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: 3 complete abstracts (613 words), 9 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
An increase in the rate of synthesis of an enzyme due to the presence of an inducer which acts to derepress the gene responsible for enzyme synthesis.
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: Induction, Enzyme.
Where it fits in the MeSH classification
- Broader topics
- Gene Expression Regulation, Enzymologic
Research landscape
PubMed indexes 32,853 records tagged with the MeSH heading “Enzyme Induction” (counts retrieved 2026-10-29). 212 of them (0.6%) were published from 2020 onward, and the busiest period so far is through 1999 with 23,515 records.
Reviews account for 1,914 records (5.8%) and meta-analyses for 3. Randomized controlled trials number 124 (0.4%) 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 | 23,515 |
| 2000-2009 | 6,549 |
| 2010-2019 | 2,577 |
| 2020 onward | 212 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,914 | 5.8% |
| Meta-analyses | 3 | 0.0% |
| Randomized controlled trials | 124 | 0.4% |
Method: PubMed query "Enzyme Induction"[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 |
|---|---|---|---|---|
| l-Glutamine Attenuates DSS-Induced Colitis via Induction of MAPK Phosphatase-1 | 2018 | Research article Design not recorded in structured metadata | 43 | cc by PMID 29494494 · DOI · PMC5872706 |
| Cullin4 Is Pro-Viral during West Nile Virus Infection of Culex Mosquitoes | 2015 | Research article Design not recorded in structured metadata | 38 | cc by PMID 26325027 · DOI · PMC4556628 |
| A possible involvement of Nrf2-mediated heme oxygenase-1 up-regulation in protective effect of the proton pump inhibitor pantoprazole against indomethacin-induced gastric damage in rats | 2012 | Research article Design not recorded in structured metadata | 25 | cc by PMID 23066659 · DOI · PMC3548718 |
l-Glutamine Attenuates DSS-Induced Colitis via Induction of MAPK Phosphatase-1 [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Inflammatory bowel disease (IBD), encompassing ulcerative colitis and Crohn's disease, is a multifactorial inflammatory disease of the small intestine and colon.
- Closing excerpt
- These data indicated that Gln ameliorated DSS-induced colitis via MKP-1 induction.
- 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 (185 words)
Inflammatory bowel disease (IBD), encompassing ulcerative colitis and Crohn's disease, is a multifactorial inflammatory disease of the small intestine and colon. Many investigators have reported that l-glutamine (Gln) therapy improves outcomes of experimental colitis models, although the mechanism is not fully understood. Regarding the anti-inflammatory properties of Gln, we have shown that Gln can effectively deactivate cytosolic phospholipase A₂ (cPLA₂) by rapid induction of MAPK phosphatase (MKP)-1. In this study, we explore the possibility that Gln ameliorates dextran sulfate sodium (DSS)-induced colitis via MKP-1 induction, resulting in inhibition of cPLA₂, which has been reported to play a key role in the pathogenesis of IBD. Oral Gln intake attenuated DSS-induced colitis. Gln inhibited cPLA₂ phosphorylation, as well as colonic levels of TNF-α and leukotriene (LT)B₄. Gln administration resulted in early and enhanced MKP-1 induction. Importantly, MKP-1 small interfering RNA (siRNA), but not control siRNA, significantly abrogated the Gln-mediated (1) induction of MKP-1; (2) attenuation of colitis (colon length, histological abnormality, and inflammation; and (3) inhibition of cPLA₂ phosphorylation and colonic levels of TNF-α and LTB₄. These data indicated that Gln ameliorated DSS-induced colitis via MKP-1 induction.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29494494 · DOI · PMC5872706
Cullin4 Is Pro-Viral during West Nile Virus Infection of Culex Mosquitoes [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Although mosquitoes serve as vectors of many pathogens of public health importance, their response to viral infection is poorly understood.
- Closing excerpt
- Our results suggest a novel mechanism adopted by WNV to overcome mosquito immune response and increase viral replication.
- 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 (220 words)
Although mosquitoes serve as vectors of many pathogens of public health importance, their response to viral infection is poorly understood. It also remains to be investigated whether viruses deploy some mechanism to be able to overcome this immune response. Here, we have used an RNA-Seq approach to identify differentially regulated genes in Culex quinquefasciatus cells following West Nile virus (WNV) infection, identifying 265 transcripts from various cellular pathways that were either upregulated or downregulated. Ubiquitin-proteasomal pathway genes, comprising 12% of total differentially regulated genes, were selected for further validation by real time RT-qPCR and functional analysis. It was found that treatment of infected cells with proteasomal inhibitor, MG-132, decreased WNV titers, indicating importance of this pathway during infection process. In infection models, the Culex ortholog of mammalian Cul4A/B (cullin RING ubiquitin ligase) was found to be upregulated in vitro as well as in vivo, especially in midguts of mosquitoes. Gene knockdown using dsRNA and overexpression studies indicated that Culex Cul4 acts as a pro-viral protein by degradation of CxSTAT via ubiquitin-proteasomal pathway. We also show that gene knockdown of Culex Cul4 leads to activation of the Jak-STAT pathway in mosquitoes leading to decrease viral replication in the body as well as saliva. Our results suggest a novel mechanism adopted by WNV to overcome mosquito immune response and increase viral replication.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26325027 · DOI · PMC4556628
A possible involvement of Nrf2-mediated heme oxygenase-1 up-regulation in protective effect of the proton pump inhibitor pantoprazole against indomethacin-induced gastric damage in rats [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundProton pump is an integral membrane protein that is ubiquitous ATP binding cassette (ABC) involved in many transport processes in all living organisms, among which a specialized form of pump, so called p-type proton pump, exists in the parietal cells of stomach.
