Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (647 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The sequence at the 3' end of messenger RNA that does not code for product. This region contains transcription and translation regulating sequences.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: 3' Untranslated Region; Region, 3' Untranslated; Regions, 3' Untranslated; Untranslated Region, 3'; Untranslated Regions, 3'; 3' UTR; 3' UTRs; UTR, 3'.
Where it fits in the MeSH classification
- Broader topics
- Untranslated Regions
- Narrower topics
- AU Rich Elements
- See also
- 3' Flanking Region
Research landscape
PubMed indexes 17,048 records tagged with the MeSH heading “3' Untranslated Regions” (counts retrieved 2026-10-29). 3,061 of them (18.0%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 9,678 records.
Reviews account for 676 records (4.0%) and meta-analyses for 62. Randomized controlled trials number 22 (0.1%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 249 |
| 2000-2009 | 4,060 |
| 2010-2019 | 9,678 |
| 2020 onward | 3,061 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 676 | 4.0% |
| Meta-analyses | 62 | 0.4% |
| Randomized controlled trials | 22 | 0.1% |
Method: PubMed query "3' Untranslated Regions"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in genetics and genomics
Genetic findings vary widely in strength. A variant linked to a condition in one study may not replicate in other ancestries, and most common variants have small effects that are meaningful only in aggregate. Studies of rare, high-impact variants can support strong causal claims about a gene, while association studies describe statistical links that need functional and independent replication. Check the sample size, the ancestry of participants, whether results were replicated, and whether a laboratory or clinical outcome was actually measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Cellular stress alters 3'UTR landscape through alternative polyadenylation and isoform-specific degradation | 2018 | Research article Design not recorded in structured metadata | 128 | cc by PMID 29891946 · DOI · PMC5995920 |
| Transcriptome 3'end organization by PCF11 links alternative polyadenylation to formation and neuronal differentiation of neuroblastoma | 2018 | Research article Design not recorded in structured metadata | 99 | cc by PMID 30552333 · DOI · PMC6294251 |
| Mechanistic insights into mRNA 3'-end processing | 2019 | Review article Design not recorded in structured metadata | 94 | cc by PMID 31499460 · DOI · PMC6900580 |
| A 3'UTR-derived small RNA modulates the life cycle of the cholera toxin-encoding filamentous phage, CTXϕ | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42228528 · DOI · PMC13250501 |
Cellular stress alters 3'UTR landscape through alternative polyadenylation and isoform-specific degradation [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Most eukaryotic genes express alternative polyadenylation (APA) isoforms with different 3'UTR lengths, production of which is influenced by cellular conditions.
- Closing excerpt
- Together, our data reveal a global, 3'UTR-based mRNA stability control in stressed cells and indicate that APA can function as an adaptive mechanism to preserve mRNAs in response to stress.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (149 words)
Most eukaryotic genes express alternative polyadenylation (APA) isoforms with different 3'UTR lengths, production of which is influenced by cellular conditions. Here, we show that arsenic stress elicits global shortening of 3'UTRs through preferential usage of proximal polyadenylation sites during stress and enhanced degradation of long 3'UTR isoforms during recovery. We demonstrate that RNA-binding protein TIA1 preferentially interacts with alternative 3'UTR sequences through U-rich motifs, correlating with stress granule association and mRNA decay of long 3'UTR isoforms. By contrast, genes with shortened 3'UTRs due to stress-induced APA can evade mRNA clearance and maintain transcript abundance post stress. Furthermore, we show that stress causes distinct 3'UTR size changes in proliferating and differentiated cells, highlighting its context-specific impacts on the 3'UTR landscape. Together, our data reveal a global, 3'UTR-based mRNA stability control in stressed cells and indicate that APA can function as an adaptive mechanism to preserve mRNAs in response to stress.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29891946 · DOI · PMC5995920
Transcriptome 3'end organization by PCF11 links alternative polyadenylation to formation and neuronal differentiation of neuroblastoma [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Diversification at the transcriptome 3'end is an important and evolutionarily conserved layer of gene regulation associated with differentiation and dedifferentiation processes.
- Closing excerpt
- We provide an interactive data repository of transcriptome-wide APA covering > 170 RNAis, and an APA-network map with regulatory hubs.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (156 words)
Diversification at the transcriptome 3'end is an important and evolutionarily conserved layer of gene regulation associated with differentiation and dedifferentiation processes. Here, we identify extensive transcriptome 3'end-alterations in neuroblastoma, a tumour entity with a paucity of recurrent somatic mutations and an unusually high frequency of spontaneous regression. Utilising extensive RNAi-screening we reveal the landscape and drivers of transcriptome 3'end-diversification, discovering PCF11 as critical regulator, directing alternative polyadenylation (APA) of hundreds of transcripts including a differentiation RNA-operon. PCF11 shapes inputs converging on WNT-signalling, and governs cell cycle, proliferation, apoptosis and neurodifferentiation. Postnatal PCF11 down-regulation induces a neurodifferentiation program, and low-level PCF11 in neuroblastoma associates with favourable outcome and spontaneous tumour regression. Our findings document a critical role for APA in tumorigenesis and describe a novel mechanism for cell fate reprogramming in neuroblastoma with potentially important clinical implications. We provide an interactive data repository of transcriptome-wide APA covering > 170 RNAis, and an APA-network map with regulatory hubs.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30552333 · DOI · PMC6294251
Mechanistic insights into mRNA 3'-end processing [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The polyadenosine (poly(A)) tail found on the 3'-end of almost all eukaryotic mRNAs is important for mRNA stability and regulation of translation.
