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 (770 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
A saturated 14-carbon fatty acid occurring in most animal and vegetable fats, particularly butterfat and coconut, palm, and nutmeg oils. It is used to synthesize flavor and as an ingredient in soaps and cosmetics. (From Dorland, 28th ed)
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: Acid, Myristic; Tetradecanoic Acid; Acid, Tetradecanoic; Myristate.
Where it fits in the MeSH classification
- Broader topics
- Myristic Acids
Research landscape
PubMed indexes 1,789 records tagged with the MeSH heading “Myristic Acid” (counts retrieved 2026-10-31). 168 of them (9.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 779 records.
Reviews account for 68 records (3.8%) and meta-analyses for 1. Randomized controlled trials number 18 (1.0%) 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 | 779 |
| 2000-2009 | 472 |
| 2010-2019 | 370 |
| 2020 onward | 168 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 68 | 3.8% |
| Meta-analyses | 1 | 0.1% |
| Randomized controlled trials | 18 | 1.0% |
Method: PubMed query "Myristic Acid"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was 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 |
|---|---|---|---|---|
| Myristic acid potentiates palmitic acid-induced lipotoxicity and steatohepatitis associated with lipodystrophy by sustaning de novo ceramide synthesis | 2015 | Research article Design not recorded in structured metadata | 82 | cc by PMID 26539645 · DOI · PMC4747168 |
| The role of myristoylation in the membrane association of the Lassa virus matrix protein Z | 2006 | Research article Design not recorded in structured metadata | 77 | cc by PMID 17083745 · DOI · PMC1647273 |
| Targeting N-myristoylation for therapy of B-cell lymphomas | 2020 | Research article Design not recorded in structured metadata | 59 | cc by PMID 33093447 · DOI · PMC7582192 |
| Structural basis of co-translational N-myristoylation in humans | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 41577716 · DOI · PMC12858966 |
Myristic acid potentiates palmitic acid-induced lipotoxicity and steatohepatitis associated with lipodystrophy by sustaning de novo ceramide synthesis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Palmitic acid (PA) induces hepatocyte apoptosis and fuels de novo ceramide synthesis in the endoplasmic reticulum (ER).
- Closing excerpt
- These findings indicate a causal link between ceramide synthesis and ER stress in lipotoxicity, and imply that the consumption of diets enriched in MA and PA can cause NASH associated with lipodystrophy.
- 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 (271 words)
Palmitic acid (PA) induces hepatocyte apoptosis and fuels de novo ceramide synthesis in the endoplasmic reticulum (ER). Myristic acid (MA), a free fatty acid highly abundant in copra/palmist oils, is a predictor of nonalcoholic steatohepatitis (NASH) and stimulates ceramide synthesis. Here we investigated the synergism between MA and PA in ceramide synthesis, ER stress, lipotoxicity and NASH. Unlike PA, MA is not lipotoxic but potentiated PA-mediated lipoapoptosis, ER stress, caspase-3 activation and cytochrome c release in primary mouse hepatocytes (PMH). Moreover, MA kinetically sustained PA-induced total ceramide content by stimulating dehydroceramide desaturase and switched the ceramide profile from decreased to increased ceramide 14:0/ceramide16:0, without changing medium and long-chain ceramide species. PMH were more sensitive to equimolar ceramide14:0/ceramide16:0 exposure, which mimics the outcome of PA plus MA treatment on ceramide homeostasis, than to either ceramide alone. Treatment with myriocin to inhibit ceramide synthesis and tauroursodeoxycholic acid to prevent ER stress ameliorated PA plus MA induced apoptosis, similar to the protection afforded by the antioxidant BHA, the pan-caspase inhibitor z-VAD-Fmk and JNK inhibition. Moreover, ruthenium red protected PMH against PA and MA-induced cell death. Recapitulating in vitro findings, mice fed a diet enriched in PA plus MA exhibited lipodystrophy, hepatosplenomegaly, increased liver ceramide content and cholesterol levels, ER stress, liver damage, inflammation and fibrosis compared to mice fed diets enriched in PA or MA alone. The deleterious effects of PA plus MA-enriched diet were largely prevented by in vivo myriocin treatment. These findings indicate a causal link between ceramide synthesis and ER stress in lipotoxicity, and imply that the consumption of diets enriched in MA and PA can cause NASH associated with lipodystrophy.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26539645 · DOI · PMC4747168
The role of myristoylation in the membrane association of the Lassa virus matrix protein Z [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The Z protein is the matrix protein of arenaviruses and has been identified as the main driving force for budding.
- Closing excerpt
- Our data indicate that myristoylation of Z is critical for its binding ability to lipid membranes and thus, for effective virus budding.
- 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 (203 words)
The Z protein is the matrix protein of arenaviruses and has been identified as the main driving force for budding. Both LCMV and Lassa virus Z proteins bud from cells in the absence of other viral proteins as enveloped virus-like particles. Z accumulates near the inner surface of the plasma membrane where budding takes place. Furthermore, biochemical data have shown that Z is strongly membrane associated. The primary sequence of Z lacks a typical transmembrane domain and until now it is not understood by which mechanism Z is able to interact with cellular membranes. In this report, we analyzed the role of N-terminal myristoylation for the membrane binding of Lassa virus Z. We show that disruption of the N-terminal myristoylation signal by substituting the N-terminal glycine with alanine (Z-G2A mutant) resulted in a significant reduction of Z protein association with cellular membranes. Furthermore, removal of the myristoylation site resulted in a relocalization of Z from a punctuate distribution to a more diffuse cellular distribution pattern. Finally, treatment of Lassa virus-infected cells with various myristoylation inhibitors drastically reduced efficient Lassa virus replication. Our data indicate that myristoylation of Z is critical for its binding ability to lipid membranes and thus, for effective virus budding.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 17083745 · DOI · PMC1647273
Targeting N-myristoylation for therapy of B-cell lymphomas [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Myristoylation, the N-terminal modification of proteins with the fatty acid myristate, is critical for membrane targeting and cell signaling.
