Kemp:Research

From OpenWetWare

(Difference between revisions)
Jump to: navigation, search
Line 1: Line 1:
{{Kemp Top}}
{{Kemp Top}}
-
The Kemp lab integrates intracellular signaling and metabolism in bioengineering studies of cellular immunity, toward the goal of targeted therapeutics for immunological diseases and cancer. Using a combination of computational and experimental methods, we investigate cytokine responses in T cells from a quantitative systems perspectiveCD4+ helper T-cells produce interleukin-2 (IL-2) after ligand:receptor binding in order to activate other cells in an immune response. Increasing evidence linking chronic inflammation (a consequence of T helper cell activation) with cancer in multiple cell types highlights the need to pursue the mechanisms of T-cell activation as an avenue of cancer research. Observed changes in free radicals associated with T cell activation suggest that reactive oxygen species (ROS) play an important role in conveying receptor-ligation cues from the extracellular environment into an immune response. An understanding of the quantitative balance between signal transduction and oxidative state would provide insights into altering chemotherapy-resistant cancerous cells and enhancing the immune response for desensitized T cells in disease states.
+
Aberrations in redox potential are associated with cancerous phenotypes, resulting in a resistance towards chemotherapeutic drugsReactive oxygen species (ROS) such as hydrogen peroxide and superoxide that are generated by ligation events across a diverse range of receptor families and redox couples provide a means of translating the presence of ROS into useful signals in the cell. Thioredoxin and glutathione-mediated post-translational modifications of proteins (thiolation and glutathiolation, respectively) have been shown to functionally alter the activity of certain proteins. However, few proteins have been investigated in depth to understand this relationship. More broadly, an in-depth quantitative analysis of how redox-related effects systemically influence the regulation of a receptor signaling pathway has never been undertaken. Challenges in quantificatifying post-translational events and discerning the effects of one redox couple from another have compounded the difficulties in understanding the role of redox-potential in cellular signaling, mandating a modeling-based approach for gaining insight into these biological processes.
 +
<br> <br>
 +
The Kemp lab uses computational modeling and wet-lab experimentation to investigate  how thiolation/glutathiolation of proteins influences the information flow from receptors to the nucleus. We study these effects in the context of T cell activation and cytokine response through TCR ligation. Research projects include: <br>
 +
 
 +
* modeling of NF-kB regulation through thioredoxin <br>
 +
* development of new techniques to monitor glutathiolation of proteins <br>
 +
* systemic influences of ROS on cellular phosphorylation levels

Revision as of 18:26, 6 December 2006

The Kemp Lab

Redox Systems Biology at Georgia Tech

Research        Publications        Lab Members        Positions        News        Links        Contact        Home      



Aberrations in redox potential are associated with cancerous phenotypes, resulting in a resistance towards chemotherapeutic drugs. Reactive oxygen species (ROS) such as hydrogen peroxide and superoxide that are generated by ligation events across a diverse range of receptor families and redox couples provide a means of translating the presence of ROS into useful signals in the cell. Thioredoxin and glutathione-mediated post-translational modifications of proteins (thiolation and glutathiolation, respectively) have been shown to functionally alter the activity of certain proteins. However, few proteins have been investigated in depth to understand this relationship. More broadly, an in-depth quantitative analysis of how redox-related effects systemically influence the regulation of a receptor signaling pathway has never been undertaken. Challenges in quantificatifying post-translational events and discerning the effects of one redox couple from another have compounded the difficulties in understanding the role of redox-potential in cellular signaling, mandating a modeling-based approach for gaining insight into these biological processes.

The Kemp lab uses computational modeling and wet-lab experimentation to investigate how thiolation/glutathiolation of proteins influences the information flow from receptors to the nucleus. We study these effects in the context of T cell activation and cytokine response through TCR ligation. Research projects include:

  • modeling of NF-kB regulation through thioredoxin
  • development of new techniques to monitor glutathiolation of proteins
  • systemic influences of ROS on cellular phosphorylation levels
Personal tools