When Barbara Alving, the former head of National Center for Research Resources (NCRR), spoke at Harvard last spring, an audience member complained that even Harvard’s superstar scientists couldn’t get NIH grants. Alving, whose NIH agency was about to be shuttered suggested scientists get used to it – NIH funding would be tight for a while.
A search on the NIH data base proves her right. While the agency funded 403 new projects in Massachusetts in 2010, that number dropped to 335 in 2011.
Does that make the grant winners super superstars? Or was the research in the labs at the right place at the right time? So many variables go into NIH funding, it can be hard to tell. Still it’s worth looking at where the money is going.
The 11 new winners so far for 2012 are looking into influenza, herpes, DNA replication timing, structural vaccinology for malaria and the search for biologically active antitumor and anti-infective agents in natural products. Our data is current as of this morning, but the numbers change constantly as NIH adds new grants to the database. Grants went to Boston University, UMass med school and Brandeis University. But, Harvard-linked researchers – and infectious disease — dominate the list.
At $530,282, the biggest new grant so far this year went to Harvard chemist Suzanne L. Walker for research into the “structure, function and inhibition of human o-glcnac transferase.”
From the application: “O-GlcNAc transferase (OGT) is an essential mammalian enzyme that catalyzes a unique post-translational modification, O-GlcNAcylation. This modification mediates critical cellular processes involved in nutrient signaling, stress responses, and cell division. Aberrant O-GlcNAcylation has been linked to many diseases, and the work proposed here will lead to the development of small molecule inhibitors to probe OGT’s biological roles and potential as a therapeutic target.”
Harvard is also offering dibs on her finding to drug developers through the school’s tech transfer program.
Walker’s group is currently investigating the target specificity of one class of inhibitor.These compounds will be useful as cellular probes of OGT biology. In parallel with these efforts, the group is optimizing another class of OGT inhibitors. Through a combination of analog synthesis and structure-based design, this class of OGT inhibitor has sub-micromolar IC50, is non-toxic to mammalian cells, and inhibits OGT activity in HEK cells. More on that here.
Coming in second for January 2012 is another Harvard project, Samuel Behar’s work on TB immunity, which won a $528,749 grant.
From the application : Apoptosis and efferocytosis: Regulators of immunity to tuberculosis. Pulmonary tuberculosis, a disease caused by Mycobacterium tuberculosis, is a threat to global health. The disease tuberculosis occurs when the immune system is no longer able to contain the infection. This research proposal seeks to understand how the immune system controls the infection. In addition we seek to determine whether the mechanisms that generate T cell immunity can be enhanced to improve the response to vaccines. Since T cell immunity is important for the control of tuberculosis, it is hoped that by understanding features of host resistance, new strategies can be developed for the treatment and prevention of tuberculosis.
Herpes simplex viruses cause considerable genital, ocular and nervous system disease, and genital herpes increases the risk of HIV infection. There are drugs that target the active growth of herpes simplex virus but none that target the latent infection. This research will define basic mechanisms of herpes simplex virus latent infection and new targets for potential drugs to treat the latent infection of these viruses.