- Closing excerpt
- Because some treated lymphoma patients experience relapse and die, targeting B-cell lymphomas with a NMT inhibitor potentially provides an additional much needed treatment option for lymphoma.
- 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)
Myristoylation, the N-terminal modification of proteins with the fatty acid myristate, is critical for membrane targeting and cell signaling. Because cancer cells often have increased N-myristoyltransferase (NMT) expression, NMTs were proposed as anti-cancer targets. To systematically investigate this, we performed robotic cancer cell line screens and discovered a marked sensitivity of hematological cancer cell lines, including B-cell lymphomas, to the potent pan-NMT inhibitor PCLX-001. PCLX-001 treatment impacts the global myristoylation of lymphoma cell proteins and inhibits early B-cell receptor (BCR) signaling events critical for survival. In addition to abrogating myristoylation of Src family kinases, PCLX-001 also promotes their degradation and, unexpectedly, that of numerous non-myristoylated BCR effectors including c-Myc, NFκB and P-ERK, leading to cancer cell death in vitro and in xenograft models. Because some treated lymphoma patients experience relapse and die, targeting B-cell lymphomas with a NMT inhibitor potentially provides an additional much needed treatment option for lymphoma.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33093447 · DOI · PMC7582192
Structural basis of co-translational N-myristoylation in humans [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Modifications of proteins occurring during translation are critical for protein localization, stability and function.
- Closing excerpt
- These insights provide a molecular foundation for the understanding of the co-translational N-myristoylation mechanism in humans.
- 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 (147 words)
Modifications of proteins occurring during translation are critical for protein localization, stability and function. N-myristoylation is an essential N-terminal lipid modification catalyzed co-translationally by N-myristoyltransferases (NMTs) which have been identified as promising drug targets. However, its molecular basis in the context of the translating ribosome is not known. Here, we reveal the structural basis for co-translational N-myristoylation by NMT1 on the human ribosome by cryo-electron microscopy (cryo-EM). We show that NMT1 binds near the peptide tunnel exit and interacts with the nascent polypeptide-associated complex (NAC). Unlike other multi-enzyme complexes that act simultaneously, we find that methionine excision by methionine aminopeptidases and N-myristoylation occur sequentially via consecutive binding to the ribosome. Furthermore, our data suggest that NMT1 remains associated with elongating nascent chains, indicating a co-translational chaperone-like function in partnership with NAC. These insights provide a molecular foundation for the understanding of the co-translational N-myristoylation mechanism in humans.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41577716 · DOI · PMC12858966
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 The biology and enzymology of protein N-myristoylation [5]
- Research article Post-translational myristoylation: Fat matters in cellular life and death [6]
- Research article Membrane localization of a rice calcium-dependent protein kinase (CDPK) is mediated by myristoylation and palmitoylation [7]
- Research article Protein N-myristoylation: functions and mechanisms in control of innate immunity [8]
- Research article Myristoylation, an Ancient Protein Modification Mirroring Eukaryogenesis and Evolution [9]
- Research article Fatty acid synthesis in African trypanosomes: a solution to the myristate mystery [10]
References
- Martínez L, Torres S, Baulies A, Alarcón-Vila C, Elena M, Fabriàs G, et al.. Myristic acid potentiates palmitic acid-induced lipotoxicity and steatohepatitis associated with lipodystrophy by sustaning de novo ceramide synthesis. . 2015. PMID 26539645 · DOI · PMC4747168
- Strecker T, Maisa A, Daffis S, Eichler R, Lenz O, Garten W. The role of myristoylation in the membrane association of the Lassa virus matrix protein Z. . 2006. PMID 17083745 · DOI · PMC1647273
- Beauchamp E, Yap MC, Iyer A, Perinpanayagam MA, Gamma JM, Vincent KM, et al.. Targeting N-myristoylation for therapy of B-cell lymphomas. . 2020. PMID 33093447 · DOI · PMC7582192
- Denk T, Monassa P, Musial J, Berninghausen O, Beatrix B, Giglione C, et al.. Structural basis of co-translational N-myristoylation in humans. . 2026. PMID 41577716 · DOI · PMC12858966
- Farazi TA, Waksman G, Gordon JI. The biology and enzymology of protein N-myristoylation. J Biol Chem. 2001. PMID 11527981 · DOI
- Martin DD, Beauchamp E, Berthiaume LG. Post-translational myristoylation: Fat matters in cellular life and death. Biochimie. 2011. PMID 21056615 · DOI
- Martín ML, Busconi L. Membrane localization of a rice calcium-dependent protein kinase (CDPK) is mediated by myristoylation and palmitoylation. Plant J. 2000. PMID 11115124 · DOI
- Wang B, Dai T, Sun W, Wei Y, Ren J, Zhang L, et al.. Protein N-myristoylation: functions and mechanisms in control of innate immunity. Cell Mol Immunol. 2021. PMID 33731917 · DOI · PMC7966921
- Meinnel T, Dian C, Giglione C. Myristoylation, an Ancient Protein Modification Mirroring Eukaryogenesis and Evolution. Trends Biochem Sci. 2020. PMID 32305250 · DOI
- Paul KS, Jiang D, Morita YS, Englund PT. Fatty acid synthesis in African trypanosomes: a solution to the myristate mystery. Trends Parasitol. 2001. PMID 11685899 · 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 2026-10-31.
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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.