ReviewFrontiers in genetics2016
Physiological and Pathological Aging Affects Chromatin Dynamics, Structure and Function at the Nuclear Edge.
Review in Frontiers in genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Telomere Position Effect-Over Long Distances Acts as a Genome-Wide Epigenetic Regulator Through a Common Alu Element.Aging cell · 2025Article
- Migrasomes trigger innate immune activation and mediate transmission of senescence signals across human cells.Life medicine · 2023Article
- Mesenchymal stem cells derived from patients with premature aging syndromes display hallmarks of physiological aging.Life science alliance · 2022Article
- Intestinal aging is alleviated by uridine via regulating inflammation and oxidative stressCell cycle (Georgetown, Tex.) · 2022Article
- Article
- Telomere organization and the interstitial telomeric sites involvement in insects and vertebrates chromosome evolution.Genetics and molecular biology · 2022Article
- Chromatin Hubs: A biological and computational outlook.Computational and structural biotechnology journal · 2022Review
- Nuclear organization and regulation of the differentiated state.Cellular and molecular life sciences : CMLS · 2021Review
- Progesterone depletion results in Lamin B1 loss and induction of cell death in mouse trophoblast giant cells.PloS one · 2021Article
- The mechanistic role of alpha-synuclein in the nucleus: impaired nuclear function caused by familial Parkinson's disease SNCA mutations.Human molecular genetics · 2020Article
- Article
- Review
- Analysis of the 4q35 chromatin organization reveals distinct long-range interactions in patients affected with Facio-Scapulo-Humeral Dystrophy.Scientific reports · 2019Article
- Telomeres and telomerase: three decades of progress.Nature reviews. Genetics · 2019Review
- Multiplication of the SNCA locus exacerbates neuronal nuclear aging.Human molecular genetics · 2019Article
- Bring It to an End: Does Telomeres Size Matter?Cells · 2019Review
- Structural analysis of the ternary complex between lamin A/C, BAF and emerin identifies an interface disrupted in autosomal recessive progeroid diseases.Nucleic acids research · 2018Article
- Lamin B2 binding to minichromosome maintenance complex component 7 promotes non-small cell lung carcinogenesis.Oncotarget · 2017Article
- Lamina-Associated Domains: Links with Chromosome Architecture, Heterochromatin, and Gene Repression.Cell · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lamins are intermediate filaments that form a complex meshwork at the inner nuclear membrane. Mammalian cells express two types of Lamins, Lamins A/C and Lamins B, encoded by three different genes, LMNA, LMNB1, and LMNB2. Mutations in the LMNA gene are associated with a group of phenotypically diverse diseases referred to as laminopathies. Lamins interact with a large number of binding partners including proteins of the nuclear envelope but also chromatin-associated factors. Lamins not only constitute a scaffold for nuclear shape, rigidity and resistance to stress but also contribute to the organization of chromatin and chromosomal domains. We will discuss here the impact of A-type Lamins loss on alterations of chromatin organization and formation of chromatin domains and how disorganization of the lamina contributes to the patho-physiology of premature aging syndromes.
Indexed as
Identifiers
What OpenQuestion holds
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.