Picture of Phil Cole

Philip A. Cole, M.D., Ph.D.

Professor of Medicine and Biological Chemistry and Molecular Pharmacology

Our research involves the chemical biology of protein post-translational modifcations (PTMs) in the context of signaling, epigenetics, and cancer.  We develop and apply chemical approaches including protein semisynthesis and small molecule probes to the study of protein phosphorylation, acetylation, ubiquitination, and other PTMs in enzymes and cellular networks. 

Phil Cole graduated from Yale University with a B.S. in Chemistry in 1984 and then spent a year as a Churchill Scholar at the University of Cambridge.  Cole went on to obtain M.D. and Ph.D. degrees from Johns Hopkins where he pursued research in bioorganic chemistry in 1991.  Cole then entered clinical and post-doctoral training at Brigham and Women's Hospital and Harvard Medical School prior to joining Rockefeller University in 1996 as a junior lab head.  In 1999, Cole returned to Johns Hopkins as professor and director of pharmacology where he served until 2017, when he moved to Harvard Medical School and Brigham and Women's Hospital as professor of medicine and biological chemistry and molecular pharmacology.  His research interests are in the area of chemical biology, protein post-translational modifications, cell signaling, and epigenetics.

Research:

Our research involves the chemical biology of protein post-translational modifcations (PTMs) in the context of signaling, epigenetics, and cancer.  We develop and apply chemical approaches including protein semisynthesis and small molecule probes to the study of protein phosphorylation, acetylation, ubiquitination, and other PTMs in enzymes and cellular networks.  We are currently investigating the functions, regulation, and mechanisms of PTEN lipid phosphatase, Akt protein kinase, NEDD4 ubiquitin ligases, LSD1 histone demethylase, HDAC1 deacetylase, the CoREST complex, and p300/CBP acetyltransferase.  We strive to translate our findings in signaling and epigenetics to identify novel therapeutic opportunities for the treatment of cancer and other diseases.

Address: 

New Research Building

77 Avenue Louis Pasteur

Room 168C

Boston, MA 02115

Publications View
Csk, a critical link of g protein signals to actin cytoskeletal reorganization.
Authors: Authors: Lowry WE, Huang J, Ma YC, Ali S, Wang D, Williams DM, Okada M, Cole PA, Huang XY.
Dev Cell
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Serotonin N-acetyltransferase: mechanism and inhibition.
Authors: Authors: Zheng W, Cole PA.
Curr Med Chem
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Proton demand inversion in a mutant protein tyrosine kinase reaction.
Authors: Authors: Williams DM, Cole PA.
J Am Chem Soc
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Investigation of the roles of catalytic residues in serotonin N-acetyltransferase.
Authors: Authors: Scheibner KA, De Angelis J, Burley SK, Cole PA.
J Biol Chem
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Retinoids and carnosol suppress cyclooxygenase-2 transcription by CREB-binding protein/p300-dependent and -independent mechanisms.
Authors: Authors: Subbaramaiah K, Cole PA, Dannenberg AJ.
Cancer Res
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X-ray crystallographic studies of serotonin N-acetyltransferase catalysis and inhibition.
Authors: Authors: Wolf E, De Angelis J, Khalil EM, Cole PA, Burley SK.
J Mol Biol
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Impact of the American anti-smoking campaign on lung cancer mortality.
Authors: Authors: Rodu B, Cole P.
Int J Cancer
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DNA damage-dependent acetylation of p73 dictates the selective activation of apoptotic target genes.
Authors: Authors: Costanzo A, Merlo P, Pediconi N, Fulco M, Sartorelli V, Cole PA, Fontemaggi G, Fanciulli M, Schiltz L, Blandino G, Balsano C, Levrero M.
Mol Cell
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Designing bisubstrate analog inhibitors for protein kinases.
Authors: Authors: Parang K, Cole PA.
Pharmacol Ther
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Chromatin-dependent cooperativity between constitutive and inducible activation domains in CREB.
Authors: Authors: Asahara H, Santoso B, Guzman E, Du K, Cole PA, Davidson I, Montminy M.
Mol Cell Biol
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