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.
