Evidence map›Paper›PMID 20689998›Full record

ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2011

Neuronal PINCH is regulated by TNF-α and is required for neurite extension.

Asavari Jatiani, Paola Pannizzo, Elisa Gualco, Luis Del-Valle, Dianne Langford

Abstract read
In one paragraph

Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.2field-weighted citation impact, top 50% 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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Dysregulation of PINCH signaling in mesial temporal epilepsy.Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia · 2017
    Article
  7. Article
  8. Review
  9. Article
  10. Review
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

5 authors at 4 institutions in 2 countries.

Asavari JatianiDepartment of Neuroscience, Temple University School of Medicine, 3500 N. Broad St., MERB 750, Philadelphia, PA, USA.
Paola Pannizzo
Elisa Gualco
Luis Del-Valle
Dianne Langford
Temple University · USLouisiana State University · USTemple College · USUniversity of Genoa · IT

Funding

STRUCTURAL NEUROIMAGING COREP30MH062512 · NIMH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DAVID J MOORE · 2001 to 2026
$50.4M
NEUROAIDS TISSUE NETWORKR24MH059745 · NIMH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GRANT, IGOR · 1998 to 2007
$13.2M
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
Involvement of Survivin in the Development of PMLR01NS055644 · NINDS · TEMPLE UNIV OF THE COMMONWEALTH · PI DEL VALLE, LUIS · 2007 to 2011
$1.5M
NIMH NIH HHS MH059745NIMH NIH HHS MH62512NIMH NIH HHS P30 MH062512NIMH NIH HHS R01 MH085602NIMH NIH HHS R01MH085602NIMH NIH HHS R01 MH107340NINDS NIH HHS R01 NS055644
6 · The paper itself

Abstract

During HIV infection of the CNS, neurons are damaged by viral proteins, such as Tat and gp120, or by inflammatory factors, such as TNF-α, that are released from infected and/or activated glial cells. Host responses to this damage may include the induction of survival or repair mechanisms. In this context, previous studies report robust expression of a protein called particularly interesting new cysteine histidine-rich protein (PINCH), in the neurons of HIV patients' brains, compared with nearly undetectable levels in HIV-negative individuals (Rearden et al., J Neurosci Res 86:2535-2542, 2008), suggesting PINCH's involvement in neuronal signaling during HIV infection of the brain. To address potential triggers for PINCH induction in HIV patients' brains, an in vitro system mimicking some aspects of HIV infection of the CNS was utilized. We investigated neuronal PINCH expression, subcellular distribution, and biological consequences of PINCH sequestration upon challenge with Tat, gp120, and TNF-α. Our results indicate that in neurons, TNF-α stimulation increases PINCH expression and changes its subcellular localization. Furthermore, PINCH mobility is required to maintain neurite extension upon challenge with TNF-α. PINCH may function as a neuron-specific host-mediated response to challenge by HIV-related factors in the CNS.

Indexed as

Adaptor Proteins, Signal TransducingAIDS Dementia ComplexAnimalsBlotting, WesternBrainDNA-Binding ProteinsFluorescent Antibody TechniqueGene ExpressionGene Expression ProfilingGene Expression RegulationHumansImmunoprecipitationLIM Domain ProteinsMembrane ProteinsMiceMice, Inbred C57BLAdaptor Proteins, Signal TransducingDNA-Binding ProteinsLIM Domain ProteinsLIMS1 protein, humanMembrane Proteinstat Gene Products, Human Immunodeficiency VirusTumor Necrosis Factor-alpha

Identifiers

PMID20689998
PMCPMC3107369
OpenAlexW2091857386

What OpenQuestion holds

Textmetadata
LicenceTDM
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.