Evidence map›Paper›PMID 26696493›Full record

ArticleMolecular neurobiology2016

Overexpression of Telomerase Reverse Transcriptase Induces Autism-like Excitatory Phenotypes in Mice.

Ki Chan Kim, Jeehae Rhee, Jong-Eun Park, Dong-Keun Lee, Chang Soon Choi, Ji-Woon Kim, Han-Woong Lee, Mi-Ryoung Song, Hee Jeong Yoo, ChiHye Chung and 1 more

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2016. 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
1.3field-weighted citation impact, top 19% 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, 18 citations in OpenAlex.

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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

11 authors at 4 institutions in 1 country.

Ki Chan KimCenter for Neuroscience Research, SMART Institute of Advanced Biomedical Sciences, Konkuk University, Seoul, South Korea.
Jeehae RheeDepartment of Biological Sciences, Konkuk University, Seoul, South Korea.
Jong-Eun ParkDepartment of Neuropsychiatry, Seoul National University Bungdang Hospital, Seongnam, South Korea.
Dong-Keun LeeSchool of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, South Korea.
Chang Soon ChoiCenter for Neuroscience Research, SMART Institute of Advanced Biomedical Sciences, Konkuk University, Seoul, South Korea.
Ji-Woon KimCenter for Neuroscience Research, SMART Institute of Advanced Biomedical Sciences, Konkuk University, Seoul, South Korea.
Han-Woong LeeDepartment of Biochemistry, College of Science, Yonsei University, Seoul, South Korea.
Mi-Ryoung SongSchool of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, South Korea.
Hee Jeong YooDepartment of Neuropsychiatry, Seoul National University Bungdang Hospital, Seongnam, South Korea.
ChiHye ChungDepartment of Biological Sciences, Konkuk University, Seoul, South Korea.
Chan Young ShinCenter for Neuroscience Research, SMART Institute of Advanced Biomedical Sciences, Konkuk University, Seoul, South Korea. chanyshin@kku.ac.kr.
Konkuk University · KRGwangju Institute of Science and Technology · KRSeoul National University Bundang Hospital · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In addition to its classical role as a regulator of telomere length, recent reports suggest that telomerase reverse transcriptase (TERT) plays a role in the transcriptional regulation of gene expression such as β-catenin-responsive pathways. Silencing or over-expression of TERT in cultured NPCs demonstrated that TERT induced glutamatergic neuronal differentiation. During embryonic brain development, expression of transcription factors involved in glutamatergic neuronal differentiation was increased in mice over-expressing TERT (TERT-tg mice). We observed increased expression of NMDA receptor subunits and phosphorylation of α-CaMKII in TERT-tg mice. TERT-tg mice showed autism spectrum disorder (ASD)-like behavioral phenotypes as well as lowered threshold against electrically induced seizure. Interestingly, the NMDA receptor antagonist memantine restored behavioral abnormalities in TERT-tg mice. Consistent with the alteration in excitatory/inhibitory (E/I) ratio, TERT-tg mice showed autism-like behaviors, abnormal synaptic organization, and function in mPFC suggesting the role of altered TERT activity in the manifestation of ASD, which is further supported by the significant association of certain SNPs in Korean ASD patients.

Indexed as

AnimalsAutistic DisorderBehavior, AnimalBrainCell DifferentiationCells, CulturedEmbryonic DevelopmentGene Knockdown TechniquesGene SilencingGlutamatesGreen Fluorescent ProteinsHumansMemantineMice, TransgenicNeuronsPhenotypeGlutamatesGreen Fluorescent ProteinsMemantineReceptors, N-Methyl-D-AspartateRNA, Small InterferingTelomeraseTranscription FactorsAutism spectrum disorderExcitatory/Inhibitory imbalanceGlutamatergic neuronMemantineNMDA receptorTelomerase reverse transcriptase

Identifiers

PMID26696493
OpenAlexW2201775718

What OpenQuestion holds

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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.