Evidence map›Paper›PMID 30857970›Full record

ReviewJournal of molecular biology2019

RNA Splicing: A New Paradigm in Host-Pathogen Interactions.

Komal Chauhan, Haroon Kalam, Ravi Dutt, Dhiraj Kumar

Abstract readReview
In one paragraph

Review in Journal of molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing 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

55 citing papers in PubMed.

  1. Article
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  6. AProceedings of the National Academy of Sciences of the United States of America · 2025
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  13. Review
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  15. Frontiers in immunology · 2024
    Article
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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

4 authors.

Komal ChauhanCellular Immunology Group, International Centre for Genetic Engineering and Biotechnology, Aruna Asaf Ali Marg, New Delhi 110067, India.
Haroon KalamCellular Immunology Group, International Centre for Genetic Engineering and Biotechnology, Aruna Asaf Ali Marg, New Delhi 110067, India.
Ravi DuttCellular Immunology Group, International Centre for Genetic Engineering and Biotechnology, Aruna Asaf Ali Marg, New Delhi 110067, India.
Dhiraj KumarCellular Immunology Group, International Centre for Genetic Engineering and Biotechnology, Aruna Asaf Ali Marg, New Delhi 110067, India. Electronic address: dhiraj@icgeb.res.in.

Funding

DBT-Wellcome Trust India Alliance IA/S/17/1/503071Wellcome Trust
6 · The paper itself

Abstract

RNA splicing brings diversity to the eukaryotic proteome. Different spliced variants of a gene may differ in their structure, function, localization, and stability influencing protein stoichiometry and physiological outcomes. Alternate spliced variants of different genes are known to associate with various chronic pathologies including cancer. Emerging evidence suggests precise regulation of splicing as fundamental to normal well-being. In this context, infection-induced alternative splicing has emerged as a new pivot of host function, which pathogenic microbes can alter-directly or indirectly-to tweak the host immune responses against the pathogen. The implications of these findings are vast, and although not explored much in the case of pathogenic infections, we present here examples from splicing mediated regulation of immune responses across a variety of conditions and explore how this fascinating finding brings a new paradigm to host-pathogen interactions.

Indexed as

Alternative SplicingAnimalsBacterial InfectionsHost-Pathogen InteractionsHumansImmunityRNAVirus DiseasesRNAAlternative SplicingGene ExpressionImmune responseInfectionSplicing factors

Identifiers

PMID30857970
PMCPMC7115970

What OpenQuestion holds

Textmetadata
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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.