Allison L. Brill

Allison L. Brill, PhD

Technology Specialist | Biotechnology
617.646.8395 LinkedIn Profile


  • BS, Genetics, University of Wisconsin
  • PhD, Cellular and Molecular Physiology, Yale University

Key Technologies

  • Cell Biology
  • Molecular Metabolism
  • Pathology
  • Physiology
  • Pharmacology
  • Diabetes
  • Immune Regulation of Liver Disease 
  • Optical Phenotyping
  • Genetic Screens
  • Disease Models

Practice Groups


  • Boston


Allison Brill assists the firm in biotechnology patent prosecution. Allison has extensive knowledge in the areas of cell biology, molecular metabolism, pathology, physiology, pharmacology, diabetes, and liver disease.

Prior to joining Wolf Greenfield, Allison trained as a postdoctoral associate at Pfizer and the Broad Institute of MIT and Harvard, where she studied genetic causes of immune-mediated fatty liver disease and helped develop new technologies in optical phenotyping. Allison earned her PhD from Yale University’s Department of Cellular & Molecular Physiology. Her research focused on calcium-mediated regulation of mitophagy in non-alcoholic fatty liver disease as well as mitochondrial dysfunction in kidney disease.


  • NIDDK F31 National Research Service Award Individual Predoctoral Fellowship
  • Molecular Endocrinology Award for Outstanding Publication of 2016


Scientific Publications

  • Carpio, M.A.*, Means, R.E.*, Brill, A.L., Sainz, A., Ehrlich, B.E., and Katz, S.G. (2021). “BOK controls apoptosis by calcium transfer through ER- mitochondrial contact sites.” Cell Rep. 34(10):108827.
  • Schaid, M.D., Green, C.L., Peter, D., Gallagher, S., Guthery, E.E., Carbajal, K.A., Harrington, J.M., Kelly, G.M., Reuter, A.J., Wehner, M.L., Brill, A.L., Neuman, J.C., Lamming, D.W., and Kimple, M.E. (2021). “Agonist-independent Gαz activity negatively regulates β-cell compensation in a diet-induced obesity model of type 2 diabetes.” J Biol Chem. 296:100056.
  • Truchan, N.A., Fenske, F.J., Sandhu, H.K., Weeks, A.M., Patibandla, C., Wancewicz, B., Pabich, S., Reuter, A., Harrington, J.M., Brill, A.L., Peter, D.C., Nall, R., Daniels, M., Punt, M., Kaiser, C.E., Cox, E.D., Ge, Y., Davis, D.B.*, and Kimple, M.E.* (2021). “Human islet expression levels of Prostaglandin E2 synthetic enzymes, but not Prostaglandin EP3 Receptor, are positively correlated with markers of b-cell function and mass in nondiabetic obesity.” ACS Pharmacology & Translational Science. 4 (4), 1338-1348.
  • Brill, A. L., Fischer, T.T., Walters, J.M., Marlier, A., Sewanan, L.R., Robert, M.E., Wilson, P.C., Chung, H.J., Campbell, S.G., Cantley, L.G., and Ehrlich, B.E. (2020). "Polycystin 2 is increased in disease to protect against stress-induced cell death." Sci Rep. 10(1): 386.
  • Perry, R.J., Zhang, D., Guerra, M.T., Brill, A.L., Goedeke, L., Nasiri, A.R., Rabin-Court, A., Wang, Y., Peng, L., Dufour, S., Zhang, Y., Zhang, X.M., Butrico, G.M., Toussaint, K., Nozaki, Y., Cline, G.W., Petersen, K.F., Nathanson, M.H., Ehrlich, B.E., and Shulman, G.I. (2020). “Glucagon stimulates gluconeogenesis by InsP3R-I mediated hepatic lipolysis.” Nature 579(7798): 279-283.
  • Grosshans, H.K., Fischer, T.T., Steinle, J.A., Brill, A.L., and Ehrlich, B.E. (2020). “Neuronal Calcium Sensor 1 is up-regulated in response to stress to promote cell survival and motility in cancer cells.” Mol Oncol. doi: 10.1002/1878-0261.12678.
  • Ng, R., Sewanan, L.R., Brill, A.L., Stankey, P., Li, X., Qyang, Y., Ehrlich, B.E., and Campbell, S.G. (2020). "Contractile work directly modulates mitochondrial protein levels in human engineered heart tissues." American journal of physiology. Heart and circulatory physiology 318(6): H1516-h1524.
  • Brill, A.L.*, Kuo, I.Y*., Lemos, F.O., Jiang, J.Y., Falcone, J.L., Kimmerling, E.P., Cai, Y., Dong, K., Kaplan, D.L., Wallace, D.P., Hofer, A.M., and Ehrlich, B.E. (2019). “Polycystin 2 regulates mitochondrial calcium signaling, bioenergetics, and dynamics through mitofusin 2.” Sci Signaling. 12, eaat7397.
  • Neuman, J.C., Schaid, M.D., Brill, A.L., Fenske, R.J., Kibbe, C.R., Fontaine, D.A., Sdao, S.M., Brar, H.K., Connors, K.M., Wienkes, H.N., Eliceiri, K.W., Merrins, M.J., Davis, D.B., and Kimple, M.E. (2017). “Enriching Islet Phospholipids with Eicosapentaenoic Acid Reduces Prostaglandin E2 Signaling and Enhances Diabetic b-Cell Function.” Diabetes. 66(6):1572-1585.
  • Fenske, R.J., Cadena, M.T., Harenda, Q.E., Wienkes, H.N., Carbajal, K., Schaid, M.D., Laundre, E., Brill, A.L., Truchan, N.A., Brar, H.K., Wisinski, J.A., Jinjin, C., Graham, T.E., Engin, F., and Kimple, M.E. (2017). “The Inhibitory G-protein α-subunit, Gαz, promotes Type 1 diabetes-like pathophysiology in NOD mice.” Endocrinology. 158(6):1645-1658.
  • Brill, A.L., Wisinski, J.A., Cadena, M.T., Thompson, M.F., Fenske, R.J., Brar, H.K., Schaid, M.D., Pasker, R.L., and Kimple, M.E. (2016). “Synergy Between Gαz Deficiency and GLP-1 Analog Treatment in Preserving Functional b-Cell Mass in Experimental Diabetes.” Mol Endocrinol. 30(5):543-556.
  • Pierre, J.F.*, Neuman, J.C.*, Brill, A.L., Brar, H.K., Thompson, M.F., Cadena, M.T., Connors, K.M., Busch, R.A., Heneghan, A.F., Cham, C.M., Jones, E.K., Groblewski, G.E., Chang, E.B., and Kudsk, K.A., Kimple, M.E. (2015). “The Gastrin Releasing Peptide Analog, Bombesin, Preserves the Exocrine Pancreas and Enteroendocrine Cell-Pancreas Axis during Parenteral Nutrition.” Am J Physiol: Gastrointest. Liver Physiol. 309(6):G431-442.


Tennis, baking, travel, and finding fun spots to eat new foods!