Evidence map›Paper›PMID 27144290›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2016

The Nuclear Receptor, Nor-1, Induces the Physiological Responses Associated With Exercise.

Joel M Goode, Michael A Pearen, Zewen K Tuong, Shu-Ching M Wang, Tae Gyu Oh, Emily X Shao, George E O Muscat

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 22% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. NOR-1 as a Context-Dependent Rheostat of Vascular and Cardiac Remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  4. Article
  5. NR4A3 suppresses bladder cancer progression by modulating autophagyEuropean journal of histochemistry : EJH · 2025
    Article
  6. NOR-1 Overexpression Elevates Myoglobin Expression via PERM1 and Enhances Mitochondrial Function and Endurance in Skeletal Muscles of Aged Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  7. Review
  8. βFrontiers in physiology · 2024
    Article
  9. Review
  10. Exercise metabolism and adaptation in skeletal muscle.Nature reviews. Molecular cell biology · 2023
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
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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

7 authors at 1 institution in 1 country.

Joel M GoodeInstitute for Molecular Bioscience (J.M.G., M.A.P., Z.K.T., S.-C.W., T.G.O., E.X.S., G.E.O.M.), The University of Queensland, Queensland 4072, Australia; and QIMR Berghofer Medical Research Institute (M.A.P.), Royal Brisbane Hospital, Queensland 4029, Australia.
Michael A PearenInstitute for Molecular Bioscience (J.M.G., M.A.P., Z.K.T., S.-C.W., T.G.O., E.X.S., G.E.O.M.), The University of Queensland, Queensland 4072, Australia; and QIMR Berghofer Medical Research Institute (M.A.P.), Royal Brisbane Hospital, Queensland 4029, Australia.
Zewen K TuongInstitute for Molecular Bioscience (J.M.G., M.A.P., Z.K.T., S.-C.W., T.G.O., E.X.S., G.E.O.M.), The University of Queensland, Queensland 4072, Australia; and QIMR Berghofer Medical Research Institute (M.A.P.), Royal Brisbane Hospital, Queensland 4029, Australia.
Shu-Ching M WangInstitute for Molecular Bioscience (J.M.G., M.A.P., Z.K.T., S.-C.W., T.G.O., E.X.S., G.E.O.M.), The University of Queensland, Queensland 4072, Australia; and QIMR Berghofer Medical Research Institute (M.A.P.), Royal Brisbane Hospital, Queensland 4029, Australia.
Tae Gyu OhInstitute for Molecular Bioscience (J.M.G., M.A.P., Z.K.T., S.-C.W., T.G.O., E.X.S., G.E.O.M.), The University of Queensland, Queensland 4072, Australia; and QIMR Berghofer Medical Research Institute (M.A.P.), Royal Brisbane Hospital, Queensland 4029, Australia.
Emily X ShaoInstitute for Molecular Bioscience (J.M.G., M.A.P., Z.K.T., S.-C.W., T.G.O., E.X.S., G.E.O.M.), The University of Queensland, Queensland 4072, Australia; and QIMR Berghofer Medical Research Institute (M.A.P.), Royal Brisbane Hospital, Queensland 4029, Australia.
George E O MuscatInstitute for Molecular Bioscience (J.M.G., M.A.P., Z.K.T., S.-C.W., T.G.O., E.X.S., G.E.O.M.), The University of Queensland, Queensland 4072, Australia; and QIMR Berghofer Medical Research Institute (M.A.P.), Royal Brisbane Hospital, Queensland 4029, Australia.
University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle remodels metabolic capacity, contractile and exercise phenotype in response to physiological demands. This adaptive remodeling response to physical activity can ameliorate/prevent diseases associated with poor diet and lifestyle. Our previous work demonstrated that skeletal muscle-specific transgenic expression of the neuron-derived orphan nuclear receptor, Nor-1 drives muscle reprogramming, improves exercise endurance, and oxidative metabolism. The current manuscript investigates the association between exercise, Nor-1 expression and the role of Nor-1 in adaptive remodeling. We demonstrate that Nor-1 expression is induced by exercise and is dependent on calcium/calcineurin signaling (in vitro and in vivo). Analysis of fatigue-resistant transgenic mice that express Nor-1 in skeletal muscle revealed increased hypertrophy and vascularization of muscle tissue. Moreover, we demonstrate that transgenic Nor-1 expression is associated with increased intracellular recycling, ie, autophagy, involving 1) increased expression of light chain 3A or LC3A-II, autophagy protein 5, and autophagy protein 12 in quadriceps femoris muscle extracts from Tg-Nor-1 (relative to Wild-type (WT) littermates); 2) decreased p62 expression indicative of increased autophagolysosome assembly; and 3) decreased mammalian target of rapamycin complex 1 activity. Transfection of LC3A-GFP-RFP chimeric plasmid demonstrated that autophagolysosome formation was significantly increased by Nor-1 expression. Furthermore, we demonstrated a single bout of exercise induced LC3A-II expression in skeletal muscle from C57BL/6 WT mice. This study, when combined with our previous studies, demonstrates that Nor-1 expression drives multiple physiological changes/pathways that are critical to the beneficial responses of muscle to exercise and provides insights into potential pharmacological manipulation of muscle reprogramming for the treatment of lifestyle induced chronic diseases.

Indexed as

Physical Conditioning, AnimalAnimalsAutophagosomesAutophagyCalcineurinCalciumCell LineDNA-Binding ProteinsHypertrophyLysosomesMechanistic Target of Rapamycin Complex 1Mice, Inbred C57BLMice, TransgenicMicrotubule-Associated ProteinsModels, BiologicalMuscle, SkeletalCalcineurinCalciumDNA-Binding ProteinsMap1lc3b protein, mouseMechanistic Target of Rapamycin Complex 1Microtubule-Associated ProteinsNerve Tissue ProteinsNr4a3 protein, mouseReceptors, SteroidReceptors, Thyroid HormoneRNA, MessengerSirolimus

Identifiers

PMID27144290
PMCPMC5414640
OpenAlexW2345500353

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.