Neurogenetics, Development and Evolution
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PETER JOHN MCKINNON, Ph.D.
- Associate Member
- Department of Genetics and Tumor Cell Biology
- St. Jude Children's Research Hospital
- Affiliated Associate Professor
- Department of Anatomy and Neurobiology
- The University of Tennessee College of Medicine
Address
- St. Jude Children's Research Hospital
- MS331, Room D3055F
- 332 N. Lauderdale
- Memphis, TN 38105
- Tel: (901) 495-2700; Fax: (901) 526-2907
Education
- Ph.D. Institution: The Flinders Universiry of South Australia, Adelaide, Australia
- Postdoctoral: The Roche Institute of Molecular Biology, Nutley, New Jersey
Research Interests
Our research focus is an analysis of selected molecules that are important for the develop-mental and maintenance of the central nervous system (CNS). In one line of research, we are interested in the molecular events leading to neurodegeneration in the human syndrome ataxia-telangiectasis (A-T). A-T is a multisystem disease characterized by cancer, immune defects and a profound progressive neurodegeneration. Recently the gene mutated in A-T has been identifed and found to be related to a number of critical cellular signaling molecules collectively termed the PI3-kinases. However, the role of this gene in the nervous system is unclear. Using techniques such as gene-targeting and the yeast two-hybrid system, we aim to identify important components of the signal transduction pathway involving Atm, and to understand their role in the nervous system. This will provide key information regarding basic mechanisms of neuronal development and maintenance.
In another line of research, the function of the astrocyte extracellular matrix (ECM) following perturbation of CNS homeostasis is being investigated. Astrocytes respond to CNS injury by undergoing reactive astroctyosis; a pronounced response that occurs following both neurodegeneration and a spectrum of other insults that perturb CNS homeostasis, such as epilepsy, Parkinson' and Alzheimer's diesease. However, little is know about the molecular events that underlie this response, or indeed the role of astrocytosis in nervous system recovery from injury. We have shown that members of a relatively new family of astrocyte ECM proteins (the SPARC family) may be directly involved in reactive astrocytosis. The long term goal of this research is to define the molecular events that are important for reactive astrocytosis, and to understand the implications of reactive astrocytosis for the nervous system.
Links
- St Jude Faculty - Peter John McKinnon
Recent Publications
- Frappart PO, McKinnon PJ.
Mouse models of DNA double-strand break repair and neurological disease.
DNA Repair (Amst). 2008 Jul 1;7(7):1051-60. Epub 2008 May 23. Review.
PMID: 18458002
- Katyal S, McKinnon PJ.
DNA strand breaks, neurodegeneration and aging in the brain.
Mech Ageing Dev. 2008 Jul-Aug;129(7-8):483-91. Epub 2008 Mar 25. Review.
PMID: 18455751
- Wilson DM 3rd, Bohr VA, McKinnon PJ.
DNA damage, DNA repair, ageing and age-related disease.
Mech Ageing Dev. 2008 Jul-Aug;129(7-8):349-52. Epub 2008 Mar 4. No abstract
available.
PMID: 18420253
- Green DR, McKinnon PJ.
A survivor hits the breaks.
Mol Cell. 2008 Feb 29;29(4):411-2.
PMID: 18313378
- Phillips ER, McKinnon PJ.
DNA double-strand break repair and development.
Oncogene. 2007 Dec 10;26(56):7799-808. Review.
PMID: 18066093
- Desmots F, Russell HR, Michel D, McKinnon PJ.
Scythe regulates apoptosis-inducing factor stability during endoplasmic
reticulum stress-induced apoptosis.
J Biol Chem. 2008 Feb 8;283(6):3264-71. Epub 2007 Dec 3.
PMID: 18056262
view complete list of references (pubmed link)
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