Peter Jackson Ph.D. Professor of Microbiology & Immunology and of Pathology: Fellow, Stanford Cancer Center, Stanford Chemistry, Engineering and Medicine Institute: Director of Proteomics, Stanford University and Stanford Cancer Center

Research description: Dr. Jackson’s laboratory focuses on identifying biochemical and cell biological mechanisms to identify druggable targets for cancer, tissue regeneration, and human genetic diseases including ciliopathies.  His laboratory first identified cell cycle mechanisms, including control of cyclin A accumulation and S phase by Emi1, a critical inhibitor of the Anaphase Promoting Complex, the E3 ubiquitin ligase for mitotic cyclins.  Later, his laboratory purified and discovered the BBSome, a complex composed of multiple disease proteins from Bardet-Biedl syndrome, providing a consolidated explanation for the disease and a first mechanism explaining GPCR trafficking in cilia.  The lab published the first comprehensive analysis of the nephronophthisis/Joubert/ Meckel-Gruber ciliopathies connecting cystic diseases of the kidney, pancreas and liver to new ciliary trafficking and signaling pathways for G proteins and the Sonic Hedgehog (Shh) pathway.  The lab discovered that the Tubby/Tulp3 family of phosphoinositide binding proteins controlled GPCR trafficking into cilia, leading to the discovery of GPR161, a new GPCR and negative regulator of the Shh pathway.  The lab continues to focus on cystic diseases of the kidney and pancreas and how cystic tissue is a precursor to cancer. Current work includes defining critical GPCRs in renal collecting tubules and pancreatic ducts, and the role these molecules play in renal and pancreatic cancers. 

Dr. Jackson worked for eight years in drug discovery at Genentech, initiating small molecule inhibitor programs for cancer targets related to the cell cycle, tumor metabolism, stress, and KRAS pathways. The group published one of the first KRAS chemical inhibitors and developed inhibitors of p97/VCP, Chk1, NAMPT, and LDHA targets. His current group is using proteomics to build protein networks for Kras signaling in non-small cell lung and pancreatic cancers, two major indications driven by mutation of the Kras oncogene.  A current focus is identifying mechanisms for endocytosis and exocytosis in Kras tumors, the Kras secretome and associated targets in tumor cells.

Dr. Jackson’s group has active collaborations with other members of the PCRG, including Drs. Seung Kim (focusing on cilia in the pancreas), Laura Attardi (using proteomics to explore the p53 tumor suppressor), Max Diehn (identifying key cancer proteins whose genes are found in circulating tumor cells), Monte Winslow (building mouse model for Kras-driven tumors), Amato Giaccia (on hypoxia in tumors), and with Terri Longacre and Stefanie Jeffrey looking for tumor markers by proteomics.

Selected relevant publications (Stanford PCRG members in bold):

  1. Reimann, J. D. R., E. Freed, J. Hsu, E. R. Kramer, J. M. Peters, and P. K. Jackson (2001).  Emi1 is a mitotic regulator that interacts with Cdc20 and inhibits the anaphase promoting complex. Cell 105: 645-55. 

  2. Nachury, M.V., A. V. Loktev., J. F. Bazan, V. C. Sheffield, and P. K. Jackson (2007). A core complex of conserved BBS proteins links phosphoinositide signaling to primary cilium biogenesis. Cell 129, 1201-13.

  3. Mukhopadhyay, S., X. Wen, B. Chih, C. D. Nelson, W. S. Lane, S. J. Scales, and P. K. Jackson (2010). TULP3 bridges the IFT-A complex and the membrane phosphoinosities to promote trafficking of G protein-coupled receptors into primary cilia.  Genes & Development. 24:2180-93.

  4. Sang, L., et. al J. F. Reiter, and P. K. Jackson (2011). Mapping the NPHP-JBTS-MKS Protein Network Reveals Ciliopathy Disease Genes and Pathways. Cell 145: 513-28.

  5. Maurer, T., et. al, P. K. Jackson, J. Rudolph, W. Wang, and G. Fang (2012). Small molecule ligands bind to a malleable pocket in Ras and inhibit its nucleotide exchange.  Proc. Natl. Acad. Sci. USA 109: 5299-304.

  6. Mukhopadhyay, S., X. Wen, Ratti N, Loktev A, Rangell L, S. J. Scales, and P. K. Jackson (2013). The ciliary G-protein-coupled receptor Gpr161 negatively regulates the Sonic hedgehog pathway via cAMP signaling.  Cell 152: 210-23.

  7. Tomoharu Kanie, Keene L Abbott, Nancie Ann Mooney, Edward Douglas Plowey, Janos Demeter, Peter K Jackson (2017).  The CEP19-RABL2 GTPase complex binds IFT-B to initiate intraflagellar transport at  the ciliary base.  Developmental Cell, 42:22-36.

  8. Elizabeth Y. Qin, et. al, Hannes Vogel, Peter K.  Jackson, Michelle Monje (2017).  Glioma Invasion of the Subventricular Zone is Mediated by Neural Precursor Cell-Derived Pleiotrophin, Cell 70:845-859.