Grant: $10,950 - National Institutes of Health - Jun. 1, 2009
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Award Description: The award supported summer research of undergraduate student. It was a great educational opportunity for students, which allowed hands-on laboratory research experience and active contribution to laboratory work. In addition the student was able to participate in departmental seminars and discuss research with other members of laboratory. Being a part of an active research environment gives a new perspective on science and future carrier choices.
Project Description: Recent research from our laboratory demonstrated that sustained activation of Protein Kinase C (PKC) globally affected endocytic trafficking leading to PKC-dependent sequestration of various plasma membrane lipids and proteins including PKC itself, to a novel subset of Rab11-positive recycling endosomes named the pericentrion. Mammalian target of rapamycin compex 1 (mTORC1) is well known to control cell growth, proliferation, protein synthesis upon activation with growth factors, insulin, or serum. Independent studies implicated PKC in regulation of mTORC1 activity. In addition a recent report implicated that activation of mTORC1 requires translocation of its components to intracellular endosomal compartment. The goal of this project was to investigate if sustained stimulation of PKC that leads to pericentrion formation plays a role in mTORC1 regulation of cell growth. First, the student determined the ability of sustained PKC and PLD stimulation by PMA, FBS, and Gq-coupled GPCR agonist such as 5-HT to induce translocation of mTOR and/or key components of the mTORC1 complex (e.g. raptor) to the pericentrion (colocalization studies). Next,he investigated if activation of mTOR (measured by phosphorylation of S6K) requires PKC and PLD (inhibitors, RNAi and DN constructs). Preliminary results obtained confirmed role of PKC in activation of mTORC1 after treatment with phorbol ester (PMA) and fetal bovine serum (FBS) as shown by activation of S-6 kinase. This was done by use of specific inhibitors of PKC (Gö6976 and ruboxistaurin). Also, role of PLD was confirmed by inhibition of PLD with 1-butanol. Most importantly, inhibition of pericentrion formation by inhibition of clathrin-dependent endocytosis, ceramide treatment and inhibition of microtubules polymerization were also able to inhibit activation of mTORC1 pathway.
Infrastructure Description: N/A
Jobs Summary: Student (Total jobs reported: 0)
Project Status: More than 50% Completed
This award's data was last updated on Jun. 1, 2009. Help expand these official descriptions using the wiki below.