Evidence map›Paper›PMID 25349423›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Role for NUP62 depletion and PYK2 redistribution in dendritic retraction resulting from chronic stress.

Yayoi Kinoshita, Richard G Hunter, Jason D Gray, Roxana Mesias, Bruce S McEwen, Deanna L Benson, D Stave Kohtz

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

26 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. SKA2 enhances stress-related glucocorticoid receptor signaling through FKBP4-FKBP5 interactions in neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Advances in the understanding of nuclear pore complexes in human diseases.Journal of cancer research and clinical oncology · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Sca1Stem cell reviews and reports · 2021
    Article
  12. Review
  13. Review
  14. Revisiting the Stress Concept: Implications for Affective Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Review
  15. Review
  16. Alzheimer's Disease Risk Factor Pyk2 Mediates Amyloid-β-Induced Synaptic Dysfunction and Loss.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  17. Article
  18. Review
  19. Article
  20. 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

7 authors at 3 institutions in 1 country.

Yayoi KinoshitaDepartment of Pathology and.
Richard G HunterHarold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, Rockefeller University, New York, NY 10065; and Department of Psychology, University of Massachusetts, Boston, MA 02125.
Jason D GrayHarold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, Rockefeller University, New York, NY 10065; and.
Roxana MesiasDepartment of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029;
Bruce S McEwenDepartment of Psychology, University of Massachusetts, Boston, MA 02125 stave.kohtz@gmail.com mcewen@mail.rockefeller.edu.
Deanna L BensonDepartment of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029;
D Stave KohtzDepartment of Pathology and stave.kohtz@gmail.com mcewen@mail.rockefeller.edu.
Allen Institute for Brain Science · USRockefeller University · USUniversity of Massachusetts Boston · US

Funding

STRESS, ADRENAL STEROIDS AND THE BRAINR01MH041256 · NIMH · ROCKEFELLER UNIVERSITY · PI MCEWEN, BRUCE S. · 1986 to 2015
$4.3M
Role of Sema7A in functional organization of neocortexR01MH095229 · NIMH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BENSON, DEANNA L, HUNTLEY, GEORGE W. · 2012 to 2013
$790k
Nuclear Pore Complex Architecture and Drug Resistance in Ovarian CarcinomasR03CA141318 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI KOHTZ, DONALD STAVE · 2010 to 2011
$167k
NCI NIH HHS R03 CA141318NCI NIH HHS R03CA141318NIMH NIH HHS R01 MH041256NIMH NIH HHS R01 MH095229NIMH NIH HHS R01 MH41256
6 · The paper itself

Abstract

Genetic evidence suggests cell-type-specific functions for certain nucleoporins, and gene expression profiling has revealed that nucleoporin p62 (NUP62) transcripts are decreased in the prefrontal cortex of major depressives. Chronic stress, which can precipitate depression, induces changes in the architecture and plasticity of apical dendrites that are particularly evident in the CA3 region of the hippocampus. Genetically targeted translating ribosome affinity purification revealed a selective reduction in translated Nup62 transcripts in CA3 of chronically stressed mice, and the Nup62 protein content of nuclei extracted from whole hippocampus was found to be decreased in chronically stressed rats. In cultured cells, phosphorylation of a FAK/proline-rich tyrosine kinase 2 (PYK2) consensus site in the alpha-helical domain of NUP62 (human Y422) is shown to be associated with shedding of NUP62 from the nuclear pore complex (NPC) and/or retention of NUP62 in the cytoplasm. Increased levels of phospho-Y425 Nup62 were observed in cytoplasmic fractions of hippocampi from chronically stressed rats, and immunofluorescence microscopy revealed redistribution of activated Pyk2 to the perinuclear region of stressed pyramidal neurons. Depletion of Nup62 from cultured embryonic day 18 rat hippocampal and cortical neurons resulted in simplification and retraction of dendritic arbors, without disruption of axon initial segment integrity. Thus, at least two types of mechanisms--one affecting expression and the other association with the NPC--could contribute to loss of NUP62 from CA3 pyramidal neurons during chronic stress. Their combined actions may account for the enhanced responsiveness of CA3 apical dendrites to chronic stress and may either be pathogenic or serve to protect CA3 neurons from permanent damage.

Indexed as

AnimalsAxonsCA3 Region, HippocampalChronic DiseaseDendritesFocal Adhesion Kinase 2HumansMembrane GlycoproteinsMiceNuclear Pore Complex ProteinsPyramidal CellsRatsRats, Sprague-DawleyStress, PsychologicalFocal Adhesion Kinase 2Membrane GlycoproteinsNuclear Pore Complex Proteinsnuclear pore protein p62NUP62 protein, mousePtk2b protein, mousechronic stressdendrite retractionhippocampusnucleoporin p62proline-rich tyrosine kinase 2

Identifiers

PMID25349423
PMCPMC4234548
OpenAlexW2054226017

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.