Articles tagged with Extracellular Matrix Proteins
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Researchers have gained detailed insights into RBP3's structure and mechanism of action, shedding light on its role in protecting the retina from diseases. The study suggests potential therapies to slow or stop retinal degeneration, including RP and myopia.
Researchers have developed a new way to grow organoids using Invasin, a protein produced by bacteria, mimicking the original organ with its variety of cell types. This study provides an affordable, standardized and animal-free alternative to currently used methods.
Dr. Gail Cornwall is investigating the structure of the brain extracellular matrix, a network of proteins and polysaccharides found in the space between neurons and glia. Her research aims to identify novel structural elements and mechanisms that enable brain plasticity and sex-specific responses.
Researchers at Sanford Burnham Prebys found that pancreatic cancer cells rely on a specific nutrient, glutamine, to fuel their unchecked growth. The study identified two enzymes, aPKC zeta and iota, that play a regulatory role in the process of macropinocytosis, allowing cancer cells to scavenge alternative resources.
Researchers have created a comprehensive database of protein changes in mice tissues due to aging, providing new insights into age-related diseases. The study reveals proteins that increase with age and improve understanding of the molecular mechanisms underlying aging.
Researchers from Brazil's Center for Research on Redox Processes in Biomedicine found that high blood sugar can cause thrombosis by altering endothelial function and promoting platelet adhesion. They identified a specific molecular mechanism involving protein disulfide isomerase A1 as a key regulator of this process.
A new genetic labeling tool has revealed patterns in brain extracellular matrix (ECM) in mice, including differences in matrix deposition on various neuron types. The tool allows for detection of changes in ECM over time, providing insights into brain development and function.
Researchers have developed a multi-component hydrogel scaffold to mimic the amyloid-beta containing microenvironment associated with AD. The study found elevated levels of neuroinflammation and apoptosis markers in healthy neuronal progenitor cells cultured within this environment.
A study found that targeting heparan sulfate-modified proteins improves cell repair, rescues neuron loss and reverses cellular changes associated with neurodegenerative diseases. Disrupting these proteins promotes autophagy-dependent cell repair and reverses early cellular problems in models of Alzheimer's.
Bromination of extracellular matrix proteins is a physiological modification dependent on peroxidasin, revealing a possible role for protein bromination in pulmonary fibrosis and non-fibrotic lung tissue. This study extends knowledge of halogenation's importance in the mammalian organism.
Studies on knockout mice have shown that removal of specific matrix proteins leads to visual deficits, including impaired motion processing and synaptic imbalance. This research contributes to a better understanding of visual processing mechanisms, potentially offering new therapeutic approaches.
Researchers at Kyoto University have observed a unique phenomenon where talin constantly moves over focal adhesions as a single unit, contradicting prevailing notions. This discovery reveals that talin manages to simultaneously maintain the intercellular connection while transmitting force through dynamic molecular stretching.
A new study from Tulane University found that perlecan LG3, a protein commonly found in blood vessels and the brain, forms a stable bond with the COVID spike protein, enhancing the virus's ability to bind with cells. This discovery may lead to new forms of treatment or prevention for COVID-19.
Scientists have deciphered the assemblage of apical extracellular matrices in roundworms at the nanoscale using advanced microscopy. Defects in struts result in unnatural layer swelling, and the researchers found that collagens play a crucial role in maintaining matrix structure.
Researchers shed light on TIMP2's role in regulating hippocampal plasticity and function, which decreases with age. Targeting the extracellular matrix may improve plasticity in the brain, offering new directions for mitigating neurodegenerative disorders.
Researchers found a total of 4,721 proteins altered with age in the murine ovary, including upregulated ECM proteins associated with fibrosis. Age-dependent changes also affect immune response pathways and unique immune cell populations.
A team of researchers found that fibroblast cells cultured on substrates with varying degrees of stiffness exhibit changes in cell structure, function, and TGF-β activity, which regulates ECM architecture. This study provides insights into how mechanical forces influence wound healing and tissue development.
A University of Virginia team has developed a new analytical tool using hydrogels to cultivate vascular sprouting from mouse lung tissue, providing new insight into idiopathic pulmonary fibrosis. The research aims to understand the biomechanical and biochemical cues to blood vessels in the lungs during disease progression.
A groundbreaking study by UNIST researchers reveals that high levels of endotrophin in fat cells disrupt autophagy, leading to inflammation and insulin resistance. Inhibiting ATG7 protein function or neutralizing endotrophin shows promise as a potential treatment for obesity-related metabolic diseases.
A Kyoto University team reveals the Dumpy protein as the key factor in controlling 3D tissue structures through external cues. This finding challenges traditional understanding of morphogenesis and opens up new avenues for manufacturing controllable 3D tissue folding with coordinated cell behaviors.
Extracellular vesicles from fibrotic lungs can activate dormant fibroblasts in healthy lungs, initiating fibrosis development and spreading. The study's findings support the potential use of EVs as a targeted drug therapy platform to slow fibrosis progression and improve patient outcomes.
Scientists have created human brain organoids free of animal cells, which could greatly improve the study and treatment of neurodegenerative conditions. The novel method uses an engineered extracellular matrix to support stem cell growth, resulting in more accurate models of brain development.
Researchers found that epigallocatechin gallate (EGCG) reduces protein levels of fibronectin by 46-52% and disrupts pathways involved in fibroid tumor cell growth. EGCG supplements may provide an easily accessible and natural way to relieve symptoms and slow fibroid growth.
Researchers from Kyushu University found that the single mechanosensitive protein VGLL3 induces fibrosis, thickening and scarring tissue. The study suggests targeting this protein could lead to new treatments against fibrosis.
Researchers at Aston University are working with Isterian Biotech to develop small molecule inhibitors targeting transglutaminase 2, a key enzyme in fibrosis. The goal is to stop or reverse pathological crosslinking of proteins that lead to fibrotic diseases such as idiopathic pulmonary fibrosis.
A new molecule called embigin has been discovered to regulate sebaceous gland progenitor cell function. Embigin binds to fibronectin and directs transport proteins for lipid synthesis, playing a crucial role in sebum production.
Researchers at Brown University have developed a new laboratory test model to investigate fibrosis treatments without the use of animals. The model uses human cells and replicates not only the structure of human tissue but also its mechanics, enabling scientists to study the underlying mechanisms of fibrosis and test potential treatments.
Researchers find biglycan acts as endogenous ligand of Toll-like receptor 4 in macrophages, increasing responses and leading to improved survival in sepsis. Mice lacking biglycan show increased survival benefit, highlighting the protein's pro-inflammatory role.
Computer simulations reveal a tension-activated switch mechanism that regulates fibronectin's cell-binding function, similar to untying a shoelace. The researchers' findings provide new insight into how nature may use molecular mechanics to control biological activity.
Researchers at the University of Michigan have identified a protein that causes progressive retinal degeneration and functional blindness in children with Usher syndrome. Understanding the function of this protein may lead to new treatments for people with Usher syndrome and other types of retinal degeneration.