Evidence map›Paper›PMID 21061916›Full record

ArticleGene expression2010

Domain within the C protein of human parainfluenza virus type 3 that regulates interferon signaling.

Hongxia Mao, Santanu Chattopadhyay, Amiya K Banerjee

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

Article in Gene expression, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 37% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Review
  3. 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

3 authors at 1 institution in 1 country.

Hongxia MaoVirology Section, Department of Molecular Genetics, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.
Santanu Chattopadhyay
Amiya K Banerjee
Cleveland Clinic · US

Funding

NIAID NIH HHS AI 32037
6 · The paper itself

Abstract

Human parainfluenza virus type 3 (HPIV3), one of the paramyxoviruses, uses its accessory C protein as an antagonist against interferon (IFN)-mediated host innate immunity. We have previously shown that the C protein significantly decreased the IFN-induced phosphorylation of signal transducer and activator of transcription (Stat) 1 and the formation of gamma IFN activation factor (GAF) complex, thus abrogating the antiviral activity of the IFNs against vesicular stomatitis virus (VSV) replication. Here, by mutational analyses we demonstrated that the N-terminal truncation of the C protein (CNdelta25 and CNdelta50) substantially (approximately 50%) recovers the IFN-induced responses, suggesting the critical role of the N-terminal region of the C protein in IFN signaling. Furthermore, our results indicate that the charged amino acid residues within the N-terminal region of the C protein regulate the antagonistic effect of the C protein on IFN signaling.

Indexed as

Signal TransductionAmino Acid SequenceAntiviral AgentsHeLa CellsHumansInterferonsMutant ProteinsParainfluenza Virus 3, HumanPhosphorylationProtein Structure, TertiarySTAT1 Transcription FactorStructure-Activity RelationshipTranscription, GeneticTYK2 KinaseVesiculovirusViral ProteinsAntiviral AgentsInterferonsMutant ProteinsSTAT1 protein, humanSTAT1 Transcription FactorTYK2 KinaseTYK2 protein, humanViral Proteins

Identifiers

PMID21061916
PMCPMC6043821
OpenAlexW2328474352

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.