Articles tagged with Chromatin
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A team of researchers at Florida State University has made a groundbreaking discovery in the field of plant genetics, shedding light on how plants regulate their genetic material. The study found that certain regions of DNA are hypersensitive to enzymes, allowing scientists to identify new biochemical signatures and gain a better under...
Researchers have successfully treated a genetic form of intellectual disability in mice using an anticancer drug, suggesting a potential new approach for the human condition. The study's findings indicate that altering the balance between chromatin's open and closed states could be key to treating Mendelian disorders of the epigenetic ...
Three analyses compare how human, worm, and fruit fly genomes are read out and organized into chromosomes, adding billions of entries to a publicly available archive. Scientists discovered common features that apply to all organisms, offering insights into human development and disease.
Researchers at Duke University discovered that the host determines which genes are open in the gut, while microbes regulate their usage, indicating a cooperative environment where both parties interact to thrive. This study has significant implications for understanding the intricate relationships between hosts and microbiomes.
A study sequencing the exome of 231 schizophrenia patients and their unaffected parents found that collective damage across several genes contributes to the disease. This discovery could lead to early detection and treatment strategies.
Researchers at Cold Spring Harbor Laboratory discovered a protein called Chd5 that plays a crucial role in chromatin remodeling during sperm development. The team found that Chd5 is essential for maintaining the genetic information of male fertility, and its absence can lead to infertility and increased risk of disease.
Researchers identify machinery of epigenetic inheritance, a process by which traits are passed between generations without DNA sequence changes. The discovery reveals that chemical marks on chromatin serve as molecular memory, allowing cells to recognize and remember to silence specific genes in each new generation.
Researchers identified an enzyme called TLK1 that regulates the transport of histones to DNA copying hubs, crucial for maintaining normal gene function. The study found that TLK1 boosts the supply of histones at critical time points, ensuring correct chromatin architecture and cellular identity.
Researchers found that ANP32E strips histone H2A.Z from DNA, altering gene expression and leading to improper chromatin structure in cells lacking the protein. This discovery could reveal novel therapeutic strategies for diseases and cancers.
Researchers present new pain management treatment for SCD patients using selectin inhibitors, while also exploring targeted gene therapy strategies to produce healthy hemoglobin. These advances aim to improve the long-term outlook and quality of life for hundreds of thousands of patients worldwide.
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.
The study reveals HDAC3 plays a key role in regulating gene expression, chromatin structure, and genome stability. Disruption of HDAC3 expression leads to impaired hematopoiesis, highlighting its importance in stem cell functions and bone marrow failure syndromes.
Researchers found that actin's monomeric form interacts with chromatin to regulate gene expression and genome stability. The discovery challenges the dogma that actin functions through polymerization, revealing a novel mechanism for nuclear actin.
Researchers at CSHL have discovered how Chd5 exerts its beneficial effects by binding to histone H3, preventing cancer initiation and promoting tumor suppression. This finding has important implications for treating diverse human cancers.
A study published in Cell Reports found that the position of a gene within chromatin affects its expression, contradicting the concept of a singular 'histone code'. The researchers inserted the same gene into 90 different locations in yeast chromosome and discovered significant differences in gene activity.
Researchers identified hundreds of regions in the human genome with unique chromatin structures that control cognitive behavior and expression. These findings provide new insights into diseases like Alzheimer's and autism.
Researchers identified a new mechanism allowing the toxic DUX4 protein to be produced in skeletal muscle, causing progressive muscle weakness. Mutations in the SMCHD1 gene cause chromatin relaxation, leading to DUX4 production.
Researchers have made a breakthrough in nuclear reprogramming by identifying histone H3.3 as a key player in reverting nuclei to a pluripotent state, capable of becoming any cell type. This discovery has significant implications for regenerative medicine and cancer treatment.
A study reveals that repressor proteins like Set2 recruit de-acetylases and chromatin remodelers Isw1 to block histone exchange and prevent erroneous transcription. This mechanism is crucial for maintaining accurate gene expression, which is often disrupted in diseases such as cancer.
Researchers discovered a 'switch' called MOZ that modifies the Tbx1 gene, essential for normal heart development, to explain variations in DiGeorge syndrome severity. The study found that MOZ activity can be influenced by environmental factors, such as diet, particularly vitamin A, which can exacerbate birth defects.
Researchers at Stowers Institute for Medical Research reveal that histone exchange occurs over a large proportion of genes, controlling gene expression. They also find that the Set2 protein plays a complex role in regulating transcription, preventing cryptic RNA transcripts and maintaining chromosomal stability.
