Brooke Emerling's Research Focus
Research in the Emerling Lab is focused on understanding key signaling and metabolic pathways involved in the regulation of cellular function under pathological conditions such as cancer. Our research program centers around dissecting the roles of the family of non-canonical phosphatidylinositol kinases, called the phosphatidylinositol-5-phosphate 4-kinases (PI5P4Ks), in cancer metabolism using a multi-disciplinary approach integrating human, mouse, and worm models. Currently, a major research project in the Emerling Lab is determining the role of the PI5P4Ks in p53 mutant cancers, especially the triple-negative breast cancer subgroup where targeted therapies have not been effective.
Brooke Emerling's Bio
Emerling received her B.A. from the University of California Santa Cruz and her Ph.D. in molecular and cellular biology from Northwestern University. Emerling did her postdoctoral training at Harvard Medical School. She then became an Instructor of Cancer Biology in Medicine at Weill Cornell Medical College in New York City, where she continued her research on lipid kinase signaling and cancer metabolism. In August 2016, Brooke joined the faculty at SBP Medical Discovery Institute as an Assistant Professor in the Cancer Metabolism and Signaling Networks Program.
Funding Awards and Collaborative Grants
Breast Cancer Research Foundation - AACR Career Development Award for Translational Breast Cancer Research
Mary Kay Foundation Innovative Translational Grant Award
Department of Defense Breast Research Program Breakthrough Award
Honors and Recognition
2014: NextGen Star – AACR Early-Career Speaker Award
2013-2016: Mastercard Ajay Banga Scientist Award
2013: AACR – Aflac Travel Fellowship Award
Phosphatidylinositol-5-Phosphate 4-Kinases Regulate Cellular Lipid Metabolism By Facilitating Autophagy.
Lundquist MR, Goncalves MD, Loughran RM, Possik E, Vijayaraghavan T, Yang A, Pauli C, Ravi A, Verma A, Yang Z, Johnson JL, Wong JCY, Ma Y, Hwang KS, Weinkove D, Divecha N, Asara JM, Elemento O, Rubin MA, Kimmelman AC, Pause A, Cantley LC, Emerling BM
Mol Cell 2018 May 3 ;70(3):531-544.e9
Sumita K, Lo YH, Takeuchi K, Senda M, Kofuji S, Ikeda Y, Terakawa J, Sasaki M, Yoshino H, Majd N, Zheng Y, Kahoud ER, Yokota T, Emerling BM, Asara JM, Ishida T, Locasale JW, Daikoku T, Anastasiou D, Senda T, Sasaki AT
Mol Cell 2016 Jan 21 ;61(2):187-98
Depletion of a putatively druggable class of phosphatidylinositol kinases inhibits growth of p53-null tumors.
Emerling BM, Hurov JB, Poulogiannis G, Tsukazawa KS, Choo-Wing R, Wulf GM, Bell EL, Shim HS, Lamia KA, Rameh LE, Bellinger G, Sasaki AT, Asara JM, Yuan X, Bullock A, Denicola GM, Song J, Brown V, Signoretti S, Cantley LC
Cell 2013 Nov 7 ;155(4):844-57
PI5P4Kα supports prostate cancer metabolism and exposes a survival vulnerability during androgen receptor inhibition.
Triscott J, Reist M, Küng L, Moselle FC, Lehner M, Gallon J, Ravi A, Arora GK, de Brot S, Lundquist M, Gallart-Ayala H, Ivanisevic J, Piscuoglio S, Cantley LC, Emerling BM, Rubin MA
Sci Adv 2023 Feb 3 ;9(5):eade8641
Llorente A, Arora GK, Grenier SF, Emerling BM
Adv Biol Regul 2023 Jan ;87:100939
Burke JE, Triscott J, Emerling BM, Hammond GRV
Nat Rev Drug Discov 2022 Nov 14 ;:1-30
Amen AM, Loughran RM, Huang CH, Lew RJ, Ravi A, Guan Y, Schatoff EM, Dow LE, Emerling BM, Fellmann C
Cell Rep Methods 2022 Jul 18 ;2(7):100239
Crucial Players for Inter-Organelle Communication: PI5P4Ks and Their Lipid Product PI-4,5-P(2) Come to the Surface.
Ravi A, Palamiuc L, Emerling BM
Front Cell Dev Biol 2021 ;9:791758
Loughran RM, Emerling BM
Adv Biol Regul 2022 Jan ;83:100839