Lisa F. Barcellos1, Stacy Caillier1, Leonard Dragone2, Melissa Elder2, Eric Vittinghoff3, Patricia Bucher1, Robin R. Lincoln1, Margaret Pericak-Vance6, Jonathan L. Haines7, Arthur Weiss4, 5, Stephen L. Hauser1
& Jorge R. Oksenberg11
Department of Neurology, University of California at San Francisco, 513 Parnassus Avenue, San Francisco, CA, 94143.
2
Department of Pediatrics, University of California at San Francisco, 513 Parnassus Avenue, San Francisco, CA, 94143.
3
Department of Epidemiology and Biostatistics, University of California at San Francisco, 513 Parnassus Avenue, San Francisco, CA, 94143.
4
Department of Microbiology and Immunology, University of California at San Francisco, 513 Parnassus Avenue, San Francisco, CA, 94143.
5
Department of Medicine, University of California at San Francisco, 513 Parnassus Avenue, San Francisco, CA, 94143.
6
Center for Human Genetics, Department of Medicine, Duke University Medical Center, Durham, North Carolina.
7
Program in Human Genetics, Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee.
Correspondence should be addressed to Jorge R. Oksenberg oksen@itsa.ucsf.edu
G nucleotide transition in exon 4 of PTPRC (encoding protein-tyrosine phosphatase receptor-type C, also known as CD45) was recently reported to be genetically associated with the development of multiple sclerosis (MS)
