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Ortega lab website

http://web.me.com/ortegaj_mcmaster/Ortega_lab_web_site/Welcome.html

The Spotlight – Under the Microscope…

After the successful graduation of three of our students this year, the Ortega lab is looking for two new graduate students to join the lab in the fall. Our lab works in understanding how the bacterial ribosome is assembled and also in the structure and function of bacterial proteases. These enzymes perform intracellular protein degradation, process that is involved in almost every aspect of the biology of the cell. These two articles below are an example of our most recent work in these areas.

• Jomaa et al. Understanding Ribosome Assembly: the Structure of in vivo Assembled Immature 30S Subunits Revealed by Cryo-electron Microscopy. (2011). RNA. Epub Feb 8,2011. Download article 1

• Li et al. Acyldepsipeptide Antibiotics Induces the Formation of a Structured Axial Channel in ClpP: a Model for the ClpX/ClpA Bound State of ClpP. (2010). Chemistry and Biology. 17: 959-969.Download article 2

If you are a motivated student, willing to make a serious contribution to research and looking for prime training in biochemistry, stop by our lab or drop a line to Dr. Joaquin Ortega (ortegaj@mcmaster.ca).

The last few months have seen some exciting developments in basic Huntington’s disease (HD) research with implications for drug development and therapy.  An ongoing study by Lise Munsie, a graduate student in the lab of Dr. Ray Truant, in collaboration with a drug company, CHDI Inc., has recently defined part of the cell stress response that is affected by the presence of mutant huntingtin; huntingtin interacts with the protein cofilin which is involved in rescuing a cell from stress (via novel live cell assays).  There is currently no way to stop or reverse the progression of HD, which affects one in 10,000 North Americans.  It is a progressive, and eventually fatal, genetic neurological disease.  HD is caused by a mutation in a single gene encoding the huntingtin protein and an affected individual has a 50% chance of passing this gene onto offspring.  HD symptoms are physical, cognitive and emotional caused by degeneration of neurons in the brain leading to death, 10-20 years post-onset.  The causal factor of HD, mutant huntingtin, has been studied for over a decade; however there has been no success in finding drugs that affect huntingtin biology.  Lise and Dr. Truant believe that huntingtin’s involvement in the cell stress response may be a target for drug discovery.   Dr. Truant’s lab is focusing on studying the normal function of huntingtin, in hopes of finding novel drug targets.  There are similar neurological disorders to HD, including Alzheimer’s disease [AD]; AD has different causal factors, however, both AD and HD are related since their main pathology is degeneration of neurons in the brain, indicating that there may be a similar mechanism of disease.  Any compounds they find that are effective in HD models will be further testable in AD models.