- Closing excerpt
- The expression of HO-1 induced by pantoprazole was significantly associated with the increased in vitro tube formation (P ConclusionThese results demonstrate that Nrf2-mediated HO-1 induction of PPIs afforded a significant protective effect against NSAIDs-induced gastric damage beyond acid suppressive actions.
- 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 (208 words)
BackgroundProton pump is an integral membrane protein that is ubiquitous ATP binding cassette (ABC) involved in many transport processes in all living organisms, among which a specialized form of pump, so called p-type proton pump, exists in the parietal cells of stomach. Though proton pump inhibitors (PPIs) are frequently prescribed to prevent nonsteroidal anti-inflammatory drugs (NSAIDs)-induced gastric damage, the acid suppressive actions do not suffice to explain.MethodsIn order to document the effects of pantoprazole, one of PPIs, on the NSAIDs-induced gastric damage, in vitro and in vivo studies were performed. Immunocytochemistry, Western blot analysis, electrophoretic mobility shift assay and RT-PCR were conducted to evaluate the induction of heme oxygenase-1 (HO-1) through Nrf2 activation in normal gastric mucosal RGM-1 cells or in vivo stomach tissues from rats treated with indomethacin and/or pantoprazole.ResultsPantoprazole activated Nrf2 through inactivation of Keap1, after which the expression of HO-1 was significantly increased in a dose-dependent manner in RGM-1 cells. Increased ARE-DNA binding activity was observed maximally at 1 h with 300 μM of pantoprazole. The expression of HO-1 induced by pantoprazole was significantly associated with the increased in vitro tube formation (P ConclusionThese results demonstrate that Nrf2-mediated HO-1 induction of PPIs afforded a significant protective effect against NSAIDs-induced gastric damage beyond acid suppressive actions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 23066659 · DOI · PMC3548718
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 Induction of phase I, II and III drug metabolism/transport by xenobiotics [4]
- Research article Modulation of Nrf2-mediated antioxidant and detoxifying enzyme induction by the green tea polyphenol EGCG [5]
- Research article Induction of drug metabolism: the role of nuclear receptors [6]
- Research article Chemoprotection against cancer by induction of phase 2 enzymes [7]
- Research article Enzyme induction with antiepileptic drugs: cause for concern? [8]
- Research article Chemoprotection against cancer by phase 2 enzyme induction [9]
References
- Jeong SY, Im YN, Youm JY, Lee HK, Im SY. l-Glutamine Attenuates DSS-Induced Colitis via Induction of MAPK Phosphatase-1. . 2018. PMID 29494494 · DOI · PMC5872706
- Paradkar PN, Duchemin JB, Rodriguez-Andres J, Trinidad L, Walker PJ. Cullin4 Is Pro-Viral during West Nile Virus Infection of Culex Mosquitoes. . 2015. PMID 26325027 · DOI · PMC4556628
- Lee HJ, Han YM, Kim EH, Kim YJ, Hahm KB. A possible involvement of Nrf2-mediated heme oxygenase-1 up-regulation in protective effect of the proton pump inhibitor pantoprazole against indomethacin-induced gastric damage in rats. . 2012. PMID 23066659 · DOI · PMC3548718
- Xu C, Li CY, Kong AN. Induction of phase I, II and III drug metabolism/transport by xenobiotics. Arch Pharm Res. 2005. PMID 15832810 · DOI
- Na HK, Surh YJ. Modulation of Nrf2-mediated antioxidant and detoxifying enzyme induction by the green tea polyphenol EGCG. Food Chem Toxicol. 2008. PMID 18082923 · DOI
- Handschin C, Meyer UA. Induction of drug metabolism: the role of nuclear receptors. Pharmacol Rev. 2003. PMID 14657421 · DOI
- Talalay P. Chemoprotection against cancer by induction of phase 2 enzymes. Biofactors. 2000. PMID 11216505 · DOI
- Brodie MJ, Mintzer S, Pack AM, Gidal BE, Vecht CJ, Schmidt D. Enzyme induction with antiepileptic drugs: cause for concern?. Epilepsia. 2013. PMID 23016553 · DOI
- Talalay P, Fahey JW, Holtzclaw WD, Prestera T, Zhang Y. Chemoprotection against cancer by phase 2 enzyme induction. Toxicol Lett. 1995. PMID 8597048 · 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.