Evidence map›Paper›PMID 33832520›Full record

ArticleMolecular brain2021

Phosphorylation of GAP-43 T172 is a molecular marker of growing axons in a wide range of mammals including primates.

Masayasu Okada, Yosuke Kawagoe, Yuta Sato, Motohiro Nozumi, Yuya Ishikawa, Atsushi Tamada, Hiroyuki Yamazaki, Yuko Sekino, Yonehiro Kanemura, Yohei Shinmyo and 5 more

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

16 citing papers in PubMed, 55 citations in OpenAlex.

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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

15 authors at 9 institutions in 1 country.

Masayasu OkadaDepartment of Neurosurgery, Brain Research Institute, School of Medicine and Graduate School of Medical/Dental Sciences, Niigata University, Niigata, Japan.
Yosuke KawagoeDepartments of Neurochemistry and Molecular Cell Biology, School of Medicine and Graduate School of Medical/Dental Sciences, Niigata University, Niigata, 951-8510, Japan.
Yuta SatoDepartments of Neurochemistry and Molecular Cell Biology, School of Medicine and Graduate School of Medical/Dental Sciences, Niigata University, Niigata, 951-8510, Japan.
Motohiro NozumiDepartments of Neurochemistry and Molecular Cell Biology, School of Medicine and Graduate School of Medical/Dental Sciences, Niigata University, Niigata, 951-8510, Japan.
Yuya IshikawaDepartments of Neurochemistry and Molecular Cell Biology, School of Medicine and Graduate School of Medical/Dental Sciences, Niigata University, Niigata, 951-8510, Japan.
Atsushi TamadaDepartments of Neurochemistry and Molecular Cell Biology, School of Medicine and Graduate School of Medical/Dental Sciences, Niigata University, Niigata, 951-8510, Japan.
Hiroyuki YamazakiDepartment of Neurobiology and Behavior, Gunma University Graduate School of Medicine, Maebashi, Japan.
Yuko SekinoLaboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo, Japan.
Yonehiro KanemuraDivision of Regenerative Medicine, Department of Biomedical Research and Innovation, Institute for Clinical Research, National Hospital Organization Osaka National Hospital, Osaka, Japan.
Yohei ShinmyoDepartment of Medical Neuroscience, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
Hiroshi KawasakiDepartment of Medical Neuroscience, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
Naoko KanekoDepartment of Developmental and Regenerative Neurobiology, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Kazunobu SawamotoDepartment of Developmental and Regenerative Neurobiology, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Yukihiko FujiiDepartment of Neurosurgery, Brain Research Institute, School of Medicine and Graduate School of Medical/Dental Sciences, Niigata University, Niigata, Japan.
Michihiro IgarashiDepartments of Neurochemistry and Molecular Cell Biology, School of Medicine and Graduate School of Medical/Dental Sciences, Niigata University, Niigata, 951-8510, Japan. tarokaja@med.niigata-u.ac.jp.ORCID 0000-0003-1474-3385
Niigata University · JPKanazawa University · JPNagoya City University · JPNiigata University Medical and Dental Hospital · JPGunma University · JPHokkaido University · JPKansai Medical University · JPOsaka National Hospital · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

GAP-43 is a vertebrate neuron-specific protein and that is strongly related to axon growth and regeneration; thus, this protein has been utilized as a classical molecular marker of these events and growth cones. Although GAP-43 was biochemically characterized more than a quarter century ago, how this protein is related to these events is still not clear. Recently, we identified many phosphorylation sites in the growth cone membrane proteins of rodent brains. Two phosphorylation sites of GAP-43, S96 and T172, were found within the top 10 hit sites among all proteins. S96 has already been characterized (Kawasaki et al., 2018), and here, phosphorylation of T172 was characterized. In vitro (cultured neurons) and in vivo, an antibody specific to phosphorylated T172 (pT172 antibody) specifically recognized cultured growth cones and growing axons in developing mouse neurons, respectively. Immunoblotting showed that pT172 antigens were more rapidly downregulated throughout development than those of pS96 antibody. From the primary structure, this phosphorylation site was predicted to be conserved in a wide range of animals including primates. In the developing marmoset brainstem and in differentiated neurons derived from human induced pluripotent stem cells, immunoreactivity with pT172 antibody revealed patterns similar to those in mice. pT172 antibody also labeled regenerating axons following sciatic nerve injury. Taken together, the T172 residue is widely conserved in a wide range of mammals including primates, and pT172 is a new candidate molecular marker for growing axons.

Indexed as

Amino Acid SequenceAnimalsAntibodiesAxonsBiomarkersBrainCallithrixCells, CulturedFerretsGAP-43 ProteinGrowth ConesHEK293 CellsHumansJNK Mitogen-Activated Protein KinasesMammalsMiceAntibodiesBiomarkersGAP-43 ProteinJNK Mitogen-Activated Protein KinasesPhosphothreonineAxon growthAxon regenerationBrain developmentGAP-43JNKPhosphorylationPrimates

Identifiers

PMID33832520
PMCPMC8034164
OpenAlexW3151489047

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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.