Postdoctoral Fellow or Associate : Manhattan, New York, NY, USA Employer: Mount Sinai School of Medicine Website: http://www.mssm.edu Location: Manhattan, New York, NY, USA Type: Postdoctoral Posted: October 20, 2011 Expires: December 01, 2011 Requisition number: Fall 2011 Postdoc Positions
job description
Postdoctoral Positions in Mouse Models of Neurodegeneration
Two positions available in the Sam Gandy, M.D., Ph.D./Michelle Ehrlich, M.D., Laboratory at the Mount Sinai School of Medicine in New York City. Projects involve development, characterization, and pathogenesis in mouse models of neurodegenerative diseases, including Alzheimer’s disease, Huntington’s disease, and primary torsion dystonia. Relevant pubs are listed below. Key requisite techniques include mouse behavior, DNA mutagenesis, RT-PCR, Northern blotting, fluorescence and light microscopy, standard immunoprotein techniques. Contact Sam Gandy and Michelle Ehrlich at <gandy.ehrlich.postdoc@gmail.com>
Kim SH, et al Forebrain striatal-specific expression of mutant huntingtin protein in vivo induces cell-autonomous age-dependent alterations in sensitivity to excitotoxicity and mitochondrial function. ASN Neuro. 2011 Jun 7;3(3):e00060. doi: 10.1042/AN20110009.
Thomas EA, et al. In vivo cell-autonomous transcriptional abnormalities revealed in mice expressing mutant huntingtin in striatal but not cortical neurons. Hum Mol Genet. 2011 Mar 15;20(6):1049-60.
Gavarini S, et al. Direct interaction between causative genes of DYT1 and DYT6 primary dystonia. Ann Neurol. 2010 Oct;68(4):549-53.
Lane RF, et al. Diabetes-associated SorCS1 regulates Alzheimer’s amyloid-beta metabolism: evidence for involvement of SorL1 and the retromer complex. J Neurosci. 2010 Sep 29;30(39):13110-5.
Gandy S, et al. Days to criterion as an indicator of toxicity associated with human Alzheimer amyloid-beta oligomers. Ann Neurol. 2010 Aug;68(2):220-30.
Kim SH, et al. Group II metabotropic glutamate receptor stimulation triggers production and release of Alzheimer’s amyloid-beta 42 from isolated intact nerve terminals. J Neurosci. 2010;30(11):3870-5.
Fuchs T, et al. Mutations in the THAP1 gene are responsible for DYT6 primary torsion dystonia. Nat Genet. 2009 Mar;41(3):286-8. Epub 2009 Feb 1. PubMed PMID: 19182804.