Evidence map›Paper›PMID 22879379›Full record

ArticleNucleic acids research2012

Inducible and reversible regulation of endogenous gene in mouse.

Ruilin Sun, Kai Zhao, Ruling Shen, Lei Cai, Xingyu Yang, Ying Kuang, Jifang Mao, Fang Huang, Zhugang Wang, Jian Fei

Abstract read
In one paragraph

Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

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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

10 authors.

Ruilin SunShanghai Research Center for Model Organisms, Shanghai 201210, People's Republic of China.
Kai Zhao
Ruling Shen
Lei Cai
Xingyu Yang
Ying Kuang
Jifang Mao
Fang Huang
Zhugang Wang
Jian Fei

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methods for generating loss-of-function mutations, such as conventional or conditional gene knockout, are widely used in deciphering gene function in vivo. By contrast, inducible and reversible regulation of endogenous gene expression has not been well established. Using a mouse model, we demonstrate that a chimeric transcriptional repressor molecule (tTS) can reversibly inhibit the expression of an endogenous gene, Nmyc. In this system, a tetracycline response element (TRE) artificially inserted near the target gene's promoter region turns the gene on and off in a tetracycline-inducible manner. Nmyc(TRE) mice were generated by inserting a TRE into the first intron of Nmyc by the knockin technique. Nmyc(TRE) mice were crossed to tTS transgenic mice to produce Nmyc(TRE/TRE): tTS embryos. In these embryos, tTS blocked Nmyc expression, and embryonic lethality was observed at E11.5d. When the dam was exposed to drinking water containing doxycycline (dox), normal endogenous Nmyc expression was rescued, and the embryo survived to birth. This novel genetic modification strategy based on the tTS-dox system for inducible and reversible regulation of endogenous mouse genes will be a powerful tool to investigate target genes that cause embryonic lethality or other defects where reversible regulation or temporary shutdown of the target gene is needed.

Indexed as

Gene Expression RegulationAnimalsCerebellar CortexDoxycyclineGene Knock-In TechniquesGenes, LethalGene TargetingGreen Fluorescent ProteinsMiceMice, Inbred C57BLMice, TransgenicProto-Oncogene Proteins c-mycRepressor ProteinsResponse ElementsSyndactylyDoxycyclineenhanced green fluorescent proteinGreen Fluorescent ProteinsMyc protein, mouseProto-Oncogene Proteins c-mycRepressor Proteinstetracycline resistance-encoding transposon repressor protein

Identifiers

PMID22879379
PMCPMC3505985

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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.