Evidence map›Paper›PMID 28779160›Full record

ArticleScientific reports2017

Age-dependent motor dysfunction due to neuron-specific disruption of stress-activated protein kinase MKK7.

Tokiwa Yamasaki, Norie Deki-Arima, Asahito Kaneko, Norio Miyamura, Mamiko Iwatsuki, Masato Matsuoka, Noriko Fujimori-Tonou, Yoshimi Okamoto-Uchida, Jun Hirayama, Jamey D Marth and 6 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. 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
2.1field-weighted citation impact, top 14% 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, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Mitochondrial ProteinFrontiers in pharmacology · 2022
    Article
  6. DualInternational journal of molecular sciences · 2021
    Article
  7. MKK7 deficiency in mature neurons impairs parental behavior in mice.Genes to cells : devoted to molecular & cellular mechanisms · 2021
    Article
  8. Review
  9. Review
  10. Article
  11. Review
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  13. Molecular basis of the functions of the mammalian neuronal growth cone revealed using new methods.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2019
    Review
  14. Article
  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

16 authors at 9 institutions in 3 countries.

Tokiwa YamasakiDepartment of Developmental and Regenerative Biology, Medical Research Institute, Tokyo Medical and Dental University (TMDU), 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Norie Deki-ArimaDepartment of Developmental and Regenerative Biology, Medical Research Institute, Tokyo Medical and Dental University (TMDU), 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Asahito KanekoLaboratory of Physiology and Pharmacology, School of Advanced Science and Engineering, Waseda University, Tokyo, Japan.
Norio MiyamuraDepartment of Developmental and Regenerative Biology, Medical Research Institute, Tokyo Medical and Dental University (TMDU), 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Mamiko IwatsukiDepartment of Hygiene and Public Health I, Tokyo Women's Medical University, Tokyo, Japan.
Masato MatsuokaDepartment of Hygiene and Public Health I, Tokyo Women's Medical University, Tokyo, Japan.
Noriko Fujimori-TonouLaboratory for Molecular Dynamics of Mental Disorders, RIKEN Brain Science Institute, Wako, Saitama, 3510198, Japan.
Yoshimi Okamoto-UchidaDepartment of Developmental and Regenerative Biology, Medical Research Institute, Tokyo Medical and Dental University (TMDU), 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Jun HirayamaDepartment of Developmental and Regenerative Biology, Medical Research Institute, Tokyo Medical and Dental University (TMDU), 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Jamey D MarthCenter for Nanomedicine, SBP Medical Discovery Institute, Department of Molecular, Cellular, and Developmental Biology, University of California Santa Barbara, Santa Barbara, California, USA.
Yuji YamanashiDivision of Genetics, Department of Cancer Biology, The Institute of Medical Science, The University of Tokyo, Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan.
Hiroshi KawasakiDepartment of Medical Neuroscience, Graduate School of Medical Sciences; Brain/Liver Interface Medicine Research Center, Kanazawa University, Kanazawa, Japan.
Koji YamanakaDepartment of Neuroscience and Pathobiology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan.ORCID 0000-0003-4655-0035
Josef M PenningerIMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria.ORCID 0000-0002-8194-3777
Shigenobu ShibataLaboratory of Physiology and Pharmacology, School of Advanced Science and Engineering, Waseda University, Tokyo, Japan.
Hiroshi NishinaDepartment of Developmental and Regenerative Biology, Medical Research Institute, Tokyo Medical and Dental University (TMDU), 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan. nishina.dbio@mri.tmd.ac.jp.
Tokyo Medical and Dental University · JPTokyo Women's Medical University · JPWaseda University · JPInstitute of Molecular Biotechnology · ATKanazawa University · JPNagoya University · JPRIKEN Center for Brain Science · JPThe University of Tokyo · JPUniversity of California, Santa Barbara · US

Funding

Protein Glycosylation in the Coagulopathy and Inflammation of SepsisP01HL131474 · NHLBI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI MARTH, JAMEY · 2016 to 2025
$26.2M
GLYCOSYLTRANSFERASE FUNCTION IN DEVELOPMENT AND DISEASER01DK048247 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JAMEY MARTH · 1994 to 2026
$9.4M
Glycoprotein Remodeling in the Vasculopathy and Coagulopathy of SepsisR01HL125352 · NHLBI · UNIVERSITY OF CALIFORNIA SANTA BARBARA · PI MARTH, JAMEY, NIZET, VICTOR · 2014 to 2018
$3.6M
NHLBI NIH HHS P01 HL131474NHLBI NIH HHS R01 HL125352NIDDK NIH HHS R01 DK048247
6 · The paper itself

Abstract

c-Jun N-terminal kinase (JNK) is a member of the mitogen-activated protein kinase family and controls various physiological processes including apoptosis. A specific upstream activator of JNKs is the mitogen-activated protein kinase kinase 7 (MKK7). It has been reported that MKK7-JNK signaling plays an important regulatory role in neural development, however, post-developmental functions in the nervous system have not been elucidated. In this study, we generated neuron-specific Mkk7 knockout mice (MKK7 cKO), which impaired constitutive activation of JNK in the nervous system. MKK7 cKO mice displayed impaired circadian behavioral rhythms and decreased locomotor activity. MKK7 cKO mice at 8 months showed motor dysfunctions such as weakness of hind-limb and gait abnormality in an age-dependent manner. Axonal degeneration in the spinal cord and muscle atrophy were also observed, along with accumulation of the axonal transport proteins JNK-interacting protein 1 and amyloid beta precursor protein in the brains and spinal cords of MKK7 cKO mice. Thus, the MKK7-JNK signaling pathway plays important roles in regulating circadian rhythms and neuronal maintenance in the adult nervous system.

Indexed as

Stress, PhysiologicalAge FactorsAnimalsBrainCircadian RhythmDisease Models, AnimalDisease ProgressionGene DeletionJNK Mitogen-Activated Protein KinasesMaleMAP Kinase Kinase 7MAP Kinase Signaling SystemMiceMice, TransgenicMotor ActivityMotor DisordersJNK Mitogen-Activated Protein KinasesMap2k7 protein, mouseMAP Kinase Kinase 7

Identifiers

PMID28779160
PMCPMC5544763
OpenAlexW2739755596

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.