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Lim, J.Y. et al.

Merlin suppresses the SRE-dependent transcription by inhibiting the activation of Ras-ERK pathway.

The neurofibromatosis type 2 (NF2) gene encodes an intracellular membrane- associated protein called merlin or schwannomin, which is known to be a tumor suppressor. Numerous studies have suggested that merlin is involved in the regulation of cell growth and proliferation. Previously, merlin/schwannomin was reported to block Ras-induced cell proliferation and anchorage-independent cell growth. Also, the N-terminus of merlin was found to suppress cell proliferation, although it appears to be less effective than full-length merlin. However, the inhibitory mechanism of merlin is unknown. In this report, merlin is shown to be effective at suppressing serum/Ras- induced and Elk-mediated SRE dependent transactivation, and serum-induced ERK phosphorylation in NIH3T3 cells. In addition, merlin inhibited serum- induced Elk phosphorylation, a downstream effector of ERKs. Also, the N-terminal deficient merlin mutant could not block serum- induced and Elk-mediated SRE dependent transactivation, although the C-terminal deficient merlin mutant could. These results suggest that merlin inhibits SRE dependent transactivation by repressing serum- induced ERK phosphorylation and its downstream effector, Elk phosphorylation. Also, the N-terminus of merlin may be important for its inhibitory effect. Our results show that merlin acts as a negative regulator of the SRE signaling pathway via the Ras-ERKs pathway.[1]

References

Merlin suppresses the SRE-dependent transcription by inhibiting the activation of Ras-ERK pathway. Lim, J.Y., Kim, H., Kim, Y.H., Kim, S.W., Huh, P.W., Lee, K.H., Jeun, S.S., Rha, H.K., Kang, J.K. Biochem. Biophys. Res. Commun. (2003) [Pubmed]

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