pp32/ I-1(PP2A) negatively regulates the Raf-1/MEK/ERK pathway.
In this study, we focus on the potential interaction of pp32/I-1(PP2A) (pp32) with the Raf-MEK-ERK signaling pathway. We show that overexpressed pp32 suppresses Raf-1 activation, thereby downregulating the level of ERK activation. This suppression of Raf-1 requires the C-terminal half of pp32. Conversely, knock-down of PP32 by siRNA enhances ERK and MEK activations. Taken together, we propose that tumor-suppression by pp32 is, at least in part, mediated by downregulation of the Raf-MEK-ERK signaling pathway.
Fukukawa
Chikako
C
Division of Biochemical Oncology and Immunology, Institute for Genetic Medicine, Hokkaido University, Kita-15, Nishi-7, Kita-ku, Sapporo 060-0815, Japan.
Tanuma
Nobuhiro
N
Okada
Tadashi
T
Kikuchi
Kunimi
K
Shima
Hiroshi
H
D000818:Animals; D015153:Blotting, Western; D019556:COS Cells; D002522:Chlorocebus aethiops; D004789:Enzyme Activation / Q000502:physiology; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism*; D006367:HeLa Cells; D006801:Humans; D009369:Neoplasms / Q000378:metabolism*; D009687:Nuclear Proteins / Q000378:metabolism*; D010750:Phosphoproteins / Q000378:metabolism; D034741:RNA, Small Interfering; D015398:Signal Transduction / Q000502:physiology*
D009687:Nuclear Proteins; D010750:Phosphoproteins; D034741:RNA, Small Interfering; D048049:Extracellular Signal-Regulated MAP Kinases