Phillip Thomas Hawkins

Phil Hawkins
Residence UK
Nationality British
Fields immunology, signal transduction
Institutions Babraham Institute

Phillip (Phil) Thomas Hawkins FRS[1] (born 5 October 1958) is a molecular biologist, senior group leader at the Babraham Institute.

Phil Hawkins has contributed much to the understanding of inositol lipids functions in eukaryotic cells. Together with his long-time collaborator Leonard R Stephens, 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.[2] 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.[3] 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.[4][5]

Life

Phil Hawkins received a BSc in Biochemistry from the University of Bristol (1980) and a PhD in Biochemistry (1983) from the University of Birmingham. After a post-doctoral training in S.K. & F. Research Ltd, he joined the Molecular Neurobiology unit of the MRC in Cambridge (UK). He joined the AFRC IAPGR (now Babraham Institute) in 1990 and became a group leader in 2003.

Awards and recognition

Phil Hawkins has received several awards, including:

References

  1. ↑ http://royalsociety.org/people/phillip-hawkins/ retrieved February 25, 2014
  2. ↑ P.T. Hawkins, T.R. Jackson, L.R. Stephens (1992) Platelet-derived growth factor stimulates synthesis of Ptdlns(3,4,5)P3 by activating a Ptdlns(4,5)P2 3-OH kinase. Nature 358, 157-159
  3. ↑ L. Stephens, A. Smrcka, F.T. Cooke, T.R. Jackson, P.C. Sternweis, P.T. Hawkins (1994) A novel phosphoinositide 3 kinase activity in myeloid-derived cells is activated by G protein βγ subunits. Cell 77, 83-93
  4. ↑ David Stokoe, Leonard R. Stephens, Terry Copeland, Piers R. J. Gaffney, Colin B. Reese, Gavin F. Painter, Andrew B. Holmes, Frank McCormick, Phillip T. Hawkins (1997) Dual Role of Phosphatidylinositol-3,4,5-trisphosphate in the Activation of Protein Kinase B. Science 277, 567-570
  5. ↑ Len Stephens, Karen Anderson, David Stokoe, Hediye Erdjument-Bromage, Gavin F. Painter, Andrew B. Holmes, Piers R.J. Gaffney, Colin B. Reese, Frank McCormick, Paul Tempst, J. Coadwell, Phillip T. Hawkins (1998) Protein Kinase B Kinases That Mediate Phosphatidylinositol 3,4,5-Trisphosphate-Dependent Activation of Protein Kinase B. Science 279, 710-714

External links

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