Evidence map›Paper›PMID 25297387›Full record

ReviewOpen biology2014

From induction to conduction: how intrinsic transcriptional priming of extrinsic neuronal connectivity shapes neuronal identity.

Jeffrey B Russ, Julia A Kaltschmidt

Abstract readReview
In one paragraph

Review in Open biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Single Nuclei Analyses Reveal Transcriptional Profiles and Marker Genes for Diverse Supraspinal Populations.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Jeffrey B RussWeill Cornell/Rockefeller University/Sloan Kettering Tri-Institutional MD-PhD Program, New York, NY 10065, USA Neuroscience Program, Weill Cornell Medical College, New York, NY 10065, USA Developmental Biology Program, Sloan Kettering Institute, New York, NY 10065, USA.
Julia A KaltschmidtNeuroscience Program, Weill Cornell Medical College, New York, NY 10065, USA Cell and Developmental Biology Program, Weill Cornell Medical College, New York, NY 10065, USA Developmental Biology Program, Sloan Kettering Institute, New York, NY 10065, USA kaltschj@mskcc.org.

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
Molecular Mechanisms Regulating Inhibitory Circuitry in the Spinal CordR01NS083998 · NINDS · STANFORD UNIVERSITY · PI KALTSCHMIDT, JULIA ANNA · 2013 to 2023
$3.6M
NCI NIH HHS P30 CA008748NIGMS NIH HHS T32 GM007739NINDS NIH HHS R01 NS083998
6 · The paper itself

Abstract

Every behaviour of an organism relies on an intricate and vastly diverse network of neurons whose identity and connectivity must be specified with extreme precision during development. Intrinsically, specification of neuronal identity depends heavily on the expression of powerful transcription factors that direct numerous features of neuronal identity, including especially properties of neuronal connectivity, such as dendritic morphology, axonal targeting or synaptic specificity, ultimately priming the neuron for incorporation into emerging circuitry. As the neuron's early connectivity is established, extrinsic signals from its pre- and postsynaptic partners feedback on the neuron to further refine its unique characteristics. As a result, disruption of one component of the circuitry during development can have vital consequences for the proper identity specification of its synaptic partners. Recent studies have begun to harness the power of various transcription factors that control neuronal cell fate, including those that specify a neuron's subtype-specific identity, seeking insight for future therapeutic strategies that aim to reconstitute damaged circuitry through neuronal reprogramming.

Indexed as

Transcription, GeneticAnimalsAxonsCell DifferentiationCell LineageCentral Nervous SystemDNA-Binding ProteinsEpigenesis, GeneticGene Expression RegulationGene Expression Regulation, DevelopmentalMiceMice, TransgenicModels, BiologicalNerve Tissue ProteinsNeuronsSynapsesDNA-Binding ProteinsNerve Tissue Proteinstranscription factor PTF1Transcription FactorsZfp312 protein, mousecircuit formationFezf2neuronal identityPtf1asubtype-specificationtranscription factors

Identifiers

PMID25297387
PMCPMC4221895

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.