Evidence map›Paper›PMID 26147533›Full record

ArticleNature neuroscience2015

Identification of a Vav2-dependent mechanism for GDNF/Ret control of mesolimbic DAT trafficking.

Shuyong Zhu, Chengjiang Zhao, Yingying Wu, Qiaoqiao Yang, Aiyun Shao, Tiepeng Wang, Jianfu Wu, Yanqing Yin, Yandong Li, Jincan Hou and 6 more

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Nature neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

33 citing papers in PubMed, 54 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

16 authors at 5 institutions in 2 countries.

Shuyong ZhuInstitute of Neuroscience, State Key Laboratory of Neuroscience, Chinese Academy of Sciences Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Chengjiang Zhao1] Institute of Neuroscience, State Key Laboratory of Neuroscience, Chinese Academy of Sciences Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China. [2] University of the Chinese Academy of Sciences, Shanghai, China.
Yingying Wu1] Institute of Neuroscience, State Key Laboratory of Neuroscience, Chinese Academy of Sciences Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China. [2] University of the Chinese Academy of Sciences, Shanghai, China.
Qiaoqiao Yang1] Institute of Neuroscience, State Key Laboratory of Neuroscience, Chinese Academy of Sciences Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China. [2] Department of Anatomy, Histology and Embryology, Shanghai Medical School, Fudan University, Shanghai, China.
Aiyun ShaoInstitute of Neuroscience, State Key Laboratory of Neuroscience, Chinese Academy of Sciences Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Tiepeng WangInstitute of Neuroscience, State Key Laboratory of Neuroscience, Chinese Academy of Sciences Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Jianfu WuInstitute of Neuroscience, State Key Laboratory of Neuroscience, Chinese Academy of Sciences Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Yanqing YinInstitute of Neuroscience, State Key Laboratory of Neuroscience, Chinese Academy of Sciences Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Yandong LiInstitute of Neuroscience, State Key Laboratory of Neuroscience, Chinese Academy of Sciences Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Jincan HouInstitute of Neuroscience, State Key Laboratory of Neuroscience, Chinese Academy of Sciences Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Xinhua Zhang1] Institute of Neuroscience, State Key Laboratory of Neuroscience, Chinese Academy of Sciences Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China. [2] Co-innovation Center of Neuroregeneration, School of Medicine, Nantong University, Nantong, China.
Guomin ZhouDepartment of Anatomy, Histology and Embryology, Shanghai Medical School, Fudan University, Shanghai, China.
Xiaosong GuCo-innovation Center of Neuroregeneration, School of Medicine, Nantong University, Nantong, China.
Xiaomin WangCenter of Parkinson's Disease, Beijing Institute for Brain Disorders, Beijing, China.
Xosé R BusteloCentro de Investigación del Cáncer, Consejo Superior de Investigaciones Científicas, University of Salamanca, Salamanca, Spain.ORCID 0000000193986072
Jiawei ZhouInstitute of Neuroscience, State Key Laboratory of Neuroscience, Chinese Academy of Sciences Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Chinese Academy of Sciences · CNNantong University · CNChinese Institute for Brain Research · CNConsejo Superior de Investigaciones Científicas · ESShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dopamine (DA) homeostasis is essential for a variety of brain activities. Dopamine transporter (DAT)-mediated DA reuptake is one of the most critical mechanisms for normal DA homeostasis. However, the molecular mechanisms underlying the regulation of DAT activity in the brain remain poorly understood. Here we show that the Rho-family guanine nucleotide exchange factor protein Vav2 is required for DAT cell surface expression and transporter activity modulated by glial cell line-derived neurotrophic factor (GDNF) and its cognate receptor Ret. Mice deficient in either Vav2 or Ret displayed elevated DAT activity, which was accompanied by an increase in intracellular DA selectively in the nucleus accumbens. Vav2(-/-) mice exposed to cocaine showed reduced DAT activity and diminished behavioral cocaine response. Our data demonstrate that Vav2 is a determinant of DAT trafficking in vivo and contributes to the maintenance of DA homeostasis in limbic DA neuron terminals.

Indexed as

AnimalsBehavior, AnimalCocaineDopamineDopamine Plasma Membrane Transport ProteinsDopaminergic NeuronsGlial Cell Line-Derived Neurotrophic FactorHomeostasisLimbic SystemMaleMiceMice, Inbred C57BLMice, KnockoutNucleus AccumbensProtein TransportProto-Oncogene Proteins c-retCocaineDopamineDopamine Plasma Membrane Transport ProteinsGdnf protein, mouseGlial Cell Line-Derived Neurotrophic FactorProto-Oncogene Proteins c-retProto-Oncogene Proteins c-vavRet protein, mouseVav2 protein, mouse

Identifiers

PMID26147533
OpenAlexW1525421750

What OpenQuestion holds

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Registered trials

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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.