Researchers at Children's Hospital of Philadelphia have developed approaches to control long-range genomic interactions during gene expression. By identifying a looping factor, they showed that chromatin looping is a cause, not an effect, of gene transcription.
Weill Cornell Medical College researchers discovered that a chromosomal rearrangement in prostate cancer cells creates a new 'fusion' gene, warping DNA structure and triggering abnormal growth. The study suggests a model for how other chromosomal translocations contribute to cancer formation.
Scientists have identified PRC2, a chromatin regulator, as a promising therapeutic target in acute myeloid leukemia. Blocking PRC2 halts uncontrolled proliferation and reactivates anti-tumor pathways, offering a potential new treatment option.
Researchers have elucidated the crystal structure of Alba2-DNA complex in archaea, revealing a hollow pipe-like structure that compacts DNA. This discovery provides valuable clues into the evolution of chromatin structure and its connection to diseases.
Scientists at EMBL have developed a new method to observe enhancer activity during development, showing that specific chromatin modifications trigger gene expression. This breakthrough provides cell-type specific information on enhancer activity and gene status in multicellular embryos.
Researchers at Max Planck Institute discovered that plant seed cells contract their nuclei and condense chromatin to resist dehydration, enabling seeds to survive harsh conditions. This mechanism allows seeds to prepare for germination when environmental conditions improve.
Researchers at USC's Keck School of Medicine discovered how estrogen activates genes in breast-cancer cells through a protein called TIP60, which recognizes methylation signals in chromatin. This finding builds upon previous work and has broader implications for gene regulation and potentially global significance.
A Stanford University School of Medicine study found that modifying proteins in a laboratory roundworm increases the life span of both the original animal and its descendants, even when the modification is no longer present. This suggests that longevity can be inherited in a non-genetic manner over several generations.
A recent study published in Nature Cell Biology has discovered that bookmarking genes before cell division accelerates their reactivation afterwards. By analyzing the kinetics of gene activation, researchers found that a histone molecule undergoes chemical modification and is preserved during mitosis, allowing for rapid reactivation.
Researchers at Stanford University School of Medicine have developed a new technique that allows them to pinpoint the exact DNA sequences and locations bound by regulatory RNAs. The study reveals the intricate world of gene expression and how RNA molecules control neighboring and distant genes.
A recent NIH award of $1.39M will support a study led by Dr. Lori A. Pile to investigate the alteration of chromatin structure during cell division, which is crucial for normal cell growth and cancer development. The findings aim to refine cancer treatments currently undergoing clinical trials.
The University of Colorado Cancer Center has successfully genetically sequenced the most prevalent type of bladder cancer, urothelial carcinoma. The team discovered mutations in genes responsible for chromatin remodeling, which are similar to those found in other cancers.
A study published in Nature Genetics identified 49 new significantly mutated genes associated with TCC, including eight genes related to chromatin remodeling. These genetic aberrations were found in 59% of individuals with TCC, suggesting a potential role for UTX gene in bladder cancer classification and diagnosis.
Researchers have discovered hundreds of new protein-coding genes and thousands of new non-protein coding RNAs in the fruit fly and roundworm genomes. The studies also identified specific chromatin signatures associated with the regulation of protein-coding genes, revealing how genes work in concert to produce complex biological processes.
A new study reveals that immune cells use chromatin to form defensive webs, catching and killing pathogens with the help of enzymes neutrophil elastase and myeloperoxidase. The discovery opens up a new understanding of how the body defends against infection.
As human cells age, their telomeres shorten, triggering massive changes in the way DNA is packaged, known as chromatin. This leads to epigenetic changes that affect gene expression and contribute to aging. Researchers have identified histone proteins as key players in this process.
The study reveals that Wilms tumor cells share epigenetic characteristics with normal kidney stem cells, highlighting the critical role of chromatin in tumor development. This discovery may provide new avenues for therapy and shed light on other pediatric cancers.
A new study reveals that chromatin regulatory proteins, Smc2 and Smc4, play a crucial role in maintaining genome stability in embryonic stem cells. The authors found that condensins promote mitotic progression and interphase chromatin compaction, leading to massive DNA damage and cell death when blocked in these cells.
A new study reveals that chromatin proteins defective in RTT, CdLS, and ATR-X syndromes are associated with each other and regulate imprinted genes. This cooperation may explain similarities between the associated human syndromes.
