ArticleJournal of molecular endocrinology2019
Cap-independent mRNA translation is upregulated in long-lived endocrine mutant mice.
Article in Journal of molecular endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
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- LONP1 regulation of mitochondrial protein folding provides insight into beta cell failure in type 2 diabetes.Nature metabolism · 2025Article
- Targeting mCurrent oncology (Toronto, Ont.) · 2025Review
- The lifespan-extending MEK1 inhibitor trametinib promotes regulation of de novo lipogenesis enzymes by chaperone-mediated autophagy.Frontiers in aging · 2025Article
- Proteomic changes induced by longevity-promoting interventions in mice.GeroScience · 2024Article
- Article
- Coordinated transcriptional upregulation of oxidative metabolism proteins in long-lived endocrine mutant mice.GeroScience · 2023Article
- Genomic Instability and Epigenetic Changes during Aging.International journal of molecular sciences · 2023Review
- Canagliflozin shares common mTOR and MAPK signaling mechanisms with other lifespan extension treatments.Life sciences · 2023Article
- Four anti-aging drugs and calorie-restricted diet produce parallel effects in fat, brain, muscle, macrophages, and plasma of young mice.GeroScience · 2023Article
- Lifespan-extending interventions induce consistent patterns of fatty acid oxidation in mouse livers.Communications biology · 2023Article
- mActa biochimica et biophysica Sinica · 2023Review
- From form to function: mAdvances in biological regulation · 2023Review
- Aging Rate Indicators: Speedometers for Aging Research in Mice.Aging biology · 2023Article
- Cap-independent translation of GPLD1 enhances markers of brain health in long-lived mutant and drug-treated mice.Aging cell · 2022Article
- Transient early life growth hormone exposure permanently alters brain, muscle, liver, macrophage, and adipocyte status in long-lived Ames dwarf mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
It has been hypothesized that transcriptional changes associated with lower mTORC1 activity in mice with reduced levels of growth hormone and insulin-like growth factor 1 are responsible for the longer healthy lifespan of these mutant mice. Cell lines and tissues from these mice show alterations in the levels of many proteins that cannot be explained by corresponding changes in mRNAs. Such post-transcriptional modulation may be the result of preferential mRNA translation by the cap-independent translation of mRNA bearing the N6-methyl-adenosine (m6A) modification. The long-lived endocrine mutants - Snell dwarf, growth hormone receptor deletion and pregnancy-associated plasma protein-A knockout - all show increases in the N6-adenosine-methyltransferases (METTL3/14) that catalyze 6-methylation of adenosine (m6A) in the 5' UTR region of select mRNAs. In addition, these mice have elevated levels of YTH domain-containing protein 1 (YTHDF1), which recognizes m6A and promotes translation by a cap-independent mechanism. Consistently, multiple proteins that can be translated by the cap-independent mechanism are found to increase in these mice, including DNA repair and mitochondrial stress response proteins, without changes in corresponding mRNA levels. Lastly, a drug that augments cap-independent translation by inhibition of cap-dependent pathways (4EGI-1) was found to elevate levels of the same set of proteins and able to render cells resistant to several forms of in vitro stress. Augmented translation by cap-independent pathways facilitated by m6A modifications may contribute to the stress resistance and increased healthy longevity of mice with diminished GH and IGF-1 signals.
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Registered trials
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.