• Laurie Cook Ph.D.
  • Assistant Professor
  • email: lcook@brockport.edu
  • Lennon Hall, Room 217, Tel: 395-5757

The goal of our laboratory is to understand the cellular mechanisms underlying hormonal signaling through G protein-coupled receptors (GPCRs). Abnormal receptor signaling can lead to cancer or disease, such as obesity. Our current work focuses on learning how cells turn off melanin-concentrating hormone signaling pathways using tissue culture cells. We use both fluorescence microscopy and biochemical assays to achieve our objectives.

Research Description

My research interests can be best summarized as a desire to understand the cellular mechanisms involved in the regulation of endocrine signaling as it relates to cancer and disease. G protein-coupled receptors (GPCRs) are the largest superfamily of transmembrane proteins and regulate a wide variety of biological processes that include sensory perception, cardiovascular, immune and endocrine responses. Compromising mutations in GPCRs are responsible for diseases that include nephrogenic diabetes insipidus and retinitis pigmentosa. The goal of my laboratory is to further the understanding of G protein-coupled receptor processing, trafficking, signaling, and degradation so that novel pharmacological targets and treatments can be identified.

Melanin-concentrating hormone (MCH) was initially discovered as a hormone that induces skin lightening in teleost fish many years ago. MCH does this by causing the aggregation of melanophores in skin cells towards the inner parts of the cell. In mammals, however, MCH seems to play a much more complicated role in appetite suppression and energy expenditure via receptors localized to different regions of the brain. Humans carry two receptors for MCH. Mice lacking MCH receptor 1 seem to be somewhat protected from diet-induced obesity. This makes the MCH receptor a possible target for anti-obesity medication and, therefore, it is actively being pursued by numerous pharmaceutical companies.

Little is known about how the two receptors, MCHR1 and MCHR2, are regulated by cells. GPCRs typically undergo desensitization following agonist binding in order to prevent aberrant signaling and overstimulation of the cell. This process generally involves phosphorylation of the receptor, recruitment of beta-arrestin and internalization of the receptor-agonist complex. Desensitization may also involve degradation of the receptor. Resensitization of cells may take minutes or hours, depending upon the method of receptor renewal. The MCH receptors are known to transmit signals to downstream G proteins, however signal desensitization and receptor trafficking are poorly understood. Additionally, cytoskeletal changes must take place in order for these events to take place. We are interested in determining the molecules responsible for cytoskeletal remodeling in response to MCH. In my laboratory, we will use biochemical methods and fluorescence microscopy to address these issues using a tissue culture model system.


1. Cook LB, Shum L and Portwood S. Melanin-concentrating hormone facilitates migration of preadipocytes. Mol Cell Endo. 320: 45-50 (2010)
2. Gehret AU, Jones BW, Tran PN, Cook LB, Greuber EK, and Hinkle PM. Role of Helix 8 of the Thyrotopin-releasing hormone receptor in phosphorylation by G protein-coupled receptor kinase. Mol Pharmacol 77: 288-97 (2009)
3. Cook LB, Delorem-Axford EB and Robinson K. Caveolae as potential mediators of MCH-signaling pathways. Biochem Biophys Res Coomun. 375: 592-5 (2008)
4. Cook LB and Hinkle PM. Fate of internalized thyrotropin-releasing hormone receptors monitored with a timer fusion protein. Endocrinology. 145: 3095-100 (2004)

Research Pictures