥ and Ras, and proved its role in inflammatory events in vivo.They - in parallel with Dario Alessi - identified phosphoinositide-dependent kinase-1 as the PtdIns(3,4,5)P3-activated link between PI3K-1 activation and protein kinase B activation, a key pathway through which PtdIns(3,4,5)P3 formation regulates cell proliferation and survival.".