Evidence map›Paper›PMID 25317150›Full record

ReviewNeural regeneration research2014

Molecular mechanisms of the suppression of axon regeneration by KLF transcription factors.

Akintomide Apara, Jeffrey L Goldberg

Open access · goldAbstract readReview
In one paragraph

Review in Neural regeneration research, 2014. 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
1.9field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. CaeNeuro · 2024
    Article
  4. Review
  5. Article
  6. Optic nerve regeneration: A long view.Restorative neurology and neuroscience · 2019
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
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 at 2 institutions in 1 country.

Akintomide AparaUniversity of Miami Miller School of Medicine, Miami, FL, USA.
Jeffrey L GoldbergShiley Eye Center, University of California San Diego, La Jolla, CA, USA.
University of California, San Diego · USUniversity of Miami · US

Funding

Vision BiostatisticsP30EY022589 · NEI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Derek Stuart Welsbie · 2012 to 2026
$10.3M
Signaling Scaffolds and Survival in StrokeR01EY022129 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI GOLDBERG, JEFFREY L, KAPILOFF, MICHAEL SETH · 2012 to 2015
$2.3M
NEI NIH HHS P30 EY022589NEI NIH HHS R01 EY022129
6 · The paper itself

Abstract

Molecular mechanisms of the Krüppel-like family of transcription factors (KLFs) have been studied more in proliferating cells than in post-mitotic cells such as neurons. We recently found that KLFs regulate intrinsic axon growth ability in central nervous system (CNS) neurons including retinal ganglion cells, and hippocampal and cortical neurons. With at least 15 of 17 KLF family members expressed in neurons and at least 5 structurally unique subfamilies, it is important to determine how this complex family functions in neurons to regulate the intricate genetic programs of axon growth and regeneration. By characterizing the molecular mechanisms of the KLF family in the nervous system, including binding partners and gene targets, and comparing them to defined mechanisms defined outside the nervous system, we may better understand how KLFs regulate neurite growth and axon regeneration.

Indexed as

axon growthoptic nerveregenerationretinaretinal ganglion cellsspinal cordtranscription factors

Identifiers

PMID25317150
PMCPMC4192940
OpenAlexW2075977383

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.