The ingenuity pathway analysis (IPA) (a proprietary curation of pathways by Qiagen that estimates gene overrepresentation within specific pathways), revealed FGFR1(SP-/NLS)(TK-) dysregulation of many genes in NPCs and/or NCCs involved in pathways controlling neuronal and brain development, which were regulated during the cAMP/BDNF/GDNF-induced NCC differentiation (Table 3). These pathways included Wnt/β catenin signaling, axonal growth and guidance, ephrin, G-protein signaling, cAMP signaling, PKA signaling, CREB signaling, ERB tyrosine kinase signaling, growth hormone receptor signaling, interleukin signaling, prolactin, etc. (Table 3). In addition, inhibition with FGFR1(SP-/NLS)(TK-) revealed nFGFR1 regulation of additional developmental pathways, which were not affected by cAMP/BDNF/GDNF: Notch, Wnt/Ca++, neurotrophins/TRK, ERK/MAPK, reelin, ephrin, glucocorticoid receptors, GDNF and PDGF, as well as cell cycle and p53 controlling pathways. Overexpression of constitutively active nFGFR1(SP-/NLS) in NCCs affected genes in Notch, Ca++, GH, EGFR, CXCR4, pluripotency, and glucocorticoid signaling, neurotrophin/Trk receptors, NGF, Erk/MAPK signaling, ephrin signaling, FGF signaling, p53, and RAR signaling. Blocking nFGFR1 signaling with FGFR1(SP-/NLS)(TK-) and/or activation with FGFR1(SP-/NLS) affected genes in pathways involved in neuronal functions, such as GABA receptor signaling, calcium, melatonin, LTP, and LTD (Table 3). Thus,
