ArticleMechanisms of ageing and development2015
NRMT1 knockout mice exhibit phenotypes associated with impaired DNA repair and premature aging.
Article in Mechanisms of ageing and development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 48 citations in OpenAlex.
- Pharmacological Inhibition of N-terminal methyltransferase 1 promotes myogenic differentiation and muscle regeneration in a mouse model of Duchenne muscular dystrophy.Stem cell research & therapy · 2026Article
- Characterizations of Protein Arginine Deiminase 1 as a Substrate of NTMT1: Implications of Nα-Methylation in Protein Stability and Interaction.Journal of proteome research · 2024Article
- Exploring potential developmental origins of common neurodegenerative disorders.Biochemical Society transactions · 2024Review
- Spinal-Specific Super Enhancer in Neuropathic Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Structure-Activity Relationship Studies of Venglustat on NTMT1 Inhibition.Journal of medicinal chemistry · 2023Article
- Three's a crowd - why did three N-terminal methyltransferases evolve for one job?Journal of cell science · 2023Article
- METTLing in Stem Cell and Cancer Biology.Stem cell reviews and reports · 2023Review
- Design and characterization of PROTAC degraders specific to protein N-terminal methyltransferase 1.European journal of medicinal chemistry · 2022Article
- Age-related neurodegeneration and cognitive impairments of NRMT1 knockout mice are preceded by misregulation of RB and abnormal neural stem cell development.Cell death & disease · 2021Article
- Chemoproteomic Study Uncovers HemK2/KMT9 As a New Target for NTMT1 Bisubstrate Inhibitors.ACS chemical biology · 2021Article
- Modulation of N-terminal methyltransferase 1 by an NBiochemical and biophysical research communications · 2021Article
- Structure-based Discovery of Cell-Potent Peptidomimetic Inhibitors for Protein N-Terminal Methyltransferase 1.ACS medicinal chemistry letters · 2021Article
- Post-translational Modifications of the Protein Termini.Frontiers in cell and developmental biology · 2021Review
- Selective Peptidomimetic Inhibitors of NTMT1/2: Rational Design, Synthesis, Characterization, and Crystallographic Studies.Journal of medicinal chemistry · 2020Article
- Probing the Plasticity in the Active Site of Protein N-terminal Methyltransferase 1 Using Bisubstrate Analogues.Journal of medicinal chemistry · 2020Article
- Optimization of High-Throughput Methyltransferase Assays for the Discovery of Small Molecule Inhibitors.ACS combinatorial science · 2020Article
- Histone N-alpha terminal modifications: genome regulation at the tip of the tail.Epigenetics & chromatin · 2020Review
- Methionine metabolism and methyltransferases in the regulation of aging and lifespan extension across species.Aging cell · 2019Review
- Article
- Chemical Biology of Protein N-Terminal Methyltransferases.Chembiochem : a European journal of chemical biology · 2019Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Though defective genome maintenance and DNA repair have long been known to promote phenotypes of premature aging, the role protein methylation plays in these processes is only now emerging. We have recently identified the first N-terminal methyltransferase, NRMT1, which regulates protein-DNA interactions and is necessary for both accurate mitotic division and nucleotide excision repair. To demonstrate if complete loss of NRMT1 subsequently resulted in developmental or aging phenotypes, we constructed the first NRMT1 knockout (Nrmt1(-/-)) mouse. The majority of these mice die shortly after birth. However, the ones that survive, exhibit decreased body size, female-specific infertility, kyphosis, decreased mitochondrial function, and early-onset liver degeneration; phenotypes characteristic of other mouse models deficient in DNA repair. The livers from Nrmt1(-/-) mice produce less reactive oxygen species (ROS) than wild type controls, and Nrmt1(-/-) mouse embryonic fibroblasts show a decreased capacity for handling oxidative damage. This indicates that decreased mitochondrial function may benefit Nrmt1(-/-) mice and protect them from excess internal ROS and subsequent DNA damage. These studies position the NRMT1 knockout mouse as a useful new system for studying the effects of genomic instability and defective DNA damage repair on organismal and tissue-specific aging.
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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.