Evidence map›Paper›PMID 21744034›Full record

ArticleMolecular biotechnology2012

Nucleic acid-mediated cleavage of M1 gene of influenza A virus is significantly augmented by antisense molecules targeted to hybridize close to the cleavage site.

B Kumar, Madhu Khanna, P Kumar, V Sood, R Vyas, A C Banerjea

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Article in Molecular biotechnology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 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

6 authors.

B KumarDepartment of Respiratory Virology, Vallabhbhai Patel Chest Institute, University of Delhi, Delhi 110007, India.
Madhu Khanna
P Kumar
V Sood
R Vyas
A C Banerjea

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Influenza A virus genome segment 7 encodes protein M1, which is the matrix protein playing crucial role in the virus life cycle. Any antiviral strategy that aims at reducing, in particular, the expression of this genome segment should, in principle, reduce the infectivity of the virus. We developed a specific antiviral approach at the molecular level and designed several novel 10-23 DNAzymes (Dz) and hammerhead ribozymes (Rz), specifically targeted to cleave at the conserved domains of the influenza virus M1 RNA. We sought to use antisense molecules with the hope that it will facilitate the ribozyme-mediated cleavage. We observed that the Mg(2+)-dependent sequence-specific cleavage of M1 RNA was achieved by both the Dz and Rz in a dose-dependent manner. This combination of catalytic Dz and Rz with antisense molecules, in principle, resulted in more effective gene suppression, inhibited the whole virus replication in host cell, and thus could be exploited for therapeutic purposes.

Indexed as

AnimalsBase SequenceCell LineCloning, MolecularDNA, CatalyticDNA CleavageDNA, Single-StrandedDogsFlow CytometryGene Expression Regulation, ViralGenes, ViralInfluenza A virusMolecular Sequence DataNucleic Acid HybridizationNucleic AcidsOligonucleotides, AntisenseDNA, CatalyticDNA, Single-Strandedhammerhead ribozymeM1 protein, Influenza A virusNucleic AcidsOligonucleotides, AntisenseRNA, CatalyticRNA-cleaving DNA 10-23RNA, MessengerViral Matrix Proteins

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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.