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Data Brief. 2017 Feb 21;11:364-370. doi: 10.1016/j.dib.2017.02.040. eCollection 2017 Apr.

Data characterizing the ZMIZ1 molecular phenotype of multiple sclerosis.

Author information

1
Centre for Immunology and Allergy Research, Westmead Institute of Medical Research, University of Sydney, Sydney, New South Wales, Australia.
2
Centre for Immunology and Allergy Research, Westmead Institute of Medical Research, University of Sydney, Sydney, New South Wales, Australia; Western Clinical School, University of Sydney, Westmead Hospital, Sydney, New South Wales, Australia.
3
University of Queensland Diamantina Institute, Translational Research Institute, Australia; The Queensland Brain Institute, University of Queensland, Australia.
4
Western Australian Neuroscience Research Institute, University of Western Australia, Nedlands, Western Australia, Australia; Institute for Immunology and Infectious Diseases, Murdoch University, Murdoch, Western Australia, Australia.
5
Institute for Immunology and Infectious Diseases, Murdoch University, Murdoch, Western Australia, Australia.
6
John P. Hussman Institute for Human Genomics and the Dr. John T. Macdonald Foundation Department of Human Genetics, University of Miami, Miller School of Medicine, Miami, FL 33136, USA.
7
Department of Neurology, University of California San Francisco, USA.
8
Western Clinical School, University of Sydney, Westmead Hospital, Sydney, New South Wales, Australia.

Abstract

The data presented in this article are related to the research article entitled "The autoimmune risk gene ZMIZ1 is a vitamin D responsived marker of a molecular phenotype of multiple sclerosis" Fewings et al. (2017) [1]. Here we identify the set of genes correlated with ZMIZ1 in multiple cohorts, provide phenotypic details on those cohorts, and identify the genes negatively correlated with ZMIZ1 and the cells predominantly expressing those genes. We identify the metabolic pathways in which the molecular phenotype genes are over-represented. Finally, we present the flow cytometry gating strategy we have used to identify the immune cells from blood which are producing ZMIZ1 and RPS6.

KEYWORDS:

Gene expression; Molecular phenotype; Multiple sclerosis; ZMIZ1

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