Dr. Jackson is Professor in the Baxter Laboratory, Department of Microbiology and Immunology and Department of Pathology at Stanford University School of Medicine.  He received a BA in Mathematics and Economics from Yale College before pursuing graduate work in Chemical Physics and receiving a PhD in Biophysics from Harvard University, completing his thesis on tyrosine kinase signaling with David Baltimore at MIT’s Whitehead Institute.   Following postdoctoral work at UCSF and Harvard Medical School with Mark Kirschner, studying the cell cycle, Dr. Jackson joined the faculty at Stanford in 1995. His laboratory focuses on the biochemical and cell biological mechanisms controlling cell division, signaling, metabolic disease and cancer.  These disease studies are driven by using affinity purification/mass spectrometry construction of protein interaction networks, phosphoproteomics, quantitative imaging, and molecular studies. The lab has made discoveries of regulatory complexes and signaling in the cell cycle (Emi1, CDC14, p21-PCNA interaction, cyclin E/Cdk2), ubiquitin-dependent proteolysis (CDC34/SCF, APC), cancer (Abl, SH2/SH3, KRAS), signaling within the primary cilium and the link between cilia and human genetic diseases including Bardet-Biedl and Joubert syndromes (the BBSome, the NPHP network, Tubby/Tulp3 trafficking of ciliary GPCRs, the Arl3 and Rabl2 trafficking pathways).  

Dr. Jackson spent from 2005 to 2013 at Genentech, where he was a Director and Staff Scientist focused on validation of targets and drug discovery for cancer chemotherapy and tumor metabolism creating new small molecule inhibitors of Chk1, PARP, LDHA, NAMPT, Plk1, the first direct inhibitor of KRAS and the first allosteric inhibitor of the VCP AAA ATPase. 

He is currently focused on understanding core mechanisms driving adipogenesis and lipotoxicity in the context of ciliary signaling and using protein networks to find mechanisms and targets human genetic diseases, especially metabolic disease.  The lab has recently focused on finding key ciliary GPCRs in tissues important for obesity and metabolism including the hypothalamus, preadipocyte, muscle stem cell and endocrine pancreas.    

In March 2020, in response to the COVID-19 pandemic, the lab began to study SARS-CoV-2 discovering importance of airway cilia for presenting the ACE2 receptor and a new, fundamental pathway for how SARS-CoV-2 and other respiratory viruses cross the multiciliated airway to establish infection.  The group also showed how the virus attacks pancreatic beta cells to induce diabetes in patients with severe COVID-19 disease.  He is the founder and faculty advisor for the Stanford University Mass Spectrometry lab and directs mass spectrometry for the Stanford Cancer Center and a member of the Stanford Diabetes Center, the Stanford Cancer Center, and the Maternal and Child Health Initiative.  He has been a collaborator with Rigel, Signal, Goldfinch Biopharma, Calico and Pfizer and has been on the Scientific Advisory Board for Celgene, Juvena Therapeutics and Cullgen.  He is a longstanding member of the ASCB, has organized sessions and FASEB and Keystone meetings, Gordon Conferences on cilia, cancer and cell cycle, review broadly for major journals and has given over 400 public lectures.   He was elected as a Fellow of the American Association for the Advancement of Science (2008), the American Association of University Pathologists (Pluto Society), and Sigma Xi.