Articles tagged with Cellular Proteins
Imaging mass cytometry showcases odd numbers of proteins in kidneys of lupus patients, identifying novel markers for disease. The study found decreased and increased disease markers pointing to renal disease, with potential enlargement of glomeruli in some patients.
Research identifies key molecular signatures and pathways contributing to skeletal muscle strength loss in females with estrogen deficiency. The study found parallel patterns of inhibition and activation across various signaling pathways, including AMPK and calcium signaling.
Researchers at MIT have discovered a single scaffolding protein, TCOF1, responsible for forming a biomolecular condensate within the nucleolus. The findings suggest that this condensate played a crucial role in the evolutionary shift from a bipartite to a tripartite nucleolus 300 million years ago.
Researchers have identified a new pathway for HIV to enter the cell nucleus, and synthesized molecules that can target this pathway. The study found three proteins critical to the invasion, and their interaction, which could lead to new treatments for diseases such as Alzheimer's and cancer
Researchers identified a new approach to treat poxviruses by targeting a cellular protein, making the virus more susceptible to natural defences. Existing immunosuppressive drugs can restrict replication and spread of poxviruses.
Researchers at La Jolla Institute for Immunology have discovered the inner workings of Ebola virus replication inside host cells, revealing 'viral factories' that form clusters of viral proteins and genomes. These microscopic structures are formed in host cells and play a crucial role in the virus's life cycle.
Researchers have created a database of understudied human proteins to accelerate research. The 'unknome' database assigns a 'knownness' score to each protein based on scientific literature information. Functional screens reveal that many unknown proteins contribute to essential cellular functions.
Researchers discovered that STING, a critical immune regulator, can act as an ion channel to control immune responses. This new function allows STING to translate danger signals into ion flow, activating various defense mechanisms.
A University of Ottawa-led research team has made significant progress in understanding XLP-2, a genetic disorder that affects the immune system. The study reveals two underlying mechanisms: poor expression of Interleukin-6 and compromised T cell survival, which lead to immunodeficiency in patients.
Researchers have discovered a novel pathway that minimizes liver injury during transplantation by activating the protective CEACAM1-S version. This protective characteristic is regulated by HIF-1α and can be enhanced using molecular tools and alternative gene splicing, reducing organ injury and improving post-transplant outcomes.
A team of scientists has successfully elucidated the structure and function of LITE-1, a biomolecule used by Caenorhabditis elegans to detect danger. The researchers used artificial intelligence to predict the structure of LITE-1, which is a channel protein that forms a pore in the cell membrane allowing charged particles to pass through.
Researchers at the University of Oxford have developed a nanopore-based method to detect post-translational modification variants in proteins. The technique uses directional water flow and measures electrical current disruptions, enabling precise analysis of complex biological processes.
Researchers at Purdue University and NIH have identified 14 understudied T-reg proteins with molecular roles in disease onset, offering new avenues for understanding autoimmune diseases and cancer. Studying these proteins could lead to the development of cell-based therapies to modify their functions.
Researchers at the University of Copenhagen have discovered how a bacterium called Vibrio alginolyticus moves using sodium ions, which could lead to new targets for antibiotics. The study provides insights into the flagellum's movement and may help develop novel antibiotics to combat antibiotic resistance.
A new study uses machine learning to analyze data from DrugAge, a database of chemical compounds modulating lifespan in model organisms. The researchers create four types of datasets to predict whether or not a compound extends the lifespan of C. elegans, using features such as compound-protein interactions and Gene Ontology terms.
Researchers at EMBL Heidelberg discovered that mutations in the RBM20 gene cause familial DCM by disrupting normal RNA splicing, leading to detrimental cytoplasmic granules. Targeted gene editing via CRISPR-Cas9 and restoring nuclear localisation of RBM20 could improve therapy options for patients.
A new study reveals that the cellular chaperone protein GRP78 migrates to the nucleus under stress and alters gene activities, allowing cancer cells to become more mobile and invasive. This discovery offers potential new approaches for cancer treatment, including down-regulating GRP78 activity or preventing it from binding to ID2.
Researchers at Emory University have discovered a new paradigm for understanding how actin filaments are formed and fine-tuned in cells. They found that three proteins - formin, twinfilin, and capping protein - work together to regulate the activity of actin filaments, allowing for more precise control of cellular movement.
Researchers discovered a central regulator, DipM, controlling multiple autolysins and promoting cell constriction in Caulobacter crescentus. The study reveals DipM's role in coordinating bacterial cell wall remodeling and division processes.
Researchers identify key protein interactions that control the body's immune response during liver transplantation, leading to improved transplant survival rates. The study found that a specific communication pathway between CEACAM1 and TIM-3 proteins plays a crucial role in controlling the immune response.
The study identifies 1,074 semi-extractable RNAs potentially involved in phase-separated membraneless organelles. These RNAs are enriched in repressed heterochromatin regions and act as hubs for RNA-RNA interactions.
Researchers found that BUB1 protein regulates EGFR signaling by reducing receptor internalization, which may lead to new therapeutic interventions for EGFR-driven cancers. The study also showed that BUB1 impacts receptor recycling and degradation, affecting signaling amplitude and duration.
