ArticleNeuron2008
From neuronal activity to the actin cytoskeleton: a role for CaMKKs and betaPIX in spine morphogenesis.
Article in Neuron, 2008. 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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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.
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5 citing papers in PubMed, 14 citations in OpenAlex.
- Novel p75 neurotrophin receptor ligand stabilizes neuronal calcium, preserves mitochondrial movement and protects against HIV associated neuropathogenesis.Experimental neurology · 2016Article
- Changes in the GEF-H1 pathways after traumatic brain injury.Journal of neurotrauma · 2013Article
- Relative input strength rapidly regulates dendritic structure of chick auditory brainstem neurons.The Journal of comparative neurology · 2011Article
- Neurochemical, behavioral and architectural changes after chronic inactivation of NMDA receptors in mice.Neuroscience letters · 2010Article
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Abstract
Electrical activity plays a crucial role in neuronal circuit assembly. Activation of NMDA receptors induces the elevation of intracellular calcium, resulting in the modulation of calcium-calmodulin-dependent protein kinases (CaMKs). The CaMK pathway regulates synaptogenesis by driving the formation of dendritic spines. However, the molecular effectors downstream of this pathway have remained poorly defined. In this issue of Neuron, Saneyoshi et al. identify a new signaling complex containing CaMKK/CaMKI/betaPIX/Rac that regulates the morphogenesis of spines in an activity-dependent manner.
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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.