ArticlePloS one2011
SDF1-induced antagonism of axonal repulsion requires multiple G-protein coupled signaling components that work in parallel.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- How much do we know about the coupling of G-proteins to serotonin receptors?Molecular brain · 2014Review
- SDF1 reduces interneuron leading process branching through dual regulation of actin and microtubules.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- G-protein-coupled receptor cell signaling pathways mediating embryonic chick retinal growth cone collapse induced by lysophosphatidic acid and sphingosine-1-phosphate.Developmental neuroscience · 2014Article
- cAMP-induced expression of neuropilin1 promotes retinal axon crossing in the zebrafish optic chiasm.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
SDF1 reduces the responsiveness of axonal growth cones to repellent guidance cues in a pertussis-toxin-sensitive, cAMP-dependent manner. Here, we show that SDF1's antirepellent effect can be blocked in embryonic chick dorsal root ganglia (DRGs) by expression of peptides or proteins inhibiting either Gα(i), Gα(q), or Gβγ. SDF1 antirepellent activity is also blocked by pharmacological inhibition of PLC, a common effector protein for Gα(q). We also show that SDF1 antirepellent activity can be mimicked by overexpression of constitutively active Gα(i), Gα(q), or Gα(s). These results suggest a model in which multiple G protein components cooperate to produce the cAMP levels required for SDF1 antirepellent activity.
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Registered trials
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