ReviewCell cycle (Georgetown, Tex.)2011
Regulating the levels of key factors in cell cycle and DNA repair: new pathways revealed by lamins.
Review in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- Lamin A/C facilitates DNA damage response by modulating ATM signaling and homologous recombination pathways.Animal cells and systems · 2024Article
- Article
- Review
- Possible Mechanisms of Resistance Development to Photodynamic Therapy (PDT) In Vulvar Cancer Cells.International journal of molecular sciences · 2022Article
- Vitamin D in Triple-Negative and BRCA1-Deficient Breast Cancer-Implications for Pathogenesis and Therapy.International journal of molecular sciences · 2020Review
- Lamin A/C promotes DNA base excision repair.Nucleic acids research · 2019Article
- Cytoskeletal and nucleoskeletal interacting protein networks play critical roles in cellular function and dysfunction.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- The functional importance of lamins, actin, myosin, spectrin and the LINC complex in DNA repair.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- The Biology of the Nuclear Envelope and Its Implications in Cancer Biology.International journal of molecular sciences · 2019Review
- Review
- Spectrin and its interacting partners in nuclear structure and function.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- Causes and consequences of genomic instability in laminopathies: Replication stress and interferon response.Nucleus (Austin, Tex.) · 2018Review
- Article
- SNPs near the cysteine proteinase cathepsin O gene (CTSO) determine tamoxifen sensitivity in ERα-positive breast cancer through regulation of BRCA1.PLoS genetics · 2017Article
- Mechanisms of oncogene-induced genomic instability.Biophysical chemistry · 2017Review
- Vitamin D/vitamin D receptor axis regulates DNA repair during oncogene-induced senescence.Oncogene · 2016Article
- Methods to Monitor DNA Repair Defects and Genomic Instability in the Context of a Disrupted Nuclear Lamina.Methods in molecular biology (Clifton, N.J.) · 2016Article
- Physiological and Pathological Aging Affects Chromatin Dynamics, Structure and Function at the Nuclear Edge.Frontiers in genetics · 2016Review
- Gene expression analysis of skin grafts and cultured keratinocytes using synthetic RNA normalization reveals insights into differentiation and growth control.BMC genomics · 2015Article
- DNA repair defects and genome instability in Hutchinson-Gilford Progeria Syndrome.Current opinion in cell biology · 2015Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Spatial and temporal organization of the genome represents an additional step in the regulation of nuclear functions. The nuclear lamina, a polymeric meshwork formed by lamins (A/C and B type) and lamin-associated proteins, plays a key role in the maintenance of genome localization, structure and function. Specifically, mutations in the LMNA gene encoding lamins A/C or changes in its expression, either upregulation or silencing, are associated with defects in DNA replication, transcription and repair, as well as alterations in epigenetic modifications of chromatin. These data, together with the fact that defects in A-type lamins are associated with a whole variety of degenerative disorders, premature aging syndromes and cancer, support the notion that these proteins operate as caretakers of the genome. However, our understanding of their functions is limited due to the lack of well-defined mechanisms behind the genomic instability observed in lamin-related diseases. Here, we summarize our recent discovery of new pathways that are affected by the loss of A-type lamins. In particular, we found that A-type lamins control transcription and degradation of proteins with key roles in cell cycle regulation and DNA double-strand breaks (DSBs) repair by non-homologous end-joining (NHEJ) and homologous-recombination (HR). Importantly, the proteins regulated by A-type lamins--Rb family members, 53BP1, BRCA1 and RAD51--exert tumor suppressor functions, with their loss being associated with cancer susceptibility. Moreover, our studies revealed novel pathways that contribute to genomic instability and that can be activated in disease states independent of the status of A-type lamins.
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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.