ReviewJournal of biosciences2006
Laminopathies: multiple disorders arising from defects in nuclear architecture.
Review in Journal of biosciences, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Consensus statement on standard of care for congenital muscular dystrophies.Journal of child neurology · 2010Guideline
- Lamin A/C promotes DNA base excision repair.Nucleic acids research · 2019Article
- Mechanical regulation of mesenchymal stem cell differentiation.Journal of anatomy · 2015Review
- Association of lamin A/C with muscle gene-specific promoters in myoblasts.Biochemistry and biophysics reports · 2015Article
- Potential gene regulatory role for cyclin D3 in muscle cells.Journal of biosciences · 2015Article
- LMNA-associated cardiocutaneous progeria: an inherited autosomal dominant premature aging syndrome with late onset.American journal of medical genetics. Part A · 2013Article
- Lamin A/C haploinsufficiency modulates the differentiation potential of mouse embryonic stem cells.PloS one · 2013Article
- Oxidative stress induces an ATM-independent senescence pathway through p38 MAPK-mediated lamin B1 accumulation.The EMBO journal · 2012Article
- Lamins, laminopathies and disease mechanisms: possible role for proteasomal degradation of key regulatory proteins.Journal of biosciences · 2011Review
- RefilinB (FAM101B) targets filamin A to organize perinuclear actin networks and regulates nuclear shape.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Aging genetics and aging.Aging and disease · 2011Article
- Structure and expression of the maize (Zea mays L.) SUN-domain protein gene family: evidence for the existence of two divergent classes of SUN proteins in plants.BMC plant biology · 2010Article
- Article
- Lamin C and chromatin organization in Drosophila.Journal of genetics · 2010Article
- Mechanobiology and the microcirculation: cellular, nuclear and fluid mechanics.Microcirculation (New York, N.Y. : 1994) · 2010Review
- Deficiency of the E3 ubiquitin ligase TRIM32 in mice leads to a myopathy with a neurogenic component.Human molecular genetics · 2009Article
- Sumoylation and human disease pathogenesis.Trends in biochemical sciences · 2009Review
- Autosomal-dominant distal myopathy associated with a recurrent missense mutation in the gene encoding the nuclear matrix protein, matrin 3.American journal of human genetics · 2009Article
- Sumoylation regulates lamin A function and is lost in lamin A mutants associated with familial cardiomyopathies.The Journal of cell biology · 2008Article
- Nuclear shape, mechanics, and mechanotransduction.Circulation research · 2008Review
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lamins are the major structural proteins of the nucleus in an animal cell. In addition to being essential for nuclear integrity and assembly, lamins are involved in the organization of nuclear processes such as DNA replication, transcription and repair. Mutations in the human lamin A gene lead to highly debilitating genetic disorders that primarily affect muscle, adipose, bone or neuronal tissues and also cause premature ageing syndromes. Mutant lamins alter nuclear integrity and hinder signalling pathways involved in muscle differentiation and adipocyte differentiation, suggesting tissue-specific roles for lamins. Furthermore, cells expressing mutant lamins are impaired in their response to DNA damaging agents. Recent reports indicate that certain lamin mutations act in a dominant negative manner to cause nuclear defects and cellular toxicity, and suggest a possible role for aberrant lamins in normal ageing processes.
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.