Evidence map›Paper›PMID 25088526›Full record

ArticleScientific reports2014

Transgenic expression of the N525S-tuberin variant in Tsc2 mutant (Eker) rats causes dominant embryonic lethality.

Masatoshi Shiono, Toshiyuki Kobayashi, Riichi Takahashi, Masatsugu Ueda, Chikashi Ishioka, Okio Hino

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

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 89% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

6 authors at 3 institutions in 1 country.

Masatoshi Shiono1] Department of Clinical Oncology, Tohoku University Hospital, Tohoku University, 1-1 Seiryo-machi, Aoba-ku, Sendai, Miyagi 980-8574, Japan [2] Department of Pathology and Oncology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.
Toshiyuki KobayashiDepartment of Pathology and Oncology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.
Riichi Takahashi1] PhoenixBio Co., Ltd., 1198-4 Iwazo-machi, Utsunomiya, Tochigi 321-0973, Japan [2] Animal Resources Center, Central Institute for Experimental Animals, 3-25-12 Tonomachi, Kawasaki, Kangawa 210-0821, Japan.
Masatsugu Ueda1] PhoenixBio Co., Ltd., 1198-4 Iwazo-machi, Utsunomiya, Tochigi 321-0973, Japan [2] Transgenic Animal Division, Utsunomiya Institute, Institute of Immunology Co., Ltd., 1198-4 Iwazo-machi, Utsunomiya, Tochigi 321-0973, Japan.
Chikashi Ishioka1] Department of Clinical Oncology, Tohoku University Hospital, Tohoku University, 1-1 Seiryo-machi, Aoba-ku, Sendai, Miyagi 980-8574, Japan [2] Department of Clinical Oncology, Institute of Development, Aging, and Cancer, Tohoku University, 4-1 Seiryo-machi, Aoba-ku, Sendai, Miyagi 980-8575, Japan.
Okio HinoDepartment of Pathology and Oncology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.
Juntendo University · JPPhoenixBio (Japan) · JPTohoku University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Tsc2 product, tuberin, negatively regulates the mTOR pathway. We have exploited the Eker (Tsc2-mutant) rat system to analyse various Tsc2 mutations. Here, we focus on the N525S-Tsc2 variant (NSM), which is known to cause distinct symptoms in patients even though normal suppression of mTOR is observed. Unexpectedly, we were repeatedly unable to generate viable rats carrying the NSM transgene. Genotypic analysis revealed that most of the embryos carrying the transgene died around embryonic day after 14.5-similar to the stage of lethality observed for Eker homozygotes. Thus, the NSM transgene appeared to have a dominant lethal effect in our rat model. Further, no significant differences were observed for various signal transduction molecules in transiently expressed NSM cells compared to WT. These results indicate that a non-mTOR pathway, critical for embryogenesis, is being regulated by tuberin, providing a link between tuberin expression and the severity of Tsc2 mutation-related pathogenesis.

Indexed as

Genes, DominantGenes, LethalMutationAmino Acid SubstitutionAnimalsBase SequenceDisease Models, AnimalEmbryo, MammalianEmbryonic DevelopmentFemaleGene ExpressionHEK293 CellsHomozygoteHumansMaleMolecular Sequence DatamTOR protein, ratTOR Serine-Threonine KinasesTSC2 protein, humanTsc2 protein, ratTuberous Sclerosis Complex 2 ProteinTumor Suppressor Proteins

Identifiers

PMID25088526
PMCPMC5379989
OpenAlexW2029266475

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.