Disruption of G-protein γ5 subtype causes embryonic lethality in mice.

Disruption of G-protein γ5 subtype causes embryonic lethality in mice.
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DOI:
10.1371/journal.pone.0090970
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发表时间:
2014
期刊:
影响因子:
3.7
通讯作者:
Robishaw JD
Robishaw JD
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Moon AM;Stauffer AM;Schwindinger WF;Sheridan K;Firment A;Robishaw JD

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Heterotrimeric G-proteins modulate many processes essential for embryonic development including cellular proliferation, migration, differentiation, and survival. Although most research has focused on identifying the roles of the various αsubtypes, there is growing recognition that similarly divergent βγ dimers also regulate these processes. In this paper, we show that targeted disruption of the mouse Gng5 gene encoding the γ5 subtype produces embryonic lethality associated with severe head and heart defects. Collectively, these results add to a growing body of data that identify critical roles for the γ subunits in directing the assembly of functionally distinct G-αβγ trimers that are responsible for regulating diverse biological processes. Specifically, the finding that loss of the G-γ5 subtype is associated with a reduced number of cardiac precursor cells not only provides a causal basis for the mouse phenotype but also raises the possibility that G-βγ5 dependent signaling contributes to the pathogenesis of human congenital heart problems.
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