Articles tagged with Lamins
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A team of geneticists discovered a gene 'silencer' in junk DNA that prevents the devastating neurological disease autosomal dominant leukodystrophy (ADLD). The silencer element regulates lamin B1 expression, only affecting one type of cell, and its presence can spare patients from fatal symptoms.
Researchers at Texas A&M University have uncovered a mechanism behind cancer progression: the stiffening of tumor cell's environment. This spreading causes increased cell proliferation and tumor growth.
A new study suggests that prelamin A, a precursor of lamin A, accumulates with age and may drive normal aging. Researchers propose this protein as a target for intervention strategies to extend healthspan and lifespan.
A team of researchers identified the precise mechanism of nuclear envelope repair, finding that lamin C, BAF, and cGAS work together to facilitate rapid repair. The study provides insights into rare genetic disorders such as laminopathies and has potential applications for understanding and treating related diseases.
A study with lab-grown mouse cells reveals that lamin C plays a key role in maintaining the structural network under the cell's nucleus, ensuring proper DNA organization. This finding has significant implications for diagnosing and treating genetic disorders linked to DNA disorganization, such as progeria and muscular dystrophy.
Researchers from the CNIC and CIBERCV have created an animal model of HGPS, allowing them to study its effects and test treatments. They found that suppressing progerin expression and restoring lamin A can increase life expectancy by up to 84.5% in mice with mild symptoms, even if treatment is started late.
A study published in EMBO Molecular Medicine reveals that alterations in lamin B1 protein contribute to neurodegeneration in Huntington's disease. The researchers used innovative techniques like FANSI and ChIP-sequencing to analyze the impact of lamin B1 levels on gene transcription.
The study revealed that loss of Lamin A/C acetylation results in softened nuclei prone to mechanical pressure and eventual breaking. Nuclear blebs and micronuclei are more likely to form under these conditions, posing a risk to genetic material integrity.
A new gene therapy using CRISPR/Cas9 targets the accumulation of toxic proteins in progeria syndrome, a rare genetic disorder. The therapy improves health and life span in mice, providing insight into molecular pathways involved in accelerated aging.
Researchers visualize two distinct meshworks in the nuclear lamina, an outer layer made of lamin B1 and an inner layer of lamin A. This discovery may lead to a better understanding of genetic diseases like ADLD and how cells can compress without damaging their nuclei.
A team of biologists has shed light on how lamins maintain the relative positions of DNA segments throughout the nucleus, influencing gene expression. This finding has implications for understanding lamin-associated aging and diseases, including premature aging, neuropathies, heart defects, and organ decay.
A team of researchers has elucidated the molecular architecture of the nuclear lamina in mammalian cells using cryo-electron tomography. The study reveals a 14nm-thick layer with threadlike structures called lamin filaments, which assemble into polymers consisting of type A and B lamin proteins.
A new study has revealed multiple leads for pursuing potential treatments for Alzheimer's disease by targeting a structural flaw in brain cells. The researchers found that the tau protein aggregates in the brains of patients disrupt the lamin nucleoskeleton, leading to DNA relaxation and gene activation.
Researchers found a disordered mesh-like scaffold in Alzheimer's-affected cells, which surrounds the nucleus and controls brain cell function. This discovery may lead to new treatments for the earliest biological events leading to Alzheimer's disease.
A new study from the University of Maryland found that methylene blue can almost completely repair defects in cells with progeria and restore healthy cell function. The compound also repaired age-related damage to healthy cells, suggesting its potential as a treatment for both progeria and normal aging.
A recent study published in Nature Communications reveals that protein lamin A plays a crucial role in maintaining genomic structural stability by forming 'cross-links' that limit genetic material's freedom of movement within the nucleus. This creates a stable and linked polymeric structure promoting chromosomal integrity.
Researchers discovered that lamin-B protein plays a key role in suppressing immune responses in aging fruit flies, leading to chronic inflammation and gut hyperplasia. The findings have implications for understanding age-related immunosenescence in humans.
A study from the University of Pennsylvania School of Medicine reveals that epigenetic factors play a role in senescence, a process linked to normal aging and tumor suppression. The researchers found large-scale changes in gene expression and chromatin architecture when a nuclear protein called lamin B1 is deleted in senescent cells.
Lamins are essential proteins supporting the organization of stem cell niches, which regulate proliferation and differentiation of germline stem cells. This discovery could lead to a better understanding of diseases caused by lamin mutations and their impact on tissue degeneration.
Researchers at Johns Hopkins Medicine have identified a novel modification of the lamin A protein that disrupts normal patterns of fat distribution in familial partial lipodystrophy (FPLD). The discovery provides new insights into the mechanisms underlying FPLD, a rare disease characterized by abnormal fat accumulation in certain areas...
Researchers at Northwestern University developed a mathematical model that sheds light on the mechanisms causing bulges in cells' nuclear membranes. This study may provide potential therapies for related diseases by preventing bleb formation.
Researchers identified lamin A and lamin B receptor proteins as essential for maintaining gene position in the nucleus. Their absence causes genes to malfunction, leading to heart failure, vascular disease, and muscle wasting. This discovery may lead to new treatments for these diseases.
The study reveals two independent mechanisms for fixing heterochromatin to the inner face of the nuclear envelope, using lamin A/C and the lamin-B receptor. This discovery sheds light on how the nuclear architecture in rod cells of nocturnal animals differs from normal cells.