Researchers at the Genome Institute of Singapore have made a significant breakthrough in understanding gene expression and regulation by developing a novel technology called ChIA-PET, which successfully mapped long-range chromatin interactions throughout the human genome.
Researchers at EMBL have identified a whole family of proteins capable of directly responding to the alarm signal produced by PARP1 when DNA is damaged. Histone macroH2A1.1 plays a key role in this process, condensing chromatin around damaged areas to increase repair chances.
A recent study found that lincRNAs have a global role in genome regulation, guiding chromatin complexes to specific genomic locations. By analyzing RNA-protein interactions, researchers identified which lincRNAs are bound by chromatin-modifying enzymes and which genes are affected by their depletion.
The BRIT1 protein enables cellular repair mechanisms to fix damaged DNA by relaxing its packaging. This allows two different DNA repair pathways to access the damage, preventing flawed DNA from being passed on as the cell divides. The study suggests that targeting BRIT1 deficiency could lead to cancer treatment.
A study by Baylor College of Medicine found that retinoic acid and Neurogenin2 cooperate to activate chromatin and determine nerve progenitor cells become motor neurons. This discovery may lead to generating motor neurons from different stem cells and developing tools for drug screening.
Researchers discovered how a SUMO protein guides an enzyme complex to alter chromatin structure and regulate gene expression. The interaction between SUMO and the enzyme complex prevents aberrant gene expression, which is common in cancer and neurodegenerative diseases.
Researchers discovered the MLL-AF4 protein binds to over 169 genes in cancer cells, hijacking blood stem cell machinery and causing cancerous cell division. This understanding may lead to new drug targets for treating mixed-lineage leukemia.
The new journal Epigenetics & Chromatin publishes research on heritable changes in gene expression without altering DNA sequence. High-quality studies on human telomeres and the RNAi pathway have been published, shedding light on epigenetic inheritance and chromatin-based interactions.
The DOT1B enzyme helps epigenetically regulate VSG genes, allowing parasites to switch between coat variants. In its absence, silent genes become active, slowing down the switching process.
Researchers at the University of Illinois have developed a new technique to image cells under an electron microscope, yielding a sharper picture of chromatin structure. This method allows for enhanced staining and structural preservation, enabling scientists to study chromatin packing and gene expression in high resolution.
Scientists create whole genome maps of chromatin in embryonic stem cells, revealing a special code that underlies cell identity. The study provides a framework for mapping the complete chromatin landscape of almost any kind of cell.
A UVa-led team has discovered that chromatin packing plays a crucial role in determining gene expression timing. By analyzing the replication of genes in different cell lines, researchers found that loosely packed chromatin allows for early gene expression, while densely packed chromatin leads to late expression.
Researchers at The Wistar Institute have identified an 'insulator' - a stretch of DNA about 800 base pairs long - that serves as a physical barrier between active and inactive regions of the HSV-1 genome. This discovery may lead to strategies to manipulate the virus, and could provide targets for designing drugs to disrupt its mechanisms.
In Drosophila cells, ribosomal proteins are associated with linker histone H1 protein on chromatin. Depletion of both causes up-regulation of target genes.
Researchers at the Broad Institute found an unusual molecular structure near developmental genes that enables embryonic stem cells to maintain their unique plasticity. This 'bivalent domain' acts as a kind of gene gatekeeper, controlling the expression of crucial genes in early development.
A Brg1 mutation in mice reveals the importance of SWI/SNF complexes in beta-globin regulation and erythropoiesis. This study may provide insight into common ailments such as beta thalassemia and anemia. The findings highlight the significance of chromatin-remodeling complexes in development and physiology.
Researchers analyzed chromatin structure in human chromosomes and found similar patterns in equivalent regions of the mouse genome, revealing new insights into regulatory functions and potential connections to cancer. This study advances our understanding of how genes are turned on and off, with implications for improving human health.
Researchers found that MECP2 target gene DLX5 is overexpressed in RTT patients due to loss of silent chromatin looping and impaired imprinting. This misregulation leads to increased expression of GABA, a neurotransmitter essential for brain function.
Researchers found that mutated MeCP2 protein represses genes, specifically targeting imprinted genes like DLX5, leading to misregulation of neurotransmitter GABA production. The study links specific defects in chromatin folding to Rett Syndrome for the first time.
Researchers at The Wistar Institute have discovered a family of molecular complexes involved in the repression of extensive sets of tissue-specific genes. These complexes share two core subunits, including histone deacetylase and BHC110, which operate as co-repressors to maintain gene silencing.