Evidence map›Paper›PMID 22348105›Full record

ArticlePloS one2012

Age-dependent targeting of protein phosphatase 1 to Ca2+/calmodulin-dependent protein kinase II by spinophilin in mouse striatum.

Anthony J Baucum, Stefan Strack, Roger J Colbran

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Mechanisms of spinophilin-dependent pancreas dysregulation in obesity.American journal of physiology. Endocrinology and metabolism · 2024
    Article
  4. Regulation of Synaptic Transmission and Plasticity by Protein Phosphatase 1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. A Novel HumanThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

3 authors at 1 institution in 1 country.

Anthony J BaucumDepartment of Molecular Physiology and Biophysics, Vanderbilt-Kennedy Center, Center for Molecular Neuroscience, Vanderbilt University School of Medicine, Nashville, Tennessee, United States of America. Anthony.Baucum@vanderbilt.edu
Stefan Strack
Roger J Colbran
John F. Kennedy Center for the Performing Arts · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1986 to 2011
$28.1M
Shop Module CoreP30EY008126 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Kevin L Schey · 1989 to 2026
$19.6M
THREE-TIERED PREVENTION MODEL TO BETTER SERVE ALL STUDENP30HD015052 · NICHD · VANDERBILT UNIVERSITY · PI DYKENS, ELISABETH MAY · 1985 to 2014
$18.6M
Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
Program in NeurogenomicsT32MH065215 · NIMH · VANDERBILT UNIVERSITY · PI ROGER J COLBRAN · 2002 to 2026
$6.4M
Vanderbilt Mouse Metabolic Phenotyping CenterU2CDK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2016 to 2021
$6.3M
Mechanisms of CaM Kinase II Signal TransductionR01MH063232 · NIMH · VANDERBILT UNIVERSITY · PI COLBRAN, ROGER J · 2001 to 2015
$5.4M
TARGETING OF BRAIN PROTEIN PHOSPHATASE 1R01NS037508 · NINDS · VANDERBILT UNIVERSITY · PI COLBRAN, ROGER J · 1999 to 2002
$641k
NCI NIH HHS CA68485NCI NIH HHS P30 CA068485NEI NIH HHS EY08126NEI NIH HHS P30 EY008126NICHD NIH HHS HD15052NICHD NIH HHS P30 HD015052NIDDK NIH HHS DK20593NIDDK NIH HHS DK58404NIDDK NIH HHS DK59637NIDDK NIH HHS P30 DK020593NIDDK NIH HHS P30 DK058404NIDDK NIH HHS P60 DK020593NIDDK NIH HHS U24 DK059637NIMH NIH HHS R01 MH063232NIMH NIH HHS R01-MH063232NIMH NIH HHS T32 MH065215NIMH NIH HHS T32-MH65215NINDS NIH HHS NS037508
6 · The paper itself

Abstract

Mechanisms underlying age-dependent changes of dendritic spines on striatal medium spiny neurons are poorly understood. Spinophilin is an F-actin- and protein phosphatase 1 (PP1)-binding protein that targets PP1 to multiple downstream effectors to modulate dendritic spine morphology and function. We found that calcium/calmodulin-dependent protein kinase II (CaMKII) directly and indirectly associates with N- and C-terminal domains of spinophilin, but F-actin can displace CaMKII from the N-terminal domain. Spinophilin co-localizes PP1 with CaMKII on the F-actin cytoskeleton in heterologous cells, and spinophilin co-localizes with synaptic CaMKII in neuronal cultures. Thr286 autophosphorylation enhances the binding of CaMKII to spinophilin in vitro and in vivo. Although there is no change in total levels of Thr286 autophosphorylation, maturation from postnatal day 21 into adulthood robustly enhances the levels of CaMKII that co-immunoprecipitate with spinophilin from mouse striatal extracts. Moreover, N- and C-terminal domain fragments of spinophilin bind more CaMKII from adult vs. postnatal day 21 striatal lysates. Total levels of other proteins that interact with C-terminal domains of spinophilin decrease during maturation, perhaps reducing competition for CaMKII binding to the C-terminal domain. In contrast, total levels of α-internexin and binding of α-internexin to the spinophilin N-terminal domain increases with maturation, perhaps bridging an indirect interaction with CaMKII. Moreover, there is an increase in the levels of myosin Va, α-internexin, spinophilin, and PP1 in striatal CaMKII immune complexes isolated from adult and aged mice compared to those from postnatal day 21. These changes in spinophilin/CaMKII interactomes may contribute to changes in striatal dendritic spine density, morphology, and function during normal postnatal maturation and aging.

Indexed as

Age FactorsAgingAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Corpus StriatumDendritic SpinesMiceMicrofilament ProteinsNerve Tissue ProteinsNeurabinsPhosphorylationProtein BindingProtein Phosphatase 1Calcium-Calmodulin-Dependent Protein Kinase Type 2Microfilament ProteinsNerve Tissue ProteinsNeurabinsProtein Phosphatase 1

Identifiers

PMID22348105
PMCPMC3278457
OpenAlexW2075953074

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.