Zhijun Luo, MD, PhD
|Institution||Boston University School of Medicine|
|Address||75 E. Newton St Evans Building|
Boston MA 02118
|Title||Graduate Faculty (Primary Mentor of Grad Students)|
|Institution||Boston University School of Medicine, Division of Graduate Medical Sciences|
|Institution||Boston Medical Center|
Research Interests: Regulation of tumor cell growth and metabolism by protein phosphorylation
The overall research interest in my laboratory is to understand how protein phosphorylation regulates cell growth and metabolism, and how its alteration causes diseases such as cancer and metabolic disorders. Our ongoing research focuses on characterization of AMP-activated protein kinase and Raf kinase, both of which have been implicated in cancer and other disorders.
AMPK serves as a fuel-sensing enzyme that is activated by binding of 5’ AMP to the? gamma subunit and phosphorylation of the catalytic subunit at Thr 172 by upstream kinases such as LKB1 and CaMKK. The activation of AMPK has been shown to improve metabolic syndrome and to be implicated in control of cancer cell growth. One of our research interests is to test the hypothesis that AMPK functions as a metabolic tumor suppressor. Using microarray and proteomic approaches, we have identified several target molecules regulated by AMPK and are currently evaluating their functional relationship with AMPK and biological relevance.
Raf kinases, consisting of three isoforms, Raf-1, B-Raf and A-Raf, act as immediate downstream effectors of Ras. They are implicated in tumorigenesis, inasmuch as activating mutations of the ras genes have been found in 20-30% of overall human cancers and activated mutants of B-Raf frequently reported in human cancers. Although the linear relationship of the Ras/Raf/MEK/Erk signaling pathway has been delineated, the mechanism of Raf activation still remains elusive. We have a long standing interest in characterizing phosphorylation of Raf for its activation, and identifying kinases responsible for these phosphorylation events and downstream targets in addition to MEK1/2.
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