Evidence map›Paper›PMID 22529377›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Krüppel-like Factor 7 engineered for transcriptional activation promotes axon regeneration in the adult corticospinal tract.

Murray G Blackmore, Zimei Wang, Jessica K Lerch, Dario Motti, Yi Ping Zhang, Christopher B Shields, Jae K Lee, Jeffrey L Goldberg, Vance P Lemmon, John L Bixby

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
177citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 2% 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

177 citing papers in PubMed, 1 synthesis or guideline pooled it, 270 citations in OpenAlex.

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  18. Lipin1 depletion coordinates neuronal signaling pathways to promote motor and sensory axon regeneration after spinal cord injury.Proceedings of the National Academy of Sciences of the United States of America · 2024
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117 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 1 country.

Murray G BlackmoreDepartment of Biomedical Sciences, Marquette University, Milwaukee, WI 53201, USA. murray.blackmore@marquette.edu
Zimei Wang
Jessica K Lerch
Dario Motti
Yi Ping Zhang
Christopher B Shields
Jae K Lee
Jeffrey L Goldberg
Vance P Lemmon
John L Bixby
Neurological Surgery · USNorton Healthcare · USUniversity of Miami · USMarquette University · US

Funding

Shared Equipment ModuleP30EY014801 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Victor L Perez · 2004 to 2026
$12.2M
Kruppel-like Transcription Factors in Retinal Ganglion Cell RegenerationR01EY020913 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI GOLDBERG, JEFFREY L · 2010 to 2013
$2.2M
Novel Compounds That Overcome Glial Inhibition of Axonal RegenerationR01NS059866 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BIXBY, JOHN L · 2009 to 2013
$1.7M
NEI NIH HHS EY020913NEI NIH HHS P30 EY014801NEI NIH HHS P30-EY014801NEI NIH HHS R01 EY020913NICHD NIH HHS HD057521NINDS NIH HHS NS059866NINDS NIH HHS R01 NS059866
6 · The paper itself

Abstract

Axon regeneration in the central nervous system normally fails, in part because of a developmental decline in the intrinsic ability of CNS projection neurons to extend axons. Members of the KLF family of transcription factors regulate regenerative potential in developing CNS neurons. Expression of one family member, KLF7, is down-regulated developmentally, and overexpression of KLF7 in cortical neurons in vitro promotes axonal growth. To circumvent difficulties in achieving high neuronal expression of exogenous KLF7, we created a chimera with the VP16 transactivation domain, which displayed enhanced neuronal expression compared with the native protein while maintaining transcriptional activation and growth promotion in vitro. Overexpression of VP16-KLF7 overcame the developmental loss of regenerative ability in cortical slice cultures. Adult corticospinal tract (CST) neurons failed to up-regulate KLF7 in response to axon injury, and overexpression of VP16-KLF7 in vivo promoted both sprouting and regenerative axon growth in the CST of adult mice. These findings identify a unique means of promoting CST axon regeneration in vivo by reengineering a developmentally down-regulated, growth-promoting transcription factor.

Indexed as

AnimalsAxonsCells, CulturedEtoposideFemaleGene ExpressionGenetic EngineeringGreen Fluorescent ProteinsHEK293 CellsHerpes Simplex Virus Protein Vmw65HumansImmunohistochemistryKruppel-Like Transcription FactorsLuminescent MeasurementsMiceMice, Inbred C57BLEtoposideGreen Fluorescent ProteinsHerpes Simplex Virus Protein Vmw65Klf7 protein, mouseKruppel-Like Transcription Factors

Identifiers

PMID22529377
PMCPMC3358880
OpenAlexW2002314797

What OpenQuestion holds

Textmetadata
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.