Evidence map›Paper›PMID 23790753›Full record

ArticleNeuron2013

SAD kinases sculpt axonal arbors of sensory neurons through long- and short-term responses to neurotrophin signals.

Brendan N Lilley, Y Albert Pan, Joshua R Sanes

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Role and Impact of theInternational journal of molecular sciences · 2026
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  3. Article
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  5. Article
  6. Dynamic Regulation ofInternational journal of molecular sciences · 2023
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  8. Review
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  14. SAD-B modulates epileptic seizure by regulating AMPA receptors in patients with temporal lobe epilepsy and in the PTZ-induced epileptic model.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020
    Article
  15. Article
  16. Review
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  19. Article
  20. Molecular mechanisms underlying monosynaptic sensory-motor circuit development in the spinal cord.Developmental dynamics : an official publication of the American Association of Anatomists · 2018
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Brendan N LilleyDepartment of Molecular and Cellular Biology and Center for Brain Science, Harvard University, Cambridge, MA 02138, USA.
Y Albert Pan
Joshua R Sanes
Harvard University · US

Funding

Synaptic Choices in the Retinotectal SystemR01NS029169 · NINDS · WASHINGTON UNIVERSITY · PI SANES, JOSHUA R · 1991 to 2012
$6.0M
Extracellular Matrix and Neuromuscular DevelopmentR37NS019195 · NINDS · HARVARD UNIVERSITY · PI SANES, JOSHUA R · 2005 to 2011
$4.0M
Roles of SAD kinases in formation and maturation of multiple synaptic typesR21NS076880 · NINDS · HARVARD UNIVERSITY · PI SANES, JOSHUA R · 2011 to 2012
$465k
NINDS NIH HHS R01 NS029169NINDS NIH HHS R21 NS076880NINDS NIH HHS R37 NS019195
6 · The paper itself

Abstract

Extrinsic cues activate intrinsic signaling mechanisms to pattern neuronal shape and connectivity. We showed previously that three cytoplasmic Ser/Thr kinases, LKB1, SAD-A, and SAD-B, control early axon-dendrite polarization in forebrain neurons. Here, we assess their role in other neuronal types. We found that all three kinases are dispensable for axon formation outside of the cortex but that SAD kinases are required for formation of central axonal arbors by subsets of sensory neurons. The requirement for SAD kinases is most prominent in NT-3 dependent neurons. SAD kinases transduce NT-3 signals in two ways through distinct pathways. First, sustained NT-3/TrkC signaling increases SAD protein levels. Second, short-duration NT-3/TrkC signals transiently activate SADs by inducing dephosphorylation of C-terminal domains, thereby allowing activating phosphorylation of the kinase domain. We propose that SAD kinases integrate long- and short-duration signals from extrinsic cues to sculpt axon arbors within the CNS.

Indexed as

AMP-Activated Protein KinasesAnimalsAxonsCell PolarityCerebral CortexHeLa CellsHumansMiceNeurotrophin 3Protein Serine-Threonine KinasesReceptor, trkCSensory Receptor CellsSignal TransductionAMP-Activated Protein KinasesBrsk1 protein, mouseBrsk2 protein, mouseNeurotrophin 3Protein Serine-Threonine KinasesReceptor, trkCStk11 protein, mouse

Identifiers

PMID23790753
PMCPMC3725037
OpenAlexW2071055050

What OpenQuestion holds

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Registered trials

None linked

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.