Evidence map›Paper›PMID 25526860›Full record

ArticleMolecular neurobiology2016

CRMP1 Interacted with Spy1 During the Collapse of Growth Cones Induced by Sema3A and Acted on Regeneration After Sciatic Nerve Crush.

Li Yao, Yong-Hua Liu, Xiaohong Li, Yu-Hong Ji, Xiao-Jing Yang, Xian-Ting Hang, Zong-Mei Ding, Fang Liu, You-Hua Wang, Ai-Guo Shen

Abstract read
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In one paragraph

Article in Molecular neurobiology, 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
1.5field-weighted citation impact, top 21% 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, 22 citations in OpenAlex.

  1. Semaphorins and Their Role in Neuropathic Pain.Life (Basel, Switzerland) · 2026
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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

10 authors at 3 institutions in 1 country.

Li YaoDepartment of Orthopaedics, Affiliated Hospital of Nantong University and Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, 226001, People's Republic of China.
Yong-Hua LiuDepartment of Orthopaedics, Affiliated Hospital of Nantong University and Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, 226001, People's Republic of China.
Xiaohong LiDepartment of Orthopaedics, Affiliated Hospital of Nantong University and Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, 226001, People's Republic of China.
Yu-Hong JiDepartment of Orthopaedics, Affiliated Hospital of Nantong University and Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, 226001, People's Republic of China.
Xiao-Jing YangDepartment of Oncology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, People's Republic of China.
Xian-Ting HangDepartment of Orthopaedics, Affiliated Hospital of Nantong University and Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, 226001, People's Republic of China.
Zong-Mei DingDepartment of Orthopaedics, Affiliated Hospital of Nantong University and Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, 226001, People's Republic of China.
Fang LiuKey Laboratory of Neuroregeneration, Nantong University, Nantong, Jiangsu, 226001, People's Republic of China.
You-Hua WangDepartment of Orthopaedics, Affiliated Hospital of Nantong University and Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, 226001, People's Republic of China. wangyouhuantu@126.com.
Ai-Guo ShenDepartment of Orthopaedics, Affiliated Hospital of Nantong University and Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College of Nantong University, Nantong, Jiangsu Province, 226001, People's Republic of China. CRMP1nt@163.com.
Nantong University · CNJiangnan University · CNShanghai Sixth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CRMP1, a member of the collapsin response mediator protein family (CRMPs), was reported to regulate axon outgrowth in Sema3A signaling pathways via interactions with its co-receptor protein neuropilin-1 and plexin-As through the Fyn-cyclin-dependent kinase 5 (CDK5) cascade and the sequential phosphorylation of CRMP1 by lycogen synthase kinase-3β (GSK-3β). Using yeast two-hybrid, we identified a new molecule, Speedy A1 (Spy1), a member of the Speedy/RINGO family, with an interaction with CRMP1. Besides, for the first time, we observed the association of CRMP1 with actin. Based on this, we wondered the association of them and their function in Sema3A-induced growth cones collapse and regeneration process after SNC. During our study, we constructed overexpression plasmid and short hairpin RNA (shRNA) to question the relationship of CRMP1/Spy1 and CRMP1/actin. We observed the interactions of CRMP1/Spy1 and CRMP1/actin. Besides, we found that Spy1 could affect CRMP1 phosphorylation actived by CDK5 and that enhanced CRMP1 phosphorylation might disturb the combination of CRMP1 and actin, which would contribute to abnormal of Sema3A-induced growth cones collapse and finally lead to influent regeneration process after rat sciatic nerve crush. Through rat walk footprint test, we also observed the variance during regeneration progress, respectively. We speculated that CRMP1 interacted with Spy1 which would disturb the association of CRMP1 with actin and was involved in the collapse of growth cones induced by Sema3A and regeneration after sciatic nerve crush.

Indexed as

Nerve CrushActinsAnimalsCell Cycle ProteinsCollapsin Response Mediator Protein 1Cyclin-Dependent Kinase 5Growth ConesHEK293 CellsHumansImmunohistochemistryMutant ProteinsNerve RegenerationNerve Tissue ProteinsPhosphorylationProtein BindingProtein Structure, TertiaryActinsCell Cycle ProteinsCollapsin Response Mediator Protein 1CRMP1 protein, humanCyclin-Dependent Kinase 5Mutant ProteinsNerve Tissue ProteinsRNA, Small InterferingSemaphorin-3ASPDYA protein, humanActinCRMP1Growth cones collapseSciatic nerve crushSema3ASpy1

Identifiers

PMID25526860
OpenAlexW1993926404

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.