Figure 5.
Cdc42 is capable of regulating both mesenchymal migration and amoeboid migration due to the selective activation of Cdc42 by different GEF proteins. In melanoma cells, DOCK10 activates Cdc42, which can then interact with its downstream effector PAK2 to promote amoeboid migration through MLC2. The other well characterized signalling pathway which promotes amoeboid migration is RhoA activation of ROCK kinase. Mesenchymal migration is regulated by Rac1, via activation of WAVE2. Additionally, Cdc42 is proposed to regulate Rac1 activation via a currently uncharacterized GEF. Cdc42 mediated activation of MRCK proteins is also known to drive mesenchymal migration. Rac1 signalling to NFκB induces transcription of the IL-6 gene. IL-6 binds to IL-6R to activate JAK2, which phosphorylates Stat3, allowing it to dimerize and translocate to the nucleus, where it is transcriptionally active.
Cdc42 signalling in cell migration.

Cdc42 is capable of regulating both mesenchymal migration and amoeboid migration due to the selective activation of Cdc42 by different GEF proteins. In melanoma cells, DOCK10 activates Cdc42, which can then interact with its downstream effector PAK2 to promote amoeboid migration through MLC2. The other well characterized signalling pathway which promotes amoeboid migration is RhoA activation of ROCK kinase. Mesenchymal migration is regulated by Rac1, via activation of WAVE2. Additionally, Cdc42 is proposed to regulate Rac1 activation via a currently uncharacterized GEF. Cdc42 mediated activation of MRCK proteins is also known to drive mesenchymal migration. Rac1 signalling to NFκB induces transcription of the IL-6 gene. IL-6 binds to IL-6R to activate JAK2, which phosphorylates Stat3, allowing it to dimerize and translocate to the nucleus, where it is transcriptionally active.

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