Anton Bennett, PhD
Research & Publications
Biography
News
Research Summary
Protein tyrosine phosphorylation mediates numerous fundamental physiological events such as mitogenesis, differentiation, cell movement and apoptosis. Our laboratory is interested in how protein tyrosine phosphatases (PTPs) participate in the regulation of these cellular processes. In order to decipher how PTPs regulate mammalian cell signaling we use a broad range of approaches from molecular biology to mouse genetic strategies.
The ultimate goal of our research on protein tyrosine phosphatases is to establish whether the PTPs participate in disease processes such as cancer, cardiovascular disease, diabetes and rare diseases such as muscular dystrophy. Our long-term research goals are to identify novel mechanisms of PTP regulation in disease and to leverage this information to determine whether inhibiting these enzymes might serve as novel therapeutic targets for the treatment of human diseases.
For further information please visit the Bennett Lab website - Home | Bennett Lab (bennett-lab.org)
Extensive Research Description
Cell proliferation, cell differentiation and death are controlled by signaling pathways that are mediated by protein tyrosyl phosphorylation. The net cellular level of protein tyrosyl phosphorylation is regulated by the intrinsic and opposing activities of protein tyrosine kinases and protein tyrosine phosphatases (PTPs). Dysregulation of the net level of tyrosyl phosphorylation causes cancer, diabetes, cardiovascular disease and developmental abnormalities.
We focus our studies on how PTPs regulate cell signaling by controlling protein tyrosyl dephosphorylation. We are also exploring how PTPs participate in the pathogenesis of diseases such as obesity and diabetes, cardiovascular disease and developmental abnormalities. These research efforts are being accomplished by using integrated approaches that encompass cell biology, genetics, protein biochemistry, cell imaging and animal models. Our long-term research goals are to uncover the function of PTPs in order to identify whether these enzymes might serve as novel therapeutic targets for the treatment of human diseases.
For further information please visit the Bennett Lab website - Home | Bennett Lab (bennett-lab.org)
Coauthors
Research Interests
Cardiovascular Diseases; Musculoskeletal Diseases; Congenital, Hereditary, and Neonatal Diseases and Abnormalities; Neurosciences; Nutritional and Metabolic Diseases; Signal Transduction
Selected Publications
- Low-dose dasatinib rescues cardiac function in Noonan syndrome.Yi JS, Huang Y, Kwaczala AT, Kuo IY, Ehrlich BE, Campbell SG, Giordano FJ, Bennett AM. Low-dose dasatinib rescues cardiac function in Noonan syndrome. JCI Insight 2016, 1: e90220. PMID: 27942593, PMCID: PMC5135272, DOI: 10.1172/jci.insight.90220.
- Mining the function of protein tyrosine phosphatases in health and disease.Lee H, Yi JS, Lawan A, Min K, Bennett AM. Mining the function of protein tyrosine phosphatases in health and disease. Seminars In Cell & Developmental Biology 2015, 37: 66-72. PMID: 25263013, PMCID: PMC4339398, DOI: 10.1016/j.semcdb.2014.09.021.
- Improved regenerative myogenesis and muscular dystrophy in mice lacking Mkp5.Shi H, Verma M, Zhang L, Dong C, Flavell RA, Bennett AM. Improved regenerative myogenesis and muscular dystrophy in mice lacking Mkp5. The Journal Of Clinical Investigation 2013, 123: 2064-77. PMID: 23543058, PMCID: PMC3635719, DOI: 10.1172/JCI64375.
- Loss of mitogen-activated protein kinase phosphatase-1 protects from hepatic steatosis by repression of cell death-inducing DNA fragmentation factor A (DFFA)-like effector C (CIDEC)/fat-specific protein 27.Flach RJ, Qin H, Zhang L, Bennett AM. Loss of mitogen-activated protein kinase phosphatase-1 protects from hepatic steatosis by repression of cell death-inducing DNA fragmentation factor A (DFFA)-like effector C (CIDEC)/fat-specific protein 27. The Journal Of Biological Chemistry 2011, 286: 22195-202. PMID: 21521693, PMCID: PMC3121364, DOI: 10.1074/jbc.M110.210237.
- MAPK phosphatase-1 facilitates the loss of oxidative myofibers associated with obesity in mice.Roth RJ, Le AM, Zhang L, Kahn M, Samuel VT, Shulman GI, Bennett AM. MAPK phosphatase-1 facilitates the loss of oxidative myofibers associated with obesity in mice. The Journal Of Clinical Investigation 2009, 119: 3817-29. PMID: 19920356, PMCID: PMC2786792, DOI: 10.1172/JCI39054.