Evidence map›Paper›PMID 26435690›Full record

ArticleInternational journal of biological sciences2015

Adapted Resistance to the Knockdown Effect of shRNA-Derived Srsf3 siRNAs in Mouse Littermates.

Masahiko Ajiro, Rong Jia, Rui-Hong Wang, Chu-Xia Deng, Zhi-Ming Zheng

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 85% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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 3 institutions in 3 countries.

Masahiko Ajiro1. Tumor Virus RNA Biology Section, Gene Regulation and Chromosome Biology Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, Maryland 21702, USA.
Rong Jia1. Tumor Virus RNA Biology Section, Gene Regulation and Chromosome Biology Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, Maryland 21702, USA ; 3. Wuhan University School of Stomatology, Wuhan, Hubei, China.
Rui-Hong Wang2. Genetics of Development and Disease Branch, 10/9N105, National Institute of Diabetes, Digestive and Kidney Diseases, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, MD 20892, USA. ; 4. Faculty of Health Sciences, University of Macau, Macau SAR, China.
Chu-Xia Deng2. Genetics of Development and Disease Branch, 10/9N105, National Institute of Diabetes, Digestive and Kidney Diseases, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, MD 20892, USA. ; 4. Faculty of Health Sciences, University of Macau, Macau SAR, China.
Zhi-Ming Zheng1. Tumor Virus RNA Biology Section, Gene Regulation and Chromosome Biology Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, Maryland 21702, USA.
Center for Cancer Research · USNational Institute of Diabetes and Digestive and Kidney Diseases · USNational Cancer Institute · US

Funding

Gene Expression and Post-Transcriptional Regulation of DNA Tumor VirusesZIASC010357 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI ZHENG, ZHI-MING · 2009 to 2025
$24.3M
Intramural NIH HHS
6 · The paper itself

Abstract

Gene silencing techniques are widely used to control gene expression and have potential for RNAi-based therapeutics. In this report, transgenic mouse lines were created for conditional knockdown of Srsf3 (SRp20) expression in liver and mammary gland tissues by expressing Srsf3-specific shRNAs driven by a U6 promoter. Although a small portion of the transgenic mouse littermates were found to produce siRNAs in the targeted tissues, most of the transgenic littermates at two months of age failed to display a knockdown phenotype of Srsf3 expression in their liver and mammary gland tissues where an abundant level of Srsf3 siRNAs remained. We saw only one of four mice with liver/mammary gland expressing Srsf3 siRNA displayed a suppressed level of Srsf3 protein, but not the mRNA. Data indicate that the host resistance to a gene-specific siRNA targeting an essential gene transcript can be developed in animals, presumably as a physiological necessity to cope with the hostile perturbation.

Indexed as

AnimalsCell Line, TumorCell ProliferationFemaleGene SilencingLiverMammary Glands, AnimalMiceMice, TransgenicReverse Transcriptase Polymerase Chain ReactionRNA-Binding ProteinsRNA InterferenceRNA, Small InterferingSerine-Arginine Splicing FactorsRNA-Binding ProteinsRNA, Small InterferingSerine-Arginine Splicing FactorsSrsf3 protein, mouseshRNAsSrsf3transgenic mouse

Identifiers

PMID26435690
PMCPMC4582148
OpenAlexW2414655079

What OpenQuestion holds

Textmetadata
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.