Data for quantitative proteome analyses of NF1-deficient PC12 cells during NGF induced neural differentiation using iTRAQ

• Kobayashi Daiki

  Department of Tumor Genetics and Biology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan Department of Omics biology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan

• Araki Norie

  Department of Tumor Genetics and Biology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan

Abstract

Neurofibromatosis type 1 (NF1) tumor suppressor gene product, neurofibromin, has a function as a Ras-GAP, a negative regulator of Ras. The loss of neurofibromin is known to cause aberrant differentiation and proliferation of neural cells in NF1 patients with unknown mechanisms. To clarify the molecular mechanism of NF1 pathogenesis, we prepared a NF1 disease model using NF1 gene knockdown (KD) in PC12 cells [1,2,3], and analysed their mRNA and protein expression profiles with a unique integrated proteomics approach, comprising iTRAQ, 2D-DIGE, and DNA microarrays, using an integrated protein and gene expression analysis chart (iPEACH) [1,4]. In this study, time course quantitative proteomics of NF1-KD PC12 cells after nerve growth factor (NGF) treatments comparing with control wild cells were performed by iTRAQ quantification. The data described in this paper have been deposited to jPOST [5,6] with the identifiers JPST000067.

Journal

• Journal of Proteome Data and Methods

  Journal of Proteome Data and Methods 2 (0), 2-, 2020

  Japanese Proteomics Society

Keywords

• Neurofibromatosis type-1
• PC12
• iTRAQ

Details

• CRID: 1391130851453032064
• NII Article ID: 130007952468
• DOI: 10.14889/jpdm.2020.0002
• ISSN: 24346454
• Text Lang: en
• Data Source:
  • JaLC
  • CiNii Articles
  • KAKEN
• Abstract License Flag: Disallowed