- Closing excerpt
- Here, we describe new molecular insights into pre-mRNA recognition, cleavage and polyadenylation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (129 words)
The polyadenosine (poly(A)) tail found on the 3'-end of almost all eukaryotic mRNAs is important for mRNA stability and regulation of translation. mRNA 3'-end processing occurs co-transcriptionally and involves more than 20 proteins to specifically recognize the polyadenylation site, cleave the pre-mRNA, add a poly(A) tail, and trigger transcription termination. The polyadenylation site (PAS) defines the end of the 3'-untranslated region (3'-UTR) and, therefore, selection of the cleavage site is a critical event in regulating gene expression. Integrated structural biology approaches including biochemical reconstitution of multi-subunit complexes, cross-linking mass spectrometry, and structural analyses by X- ray crystallography and single-particle electron cryo-microscopy (cryoEM) have enabled recent progress in understanding the molecular mechanisms of the mRNA 3'-end processing machinery. Here, we describe new molecular insights into pre-mRNA recognition, cleavage and polyadenylation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31499460 · DOI · PMC6900580
A 3'UTR-derived small RNA modulates the life cycle of the cholera toxin-encoding filamentous phage, CTXϕ [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Bacteriophages (phages) are well known to be one of the major driving forces in bacterial evolution.
- Closing excerpt
- cholerae employs sRNA-mediated posttranscriptional gene regulation to coordinate CTXϕ activation with both cell density and nutrient availability.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (213 words)
Bacteriophages (phages) are well known to be one of the major driving forces in bacterial evolution. This also applies to virulent microorganisms, such as the major human pathogen Vibrio cholerae, whose pathogenic potential and epidemic proliferation largely depends on the interaction with environmental phages. Specifically, integration of the CTXϕ phage genome into the first chromosome of V. cholerae also introduced the ctxAB genes, encoding the primary toxin responsible for the severe acute diarrheal disease, cholera. Whereas the mechanisms underlying CTXϕ-associated horizontal gene transfer and transcriptional control of the ctxAB genes have been intensively studied over the past years, posttranscriptional regulation affecting the CTXϕ life cycle has not been documented. Here, we report the identification and characterization of the CisR small RNA (sRNA) that is produced from the 3'UTR (untranslated region) of the prtV gene and inhibits the expression of the CTXϕ-encoded cep mRNA. CisR-mediated repression of cep involves Hfq-assisted base-pairing of the two transcripts and results in reduced CTXϕ production under stress conditions. We further demonstrate that transcription of prtV-cisR requires both the master quorum-sensing regulator HapR and CRP (cAMP receptor protein), a global regulator of carbon metabolism. Taken together, our work provides evidence that V. cholerae employs sRNA-mediated posttranscriptional gene regulation to coordinate CTXϕ activation with both cell density and nutrient availability.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42228528 · DOI · PMC13250501
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Alternative polyadenylation of mRNA precursors [5]
- Research article AU-rich elements and associated factors: are there unifying principles? [6]
- Research article A PUF family portrait: 3'UTR regulation as a way of life [7]
- Research article Regulation by 3'-Untranslated Regions [8]
- Research article What Are 3' UTRs Doing? [9]
- Research article The power of the 3' UTR: translational control and development [10]
References
- Zheng D, Wang R, Ding Q, Wang T, Xie B, Wei L, et al.. Cellular stress alters 3'UTR landscape through alternative polyadenylation and isoform-specific degradation. . 2018. PMID 29891946 · DOI · PMC5995920
- Ogorodnikov A, Levin M, Tattikota S, Tokalov S, Hoque M, Scherzinger D, et al.. Transcriptome 3'end organization by PCF11 links alternative polyadenylation to formation and neuronal differentiation of neuroblastoma. . 2018. PMID 30552333 · DOI · PMC6294251
- Kumar A, Clerici M, Muckenfuss LM, Passmore LA, Jinek M. Mechanistic insights into mRNA 3'-end processing. . 2019. PMID 31499460 · DOI · PMC6900580
- Lippegaus A, Haycocks JRJ, O'Driscoll E, Sprenger M, Thriene K, Jung EM, et al.. A 3'UTR-derived small RNA modulates the life cycle of the cholera toxin-encoding filamentous phage, CTXϕ. . 2026. PMID 42228528 · DOI · PMC13250501
- Tian B, Manley JL. Alternative polyadenylation of mRNA precursors. Nat Rev Mol Cell Biol. 2017. PMID 27677860 · DOI · PMC5483950
- Barreau C, Paillard L, Osborne HB. AU-rich elements and associated factors: are there unifying principles?. Nucleic Acids Res. 2005. PMID 16391004 · DOI · PMC1325018
- Wickens M, Bernstein DS, Kimble J, Parker R. A PUF family portrait: 3'UTR regulation as a way of life. Trends Genet. 2002. PMID 11858839 · DOI
- Mayr C. Regulation by 3'-Untranslated Regions. Annu Rev Genet. 2017. PMID 28853924 · DOI
- Mayr C. What Are 3' UTRs Doing?. Cold Spring Harb Perspect Biol. 2019. PMID 30181377 · DOI · PMC6771366
- Kuersten S, Goodwin EB. The power of the 3' UTR: translational control and development. Nat Rev Genet. 2003. PMID 12897774 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.