Researchers have discovered that farnesyl transferase inhibitors significantly slow the progress of progeria, a rare and lethal genetic disorder. The use of these inhibitors has been shown to slow bone loss and blood vessel blockage in children with progeria.
Researchers have found that B-type lamins are necessary for proper organ development, but not for the replication and differentiation of embryonic stem cells. Mice deficient in B-type lamins were born with developmental defects, highlighting the protein's importance in tissue organization.
Researchers found that lamin filaments are essential for proper gene positioning and organization, a crucial factor in maintaining nuclear shape and function. Mutations in lamin genes cause 14 different diseases, including Emery-Dreifuss muscular dystrophy, by disrupting muscle-specific gene reorganization.
Researchers at MIT and Carnegie Mellon used molecular modeling and simulation to study the behavior of lamin A protein tails, finding that mutant protein tails are actually more stable than healthy counterparts. The discovery validates the application of civil engineering methodology to studying diseased cells.
Scientists at Salk Institute successfully generated induced pluripotent stem cells from patients with Hutchinson-Gilford Progeria Syndrome, a rare disorder that accelerates aging. The cells displayed signs of vascular aging and were differentiated into smooth muscle cells that showed premature aging phenotypes.
Scientists have created the world's first human cell model of progeria, a rare genetic disease causing severe premature ageing in children. The model reveals defects in mesenchymal stem cells and vascular smooth muscle cells that exacerbate symptoms of ageing.
Perturbation of lamin B1-Oct-1 interactions can affect the expression of genes regulated by Oct-1, leading to increased reactive oxygen species production. This could be a key mechanism underlying the aging process.
Research reveals that mutations in the LMNA gene disrupt neuromuscular junction organization, leading to muscle fiber innervation disruption. This study provides insight into the molecular mechanisms underlying Emery-Dreifuss muscular dystrophy.
The gene responsible for Progeria has led to a promising experimental drug being evaluated in 28 children with the disease. Researchers have pinpointed the genetic mutation and identified an effective therapy, potentially treating this fatal disorder.
Researchers have characterized mutant phenotypes of fly lamin genes, showing they cause neuromuscular defects and premature aging similar to human laminopathies. This study provides insight into the divergence of gene expression and function through evolution, promising greater understanding of lamin functions and diseases.
Researchers discover that infants who died of mysterious illnesses had unique LMNA gene mutations, leading to increased production of the bad protein lamin A. Treating these cells with a drug meant for progeria patients showed promising signs of improvement.
Researchers block C5a receptor to prevent or induce asthma-like symptoms in mice, identifying mechanism by which C5aR signaling prevents response. C5aR blockade also reduces severity of asthma-like symptoms after allergen exposure.
Researchers identified altered expression of proteins involved in muscle differentiation, leading to reduced myoblast differentiation potential. Forced expression of MyoD or desmin restored this defect, providing new mechanistic insight into LMNA mutations contributing to muscular dystrophy.
Researchers discover that mutant lamin A proteins interfere with key controls of gene expression and cell cycle, leading to rapid aging in HGPS patients. The study suggests that similar missteps may be part of normal human aging.
Researchers created a mouse model of EDMD to investigate gene expression changes in the heart. They found increased expression of MAP kinases, which play roles in other forms of cardiomyopathy. This discovery opens possibilities for treating lamin-related cardiomyopathies with MAP kinase inhibitors.
Researchers found that farnesyl transferase inhibitors can normalize abnormal nuclei in progeria cells. The treatment targets a genetic mutation causing lamin A protein production issues.
Scientists have made a breakthrough in understanding cell mutations that cause human diseases, particularly in children, by studying the C. elegans worm.
A study published in Proceedings of the National Academy of Sciences found that anticancer drugs can reverse the nuclear structure abnormalities caused by a rare genetic disorder, progeria. The researchers successfully treated cells with progerin, a mutated protein linked to accelerated aging, using farnesylation inhibitors.
A study published in PNAS suggests that farnesyltransferase inhibitors (FTIs) may reverse nuclear structure abnormalities in progeria cells. Researchers treated progerin-carrying skin cells with FTIs, reducing cell blebbing and improving cellular function.
A new study reveals that children with Progeria experience progressive nuclear structure and function defects due to the accumulation of defective Lamin A protein. The findings provide critical insights into the cause of heart disease and cellular aging in this fatal disease.
A second gene, zinc metalloproteinase (ZMPSTE24), has been identified as a cause of the rare skeletal disorder mandibuloacral dysplasia (MAD). Mutations in this gene may also lead to premature aging, generalized loss of body fat and early death.
Hutchinson-Gilford progeria syndrome affects 1 in 8 million newborns worldwide and is characterized by accelerated aging. The researchers identified a single-letter misspelling in the LMNA gene as the cause of this disorder.
A France-based research team has discovered the gene responsible for Hutchinson-Gilford Progeria, a disease that causes young victims to age five to ten times faster than normal. The discovery is a critical step toward developing therapies for the disorder and programs to screen individuals for the defective gene.
New research reveals nucleus is more than just a bag of chromosomes, with key findings including the discovery of rope-like proteins called lamins linked to human diseases. The study also sheds light on the orchestrated process of nuclear breakdown during cell division.