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A Nurr1-Knockout Mouse Model for Parkinson's Disease and Stem Cell Differentiation

Posted Jun 15 2010 5:00pm

Description of Invention:
The researchers have generated Nurr1-knockout mice via genomic locus inactivation using homologous recombination.

Transcription factor Nurr1 is an obligatory factor for neurotransmitter dopamine biosynthesis in ventral midbrain. From a neurological and clinical perspective, it suggests an entirely new mechanism for dopamine depletion in a region where dopamine is known to be involved in Parkinson's disease. Activation of Nurr1 may be therapeutically useful for Parkinson's disease patients; therefore, the mice would be useful in Parkinson's disease research.

Additionally, Nurr1 has been shown to be critical for development of midbrain dopaminergic neurons, and thus may contribute to stem cell-based therapies for neurological disorders. Nurr1 is also important for osteoblast differentiation, suggesting a general role in stem cell differentiation and growth.

Applications:
  • Research and drug testing for Parkinson's disease and other neurological disorders
  • Stem cell research relating to neurological and other disorders and bone formation


Inventors:
No Inventor Information Available.

Relevant Publication:
  1. MK Lee, H Choi, M Gil, VM Nikodem. Regulation of osteoblast differentiation by Nurr1 in MC3T3-E1 cell line and mouse calvarial osteoblasts. J Cell Biochem. 2006 June 1 [Epub ahead of print, doi:10.1002/jcb.20990]. [ PubMed abs ]
  2. J Jankovic, S Chen, WD Le. The role of Nurr1 in the development of dopaminergic neurons and Parkinson's disease. Prog Neurobiol. 2005 Sep-Oct, 77(1-2):128-138. Epub 2005 Oct 21, doi:10.1016/j.pneurobio.2005.09.001. [ PubMed abs ]


Licensing Status:
This technology is available under a Biological Materials License.


Portfolios:
Devices/Instrumentation
Devices/Instrumentation - Research Tools and Materials
Animal Model



For Additional Information Please Contact:
No Licensing Specialist Information Available.


Ref No: 1288

Updated: 06/2010

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