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Comment
. 2014 Mar 15;5(5):1116-7.
doi: 10.18632/oncotarget.1835.

Dopamine signaling: target in glioblastoma

Affiliations
Comment

Dopamine signaling: target in glioblastoma

Jiri Bartek et al. Oncotarget. .
No abstract available

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Figures

Figure 1
Figure 1. Targeting synergistic dependency on MAPK and dopamine signaling in glioblastoma
Canonical pro-survival and mitogenic MAPK signaling, commonly deregulated in glioblastoma, is depicted as a simplified signaling cascade of EGFR, Ras-GTP and MAPK kinases Erk1 and Erk2 (Erk1/2). At the Ras node, MAPK pathway is positively modulated by dopamine signaling. Upon ligand binding, the DRD2 receptor holds inactive small GTPase Rap1 through activation of heterotrimeric G protein alpha i2 (alpha/beta/gamma) and the GTPase-activating protein RAP (RAP-GAPII), which promote GDP-bound (inactive) Rap1. Rap1 is a Ras antagonist and its inactivation thus results in amplification of MAPK signaling. Therefore, combined targeting of both pathways can offer a promising strategy for glioblastoma therapy.

Comment on

References

    1. Li J, et al. Oncotarget. 2014;5(this issue)
    1. Stork PJ, Dillon TJ. Blood. 2005;106:2952–61. - PMC - PubMed
    1. Bartek J, Jr, et al. J Neurol Neurosurg Psychiatry. 2012;83:753–60. - PubMed
    1. Nature. 2008;455:1061–8. - PMC - PubMed
    1. De Witt Hamer PC. Neuro Oncol. 2010;12:304–16. - PMC - PubMed