The GTPase domain of Galphao contributes to the functional interaction of Galphao with the promyelocytic leukemia zinc finger protein

Won, J.H.; Ghil, Sung Ho

doi:10.2478/s11658-008-0033-6

Cited by 1 publication

(1 citation statement)

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“…After 20 h, cells were treated with 3 μM Hu210 (Tocris Bioscience, Ellisville, Mo, USA), a CB1R agonist for 6 h. Both cell lines were labeled with 10 μM BrdU (Sigma-Aldrich), 12 h before harvest. Next, cells were washed with PBS and fixed in 4% paraformaldehyde in PBS for 15 m. After fixation, cells were subjected to immunofluorescence staining against BrdU [ 46 ].…”

Section: Methodsmentioning

confidence: 99%

The alpha subunit of Go modulates cell proliferation and differentiation through interactions with Necdin

Kang

Kim

et al. 2014

Cell Commun Signal

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BackgroundHeterotrimeric GTP-binding proteins (G-proteins) play an important role in mediating signal transduction generated by neurotransmitters or hormones. Go, a member of the Gi/Go subfamily, is the most abundant G-protein found in the brain. Recently, the alpha subunit of Go (Gαo) was characterized as an inducer of neuronal differentiation. However, its underlying molecular mechanisms have remained unclear to date, since the downstream effectors of Gαo are ambiguous.ResultsA neurally differentiated embryonal carcinoma-derived protein (Necdin) was isolated as an interacting partner for Gαo from a mouse brain cDNA library using yeast two-hybrid screening. Interactions between the proteins were confirmed with several affinity binding assays, both in vitro and in vivo. Necdin interacted directly and preferentially with activated Gαo, compared to wild-type protein. Interestingly, Gαo did not interact with Gαi, despite high sequence homology between the two proteins. We subsequently analyzed whether Gαo modulates the cellular activities of Necdin. Notably, expression of Gαo significantly augmented Necdin-mediated cellular responses, such as proliferation and differentiation. Moreover, activation of type 1 cannabinoid receptor (CB1R), a Gi/oα-coupled receptor, augmented cell growth suppression, which was mediated by Gαo and Necdin in U87MG cells containing CB1R, Gαo, and Necdin as normal components.ConclusionsThese results collectively suggest that Necdin is a candidate downstream effector for Gαo. Our findings provide novel insights into the cellular roles of Gαo and its coupled receptor.

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Section: Methodsmentioning

confidence: 99%