Description
The neurofibromatosis type 1 (NF1) tumor suppressor (neurofibromin) is thought to play crucial roles in cellular Ras- and cAMP-dependent kinase (PKA)-associated signals. The absence of or alteration of the neurofibromin protein may lead to neurofibromatosis disease. Recently, a cellular neurofibromin-associating protein, NG,NG-dimethylarginine dimethylaminohydrolase (DDAH)has been identified as a cellular NO/NOS regulator which increases PKA phosphorylation of native neurofibromin in a dose-dependent manner. The PKA accessibility of neurofibromin regulated via DDAH interaction may modulate the cellular function of neurofibromin that is implicated in NF1-related pathogenesis