Evidence map›Paper›PMID 23554879›Full record

Trial reportPloS one2013

PINCH in the cellular stress response to tau-hyperphosphorylation.

Ahmet Yunus Ozdemir, Inna Rom, Jane Kovalevich, William Yen, Radhika Adiga, Rajnish S Dave, Dianne Langford

Open access · goldAbstract readClinical TrialMulticenter Study
In one paragraph

Trial report in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Dysregulation of PINCH signaling in mesial temporal epilepsy.Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia · 2017
    Article
  10. Review
  11. Blood biomarkers for brain injury: What are we measuring?Neuroscience and biobehavioral reviews · 2016
    Review
  12. 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 1 institution in 1 country.

Ahmet Yunus OzdemirTemple University School of Medicine, Department of Neuroscience, Philadelphia, Pennsylvania, USA.
Inna Rom
Jane Kovalevich
William Yen
Radhika Adiga
Rajnish S Dave
Dianne Langford
Temple University · US

Funding

Viral Gene Editing and Bioinformatics Core for Institution # 269291P30MH092177 · NIMH · TEMPLE UNIV OF THE COMMONWEALTH · PI SHOHREH AMINI · 2011 to 2026
$24.9M
California NeuroAIDS Tissue NetworkU24MH100928 · NIMH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ACHIM, CRISTIAN L, MOORE, DAVID J · 2013 to 2023
$13.9M
California NeuroAIDS Tissue Network (CNTN)U01MH083506 · NIMH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GRANT, IGOR · 2008 to 2012
$8.1M
PINCH-mediated CNS cell dysfunction and tauopathy in HIVR01MH107340 · NIMH · TEMPLE UNIV OF THE COMMONWEALTH · PI LANGFORD, DIANNE TERESA · 2016 to 2020
$2.0M
Role of PINCH in neuronal response to HIV infection of the CNSR01MH085602 · NIMH · TEMPLE UNIV OF THE COMMONWEALTH · PI LANGFORD, DIANNE TERESA · 2009 to 2013
$1.8M
NIMH NIH HHS P30 MH092177NIMH NIH HHS R01 MH085602NIMH NIH HHS R01-MH085602NIMH NIH HHS R01 MH107340NIMH NIH HHS U01 MH083506NIMH NIH HHS U24 MH100928
6 · The paper itself

Abstract

Particularly interesting new cysteine- histidine- rich protein (PINCH) is an adaptor protein that our data have shown is required for neurite extension under stressful conditions. Our previous studies also report that PINCH is recalled by neurons showing decreased levels of synaptodendritic signaling proteins such as MAP2 or synaptophysin in the brains of human immunodeficiency virus (HIV) patients. The current study addressed potential role(s) for PINCH in neurodegenerative diseases. Mass spectrometry predicted the interaction of PINCH with Tau and with members of the heat shock response. Our in vitro data confirmed that PINCH binds to hyperphosphorylated (hp) Tau and to E3 ubiquitin ligase, carboxy-terminus of heat shock-70 interacting protein. Silencing PINCH prior to induction of hp-Tau resulted in more efficient clearance of accumulating hp-Tau, suggesting that PINCH may play a role in stabilizing hp-Tau. Accumulation of hp-Tau is implicated in more than 20 neuropathological diseases including Alzheimer's disease (AD), frontotemporal dementia (FTD), and human immunodeficiency virus encephalitis (HIVE). Analyses of brain tissues from HIVE, AD and FTD patients showed that PINCH is increased and binds to hp-Tau. These studies address a new mechanism by which AD and HIV may intersect and identify PINCH as a contributing factor to the accumulation of hyperphosphorylated Tau.

Indexed as

Stress, PhysiologicalAdaptor Proteins, Signal TransducingAnimalsFemaleHumansLIM Domain ProteinsMaleMembrane ProteinsMiceMice, TransgenicMicrotubule-Associated ProteinsNeurodegenerative DiseasesPhosphorylationtau ProteinsUbiquitin-Protein LigasesAdaptor Proteins, Signal TransducingLIM Domain ProteinsLIMS1 protein, humanLims1 protein, mouseMAP2 protein, humanMembrane ProteinsMicrotubule-Associated ProteinsMtap2 protein, mousetau ProteinsUbiquitin-Protein Ligases

Identifiers

PMID23554879
PMCPMC3595241
OpenAlexW2027206789

What OpenQuestion holds

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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.