Evidence map›Paper›PMID 27651754›Full record

ReviewNeural regeneration research2016

Selective neuronal PTEN deletion: can we take the brakes off of growth without losing control?

Erin A Gutilla, Oswald Steward

Abstract readReview
In one paragraph

Review in Neural regeneration research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Anatomical Diversity of the Adult Corticospinal Tract Revealed by Single-Cell Transcriptional Profiling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  6. Review
  7. Motoneuron-Specific PTEN Deletion in Mice Induces Neuronal Hypertrophy and Also Regeneration after Facial Nerve Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Epac2 Elevation Reverses Inhibition by Chondroitin Sulfate ProteoglycansThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  13. Article
  14. Article
  15. 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.

Erin A GutillaReeve-Irvine Research Center, University of California Irvine School of Medicine, Irvine, CA, USA; Department of Anatomy & Neurobiology, University of California Irvine School of Medicine, Irvine, CA, USA.ORCID 0000-0002-8466-9902
Oswald StewardReeve-Irvine Research Center, University of California Irvine School of Medicine, Irvine, CA, USA; Department of Anatomy & Neurobiology, University of California Irvine School of Medicine, Irvine, CA, USA; Department of Neurobiology & Behavior, University of California Irvine School of Medicine, Irvine, CA, USA; Department of Neurosurgery, University of California Irvine School of Medicine, Irvine, CA, USA; Center for the Neurobiology of Learning and Memory, University of California Irvine School of Medicine, Irvine, CA, USA.ORCID 0000-0001-7069-8756

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM008620 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI GOLDIN, ALAN L · 1999 to 2023
$8.1M
Towards a therapy to regenerate corticospinal axonsR01NS073857 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI STEWARD, OSWALD · 2011 to 2015
$1.7M
NIGMS NIH HHS T32 GM008620NINDS NIH HHS R01 NS073857
6 · The paper itself

Abstract

The limited ability for injured adult axons to regenerate is a major cause for limited functional recovery after injury to the nervous system, motivating numerous efforts to uncover mechanisms capable of enhancing regeneration potential. One promising strategy involves deletion or knockdown of the phosphatase and tensin (PTEN) gene. Conditional genetic deletion of PTEN before, immediately following, or several months after spinal cord injury enables neurons of the corticospinal tract (CST) to regenerate their axons across the lesion, which is accompanied by enhanced recovery of skilled voluntary motor functions mediated by the CST. Although conditional genetic deletion or knockdown of PTEN in neurons enables axon regeneration, PTEN is a well-known tumor suppressor and mutations of the PTEN gene disrupt brain development leading to neurological abnormalities including macrocephaly, seizures, and early mortality. The long-term consequences of manipulating PTEN in the adult nervous system, as would be done for therapeutic intervention after injury, are only now being explored. Here, we summarize evidence indicating that long-term deletion of PTEN in mature neurons does not cause evident pathology; indeed, cortical neurons that have lived without PTEN for over 1 year appear robust and healthy. Studies to date provide only a first look at potential negative consequences of PTEN deletion or knockdown, but the absence of any detectable neuropathology supports guarded optimism that interventions to enable axon regeneration after injury are achievable.

Indexed as

axon regenerationcorticospinal tractmotor systemmTORPTENrecovery of functionspinal cord injury

Identifiers

PMID27651754
PMCPMC5020805

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.