Evidence map›Paper›PMID 37930508›Full record

ReviewMolecular biotechnology2024

Nonsense-Mediated mRNA Decay: Mechanistic Insights and Physiological Significance.

Ipsita Patro, Annapurna Sahoo, Bilash Ranjan Nayak, Rutupurna Das, Sanjoy Majumder, Gagan Kumar Panigrahi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. A novel nonsense mutation inFrontiers in genetics · 2025
    Article
  12. Article
  13. LowerBiology · 2024
    Article
  14. Article
  15. A frameshift mutation in the murinebioRxiv : the preprint server for biology · 2024
    Article
  16. Review
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.

Ipsita PatroSchool of Applied Sciences, Centurion University of Technology and Management, Bhubaneswar, Odisha, India.
Annapurna SahooSchool of Applied Sciences, Centurion University of Technology and Management, Bhubaneswar, Odisha, India. annapurna8121990@gmail.com.
Bilash Ranjan NayakSchool of Applied Sciences, Centurion University of Technology and Management, Bhubaneswar, Odisha, India.
Rutupurna DasSchool of Applied Sciences, Centurion University of Technology and Management, Bhubaneswar, Odisha, India.
Sanjoy MajumderSchool of Applied Sciences, Centurion University of Technology and Management, Bhubaneswar, Odisha, India.
Gagan Kumar PanigrahiSchool of Applied Sciences, Centurion University of Technology and Management, Bhubaneswar, Odisha, India. gagan.panigrahi@cutm.ac.in.ORCID http://orcid.org/0000-0003-3908-3379

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonsense-mediated mRNA decay (NMD) is an evolutionarily conserved surveillance mechanism across eukaryotes and also regulates the expression of physiological transcripts, thus involved in gene regulation. It essentially ensures recognition and removal of aberrant transcripts. Therefore, the NMD protects the cellular system by restricting the synthesis of truncated proteins, potentially by eliminating the faulty mRNAs. NMD is an evolutionarily conserved surveillance mechanism across eukaryotes and also regulates the expression of physiological transcripts, thus involved in gene regulation as well. Primarily, the NMD machinery scans and differentiates the aberrant and non-aberrant transcripts. A myriad of cellular dysfunctions arise due to production of truncated proteins, so the NMD core proteins, the up-frameshift factors (UPFs) recognizes the faulty mRNAs and further recruits factors resulting in the mRNA degradation. NMD exhibits astounding variability in its ability in regulating cellular mechanisms including both pathological and physiological events. But, the detailed underlying molecular mechanisms in NMD remains blurred and require extensive investigation to gain insights on cellular homeostasis. The complexity in understanding of NMD pathway arises due to the involvement of numerous proteins, molecular interactions and their functioning in different steps of this process. Moreover methods such as alternative splicing generates numerous isoforms of mRNA, so it makes difficulties in understanding the impact of alternative splicing on the efficiency of NMD functioning. Role of NMD in cancer development is very complex. Studies have shown that in some cases cancer cells use NMD pathway as a tool to exploit the NMD mechanism to maintain tumor microenvironment. A greater level of understanding about the intricate mechanism of how tumor used NMD pathway for their benefits, a strategy can be developed for targeting and inhibiting NMD factors involved in pro-tumor activity. There are very little amount of information available about the NMD pathway, how it discriminate mRNAs that are targeted by NMD from those that are not. This review highlights our current understanding of NMD, specifically the regulatory mechanisms and attempts to outline less explored questions that warrant further investigations. Taken as a whole, a detailed molecular understanding of the NMD mechanism could lead to wide-ranging applications for improving cellular homeostasis and paving out strategies in combating pathological disorders leaping forward toward achieving United Nations sustainable development goals (SDG 3: Good health and well-being).

Indexed as

Nonsense Mediated mRNA DecayRNA, MessengerAlternative SplicingAnimalsGene Expression RegulationHumansNeoplasmsRNA, MessengerAberrant transcriptsCellular dysfunctionsNonsense-mediated mRNA decaySurveillanceUp-frameshift factors

Identifiers

What Socratic holds

Textmetadata
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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 Socratic graph.