Evidence map›Paper›PMID 26398952›Full record

ArticleDisease models & mechanisms2015

Hyperactivity and attention deficits in mice with decreased levels of stress-inducible phosphoprotein 1 (STIP1).

Flavio H Beraldo, Anu Thomas, Benjamin Kolisnyk, Pedro H Hirata, Xavier De Jaeger, Amanda C Martyn, Jue Fan, Daniela F Goncalves, Matthew F Cowan, Talal Masood and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Disease models & mechanisms, 2015. 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
1.5field-weighted citation impact, top 17% 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, 35 citations in OpenAlex.

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  7. Functional dissociation of behavioral effects from acetylcholine and glutamate released from cholinergic striatal interneurons.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
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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

14 authors at 2 institutions in 3 countries.

Flavio H BeraldoRobarts Research Institute, The University of Western Ontario, London, Ontario N6A5B7, Canada fberaldo@robarts.ca vprado@robarts.ca mprado@robarts.ca.
Anu ThomasRobarts Research Institute, The University of Western Ontario, London, Ontario N6A5B7, Canada.
Benjamin KolisnykRobarts Research Institute, The University of Western Ontario, London, Ontario N6A5B7, Canada Program in Neuroscience, The University of Western Ontario, London, Ontario N6A5B7, Canada.
Pedro H HirataRobarts Research Institute, The University of Western Ontario, London, Ontario N6A5B7, Canada.
Xavier De JaegerRobarts Research Institute, The University of Western Ontario, London, Ontario N6A5B7, Canada.
Amanda C MartynRobarts Research Institute, The University of Western Ontario, London, Ontario N6A5B7, Canada.
Jue FanRobarts Research Institute, The University of Western Ontario, London, Ontario N6A5B7, Canada.
Daniela F GoncalvesRobarts Research Institute, The University of Western Ontario, London, Ontario N6A5B7, Canada.
Matthew F CowanRobarts Research Institute, The University of Western Ontario, London, Ontario N6A5B7, Canada.
Talal MasoodRobarts Research Institute, The University of Western Ontario, London, Ontario N6A5B7, Canada Program in Neuroscience, The University of Western Ontario, London, Ontario N6A5B7, Canada.
Vilma R MartinsDepartment of Molecular and Cell Biology, International Research Center, A.C. Camargo Cancer Center and National Institute for Translational Neuroscience Research Center, Sao Paulo, SP 01508-010, Brazil.
Robert GrosRobarts Research Institute, The University of Western Ontario, London, Ontario N6A5B7, Canada Department of Physiology and Pharmacology, The University of Western Ontario, London, Ontario N6A5B7, Canada.
Vania F PradoRobarts Research Institute, The University of Western Ontario, London, Ontario N6A5B7, Canada Program in Neuroscience, The University of Western Ontario, London, Ontario N6A5B7, Canada Department of Physiology and Pharmacology, The University of Western Ontario, London, Ontario N6A5B7, Canada Department of Anatomy and Cell Biology, The University of Western Ontario, London, Ontario N6A5B7, Canada fberaldo@robarts.ca vprado@robarts.ca mprado@robarts.ca.
Marco A M PradoRobarts Research Institute, The University of Western Ontario, London, Ontario N6A5B7, Canada Program in Neuroscience, The University of Western Ontario, London, Ontario N6A5B7, Canada Department of Physiology and Pharmacology, The University of Western Ontario, London, Ontario N6A5B7, Canada Department of Anatomy and Cell Biology, The University of Western Ontario, London, Ontario N6A5B7, Canada fberaldo@robarts.ca vprado@robarts.ca mprado@robarts.ca.
Western University · CATranslational Research in Oncology · FR

Funding

Canadian Institutes of Health Research MOP126000Canadian Institutes of Health Research MOP136930Canadian Institutes of Health Research MOP89919
6 · The paper itself

Abstract

Stress-inducible phosphoprotein I (STIP1, STI1 or HOP) is a co-chaperone intermediating Hsp70/Hsp90 exchange of client proteins, but it can also be secreted to trigger prion protein-mediated neuronal signaling. Some mothers of children with autism spectrum disorders (ASD) present antibodies against certain brain proteins, including antibodies against STIP1. Maternal antibodies can cross the fetus blood-brain barrier during pregnancy, suggesting the possibility that they can interfere with STIP1 levels and, presumably, functions. However, it is currently unknown whether abnormal levels of STIP1 have any impact in ASD-related behavior. Here, we used mice with reduced (50%) or increased STIP1 levels (fivefold) to test for potential ASD-like phenotypes. We found that increased STIP1 regulates the abundance of Hsp70 and Hsp90, whereas reduced STIP1 does not affect Hsp70, Hsp90 or the prion protein. Interestingly, BAC transgenic mice presenting fivefold more STIP1 show no major phenotype when examined in a series of behavioral tasks, including locomotor activity, elevated plus maze, Morris water maze and five-choice serial reaction time task (5-CSRTT). In contrast, mice with reduced STIP1 levels are hyperactive and have attentional deficits on the 5-CSRTT, but exhibit normal performance for the other tasks. We conclude that reduced STIP1 levels can contribute to phenotypes related to ASD. However, future experiments are needed to define whether it is decreased chaperone capacity or impaired prion protein signaling that contributes to these phenotypes.

Indexed as

Behavior, AnimalAnimalsAttention Deficit Disorder with HyperactivityDisease Models, AnimalGenetic Predisposition to DiseaseHeat-Shock ProteinsHSP70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsMaleMaze LearningMice, Inbred C57BLMice, KnockoutMotor ActivityPhenotypePrPC ProteinsReaction TimeHeat-Shock ProteinsHSP70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsPrPC ProteinsStip1 protein, mouseASDAttention deficitsAutismBACMouse modelStress-inducible phosphoprotein 1Touchscreen

Identifiers

PMID26398952
PMCPMC4631792
OpenAlexW2398212653

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.