Joaquin Espinosa

Associate Professor
HHMI Early Career Scientist

Photo of Joaquin Espinosa

Joaquin.Espinosa@Colorado.EDU
Phone: (303) 492-2857
EXT: 2-2857
LAB: 5-6610

Websites

Espinosa Lab

HHMI Research

HHMI Biography

Functional Genomics Facility

UCCC Molecular Oncology Program

Espinosa Blog at Huffington Post

Office Location

PORT B151B

Education

BS, Universidad Nacional de Mar del Plata, 1995
PhD, Universidad de Buenos Aires, 1999
PEW Charitable Trust Latin American Fellow, 2001-03
The Leukemia and Lymphoma Society Special Fellow, 2004-06

Biography

Current Positions:

Howard Hughes Medical Institute Early Career Scientist
Co-Leader, Molecular Oncology Program, University of Colorado Cancer Center (UCCC)
Director, The Functional Genomics Facility at CU-Boulder
Co-Editor in Chief, Transcription
Task Force Member, Biofrontiers Institute
Editorial Board, Molecular and Cellular Biology
Editorial Board, Cell Reports
Editorial Board, eLife

Research Interests:
Mechanisms of gene expression control and cancer biology.

Research Profile:
We are a multidimensional team of biologists. A major goal of our research is to decrease the unacceptable amount of death and sorrow caused by cancer. Nonetheless, our discoveries often lead us into other areas of biomedical research or into more fundamental biological problems without immediate clinical applications.

We understand cancer as a genetic disease caused by mutations in oncogenes and tumor suppressor genes. We believe that understanding the mechanism of action of these cancer genes will reveal strategies to reduce the burden of cancer in our society.

We abhor the use of poisonous chemotherapy and radiation to treat patients. We consider Personalized Precision Medicine employing Molecular Diagnostics and Biologically Targeted Therapies to be the only viable path toward a cure.

We employ biochemistry, molecular biology, cell biology, genetics, genomics, bioinformatics, animal models and art to investigate cancer genes. Our studies aim to produce discoveries that could be employed in the clinic for better prevention, diagnosis and treatment of cancer.

To learn more about our science, please read the selected publications below.

Selected Publications

HIF1A Employs CDK8-Mediator to Stimulate RNAPII Elongation in Response to Hypoxia.
Galbraith MD, Allen MA, Bensard CL, Wang X, Schwinn MK, Qin B, Long HW, Daniels DL, Hahn WC, Dowell RD, Espinosa JM.
Cell. 2013 Jun 6;153(6):1327-39.

A Genetic Screen Identifies TCF3/E2A and TRIAP1 as Pathway-Specific Regulators of the Cellular Response to p53 Activation.
Andrysik Z, Kim J, Tan AC, Espinosa JM.
Cell Rep. 2013 May 30;3(5):1346-54.

DNp63a represses anti-proliferative genes via H2A.Z deposition
Gallant-Behm, C.L., Ramsey, M.R., Bensard, C.L., Nojek, I., Tran, J., Liu, M., Ellisen, L.W. and Espinosa, J.M.
Genes and Development, 26(20):2325-36, 2012.

ATM and MET kinases are synthetic lethal with nongenotoxic activation of p53.
Sullivan, KD, Padilla-Just, N, Henry, RE, Porter, CC, Kim, J, Tentler, JJ, Eckhardt, SG, Tan, AC, Degregori, J, and Espinosa, JM
Nature Chemical Biology, 8:646-654. 2012

A DR4:tBID axis drives the p53 apoptotic response by promoting oligomerization of poised BAX.
Henry, R, Andrysik, Z, Paris, R, Galbraith, MD, and Espinosa, JM
EMBO Journal 31:1266-1278. 2012

Gene-specific repression of the p53 target gene PUMA via intragenic CTCF-Cohesin binding.
Gomes, NP and Espinosa, JM
Genes Dev, 24(10):1022-34. 2010

CDK8 is a positive regulator of transcriptional elongation within the serum response network.
Donner, AJ, Ebmeier, CC, Taatjes, DJ, and Espinosa, JM
Nat Struct Mol Biol, 17(2):194-201. 2010

CDK8 is a stimulus-specific positive coregulator of p53 target genes.
Donner, AJ, Szostek, S, Hoover, JM, and Espinosa, JM
Molecular Cell 27(1):121-33. 2007

Gene-specific requirement for P-TEFb activity and RNA polymerase II phosphorylation within the p53 transcriptional program.
Gomes, N, Bjerke, G, Llorente, B, Szostek, S, Emerson, BM, and Espinosa, JM
Genes and Development 20:601-612. 2006