ArticleCell cycle (Georgetown, Tex.)2012
Familial partial lipodystrophy, mandibuloacral dysplasia and restrictive dermopathy feature barrier-to-autointegration factor (BAF) nuclear redistribution.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 30 citations in OpenAlex.
- Lipodystrophic Laminopathies: From Dunnigan Disease to Progeroid Syndromes.International journal of molecular sciences · 2024Review
- The role of prelamin A post-translational maturation in stress response and 53BP1 recruitment.Frontiers in cell and developmental biology · 2022Article
- Diverse cellular functions of barrier-to-autointegration factor and its roles in disease.Journal of cell science · 2020Review
- Altered adipocyte differentiation and unbalanced autophagy in type 2 Familial Partial Lipodystrophy: an in vitro and in vivo study of adipose tissue browning.Experimental & molecular medicine · 2019Article
- Repair of nuclear ruptures requires barrier-to-autointegration factor.The Journal of cell biology · 2019Article
- Nuclear Organization in Stress and Aging.Cells · 2019Review
- Article
- The Cutting Edge: The Role of mTOR Signaling in Laminopathies.International journal of molecular sciences · 2019Review
- Ankrd2 in Mechanotransduction and Oxidative Stress Response in Skeletal Muscle: New Cues for the Pathogenesis of Muscular Laminopathies.Oxidative medicine and cellular longevity · 2019Review
- RareFrontiers in cell and developmental biology · 2019Article
- Genomic instability and DNA replication defects in progeroid syndromes.Nucleus (Austin, Tex.) · 2018Review
- Lipodystrophic syndromes due to LMNA mutations: recent developments on biomolecular aspects, pathophysiological hypotheses and therapeutic perspectives.Nucleus (Austin, Tex.) · 2018Review
- The effect of the lamin A and its mutants on nuclear structure, cell proliferation, protein stability, and mobility in embryonic cells.Chromosoma · 2017Article
- Potential therapeutic effects of the MTOR inhibitors for preventing ageing and progeria-related disorders.British journal of clinical pharmacology · 2016Review
- Barrier-to-autointegration factor (BAF) involvement in prelamin A-related chromatin organization changes.Oncotarget · 2016Article
- Physiological and Pathological Aging Affects Chromatin Dynamics, Structure and Function at the Nuclear Edge.Frontiers in genetics · 2016Review
- All-trans retinoic acid and rapamycin normalize Hutchinson Gilford progeria fibroblast phenotype.Oncotarget · 2015Article
- Barrier to Autointegration Factor (BANF1): interwoven roles in nuclear structure, genome integrity, innate immunity, stress responses and progeria.Current opinion in cell biology · 2015Review
- Modulation of TGFbeta 2 levels by lamin A in U2-OS osteoblast-like cells: understanding the osteolytic process triggered by altered lamins.Oncotarget · 2015Article
- Muscular dystrophy-associated SUN1 and SUN2 variants disrupt nuclear-cytoskeletal connections and myonuclear organization.PLoS genetics · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prelamin A processing impairment is a common feature of a restricted group of rare genetic alterations/disorders associated with a wide range of clinical phenotypes. Changes in histone posttranslational modifications, alterations in non-histone chromatin proteins and chromatin disorganization have been specifically linked to impairment of specific, distinct prelamin A processing steps, but the molecular mechanism involved in these processes is not yet understood . In this study, we show that the accumulation of wild-type prelamin A detected in restrictive dermopathy (RD), as well as the accumulation of mutated forms of prelamin A identified in familial partial lipodystrophy (FPLD) and mandibuloacral dysplasia (MADA), affect the nuclear localization of barrier-to-autointegration factor (BAF), a protein able to link lamin A precursor to chromatin remodeling functions. Our findings, in accordance with previously described results, support the hypothesis of a prelamin A involvement in BAF nuclear recruitment and suggest BAF-prelamin A complex as a protein platform usually activated in prelamin A-accumulating diseases. Finally, we demonstrate the involvement of the inner nuclear membrane protein emerin in the proper localization of BAF-prelamin A complex.
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.