Evidence map›Paper›PMID 25738396›Full record

ArticleNeuroscience research2015

Half-life of DISC1 protein and its pathological significance under hypoxia stress.

Sandeep Kumar Barodia, Sang Ki Park, Koko Ishizuka, Akira Sawa, Atsushi Kamiya

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

Article in Neuroscience research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

3 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. 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

5 authors at 2 institutions in 2 countries.

Sandeep Kumar BarodiaMolecular Psychiatry Program, Department of Psychiatry, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Baltimore, MD 21287, USA.
Sang Ki ParkMolecular Psychiatry Program, Department of Psychiatry, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Baltimore, MD 21287, USA; Department of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Koko IshizukaMolecular Psychiatry Program, Department of Psychiatry, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Baltimore, MD 21287, USA.
Akira SawaMolecular Psychiatry Program, Department of Psychiatry, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Baltimore, MD 21287, USA; Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. Electronic address: asawa1@jhmi.edu.
Atsushi KamiyaMolecular Psychiatry Program, Department of Psychiatry, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Baltimore, MD 21287, USA. Electronic address: akamiya1@jhmi.edu.
Johns Hopkins University · USPohang University of Science and Technology · KR

Funding

Project 3P50MH094268 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2011 to 2020
$19.9M
Nuclear pathway of DISC1 in major mental illnesses: biochemistry and cell biologyR01MH069853 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2004 to 2012
$3.2M
DISC1-dependent defects in neural fate, corticogenesis and cognition in psychosisR01MH105660 · NIMH · JOHNS HOPKINS UNIVERSITY · PI ISHIZUKA, KOKO, SAWA, AKIRA · 2014 to 2018
$2.8M
Oxidative stress and schizophrenia: combination of cell biology and brain imagingR01MH092443 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2011 to 2015
$1.8M
DISC1 Pathway in Dendritogenesis: Implications for Dopamine Circuit and CognitionR01MH091230 · NIMH · JOHNS HOPKINS UNIVERSITY · PI KAMIYA, ATSUSHI · 2010 to 2014
$1.6M
Defining of Neurodevelopmental Pathways Regulated by Neuregulin- DISC1 InteractioRC1MH088753 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ANTON, EVA S, SAWA, AKIRA · 2009 to 2010
$933k
Exploring depressive behavior using a natural product for novel drug targetsR21AT008547 · NCCIH · JOHNS HOPKINS UNIVERSITY · PI KAMIYA, ATSUSHI · 2014 to 2015
$439k
NCCIH NIH HHS AT-008547NCCIH NIH HHS R21 AT008547NIMH NIH HHS MH-069853NIMH NIH HHS MH-091230NIMH NIH HHS MH-092443NIMH NIH HHS MH-094268NIMH NIH HHS MH-105660NIMH NIH HHS P50 MH094268NIMH NIH HHS R01 MH069853NIMH NIH HHS R01 MH091230NIMH NIH HHS R01 MH092443NIMH NIH HHS R01 MH105660NIMH NIH HHS RC1 MH088753
6 · The paper itself

Abstract

DISC1 (disrupted in schizophrenia 1) is an intracellular scaffolding molecule which regulates multiple signaling pathways for neural cell differentiation and function. Many biological studies utilizing animal models of DISC1 have indicated that loss of DISC1 functions are associated with pathological psychiatric conditions. Thus, DISC1 protein stability is a prerequisite to its goal in governing neural function, and modulating the protein stability of DISC1 may be a key target for understanding underlying pathology, as well promising drug discovery strategies. Nonetheless, a half-life of DISC1 protein has remained unexplored. Here, we determine for the first time the half-life of DISC1, which are regulated by ubiquitin-proteasome cascade. Overexpression of PDE4B2, a binding partner of DISC1, prolonged the half-life of DISC1, whereas NDEL1 does not alter DISC1 protein stability. Notably, the half-life of DISC1 is diminished under hypoxia stress by increasing protein degradation of DISC1, suggesting that alteration of DISC1 stability may be involved in hypoxia stress-mediated pathological conditions, such as ischemic stroke.

Indexed as

AnimalsCell HypoxiaHalf-LifeIn Vitro TechniquesNerve Tissue ProteinsPC12 CellsProteolysisRatsDisc1 protein, ratNerve Tissue ProteinsDisrupted in schizophrenia 1 (DISC1)HypoxiaOxygen–glucose deprivationProtein half-lifeUbiquitin-proteasome system

Identifiers

PMID25738396
PMCPMC4486630
OpenAlexW2056527138

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.