ArticleDevelopmental biology2010
GDP-bound Galphai2 regulates spinal motor neuron differentiation through interaction with GDE2.
Article in Developmental biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Gαi2 promotes microtubule-driven incorporation of neurofilaments to stabilise nascent axons in vivo.EMBO reports · 2026Article
- Neuronal differentiation is associated with a redox-regulated increase of copper flow to the secretory pathway.Nature communications · 2016Article
- Generating spinal motor neuron diversity: a long quest for neuronal identity.Cellular and molecular life sciences : CMLS · 2014Review
- Motor neurons and the generation of spinal motor neuron diversity.Frontiers in cellular neuroscience · 2014Review
- Glycerophosphodiester phosphodiesterase domain containing 5 (GDPD5) expression correlates with malignant choline phospholipid metabolite profiles in human breast cancer.NMR in biomedicine · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Galphai proteins play major roles in the developing and mature nervous system, ranging from the control of cellular proliferation to modulating synaptic plasticity. Although best known for transducing signals from activated seven transmembrane G-protein coupled receptors (GPCRs) when bound to GTP, key cellular functions for Galphai-GDP are beginning to emerge. Here, we show that Galphai2 is expressed in motor neuron progenitors that are differentiating to form postmitotic motor neurons in the developing spinal cord. Ablation of Galphai2 causes deficits in motor neuron generation but no changes in motor neuron progenitor patterning or specification, consistent with a function for Galphai2 in regulating motor neuron differentiation. We show that Galphai2 function is mediated in part by its interaction with GDE2, a known regulator of motor neuron differentiation, and that disruption of the GDE2/Galphai2 complex in vivo causes motor neuron deficits analogous to Galphai2 ablation. Galphai2 preferentially associates with GDE2 when bound to GDP, invoking GPCR-independent functions for Galphai2 in the control of spinal motor neuron differentiation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.