Researchers have captured never-before-seen images of the CALHM1 pore, which assembles into a circular channel with flexible arms resembling octopus tentacles. The discovery reveals how fatty molecules stabilize and regulate the channel, offering potential insights into its role in taste perception and Alzheimer's disease.
Researchers at IRB Barcelona have developed new p38 inhibitors that selectively impair one of the activation pathways of the protein, allowing it to perform many of its normal functions. The inhibitors show therapeutic potential for heart diseases such as cardiac cell death and cardiotoxicity.
Researchers investigated hepatic hydrogen sulfide production in a mouse model of Hutchinson-Gilford Progeria Syndrome (HGPS) and found reduced H2S levels in RC-fed mice, with partial rescue on high-fat diet. This study suggests that accelerated aging in HGPS may be partially explained by reduced hepatic H2S levels.
A team at Penn State has identified a protein called calcium-dependent protein kinase 32 (CPK32) that modifies the cellular machinery responsible for producing cellulose. This new understanding could inform the design of more stable, cellulose-enriched materials for biofuels and other functions.
Researchers used proteomics and small RNA sequencing to analyze 103 human blood plasma samples, identifying 21 proteins and 315 small RNAs associated with aging. Combining protein and miRNA data improved age predictions (R2 = 0.70 ± 0.01), suggesting a broader range of age-related physiological changes.
A new study describes an engineered approach that makes protein aggregates amenable to spatial manipulations in both budding yeast and human cells. This system allows for the export of protein aggregates from cells, potentially protecting mother cells from toxicity and contributing to a better understanding of neurodegenerative diseases.
Scientists at the Stowers Institute for Medical Research have uncovered the structure of the first step in amyloid formation for Huntington's disease. The team proposes a new method for treating not only Huntington's but potentially dozens of other amyloid-associated diseases by preventing the initial, rate-limiting step from occurring.
A study has identified a potential treatment target for prostate cancer that is resistant to hormone therapy, a protein modification involving TRAF4. The researchers found that TRAF4 promotes the spread of cancer and may be associated with a new treatment option for patients.
Researchers updated their protein localization prediction model, MULocDeep, to provide more targeted predictions for biological discoveries. The tool helps researchers design more effective experiments and advance scientific discoveries related to drug development and treating diseases like epilepsy.
A Johns Hopkins Medicine-led team identified protein fragments that stimulate the immune system to recognize and attack HIV. The study's technique, called reductionist cell-free antigen processing, replicates the complex events in the human immune system, enabling the identification of immunodominant epitopes.
Researchers have cloned the wheat rust resistance genes Lr9 and Sr43, revealing that they encode unusual kinase fusion proteins. This breakthrough enables new options for addressing disease resistance in bread wheat and could lead to heat-resistant versions of the Sr43 gene to adapt to climate change.
A new advanced artificial intelligence system has been developed in the UK that can accurately identify protein patterns within individual cells. The HCPL system uses a deep-learning model to quickly and accurately determine subcellular structures where proteins are present.
Researchers at Mount Sinai have discovered a previously unknown way in which the brain and immune system interact in multiple sclerosis. They found that the inflammatory protein interleukin-3 (IL-3) coordinates this communication, inciting the recruitment of immune cells to the brain and exacerbating brain inflammation.
Researchers have developed a system that uses generative diffusion to create new proteins, advancing the field of generative biology. The system, called ProteinSGM, learns from image representations to generate fully new proteins, which are biophysically real and functional.
Researchers have discovered that nuclear pore IDPs form a dynamic barrier that allows essential cellular factors to pass while blocking viruses and pathogens. The team used synthetic biology, multidimensional fluorescence microscopy, and computer-based simulations to study IDPs in living cells.
Researchers at the University of Missouri identified occludin protein as a mediator for cell-to-cell transmission of coronavirus. The study found that damaged occludin protein enables virus replication and spread to neighboring cells, worsening symptoms.
Heidelberg researchers have identified key proteins that can prevent the formation of fusion pores, allowing viruses like influenza A and Ebola to be trapped in a lipid membrane. This breakthrough could lead to new approaches for preventing infections with these highly infectious viruses.
Researchers from Penn State and Ohio State University used structural biology, biophysics, and cell biology to understand how pioneer factors interact with nucleosomes. They found that a specific region of the protein helps it access DNA, making it accessible for proteins involved in gene expression.
Researchers uncover the critical link between cellular energy levels and mitochondrial damage through protein FNIP1. The study reveals that FNIP1 enables communication between AMPK and TFEB, instructing genes to remove damaged mitochondria and create new ones.
Researchers at Children's Hospital of Philadelphia discovered that viral proteins use phase separation to coordinate the complex process of replicating viral genomes and then encapsulating them in a viral particle. This process allows for the orderly and coordinated formation of infectious viral offspring.
Researchers have made significant discoveries about DELLA proteins, a family of 'promiscuous' proteins that regulate various plant functions. The study reveals complex interactions between DELLA proteins and transcription factors, which could lead to designing new crops with improved resilience and yields.
Research reveals that cold activates cellular cleansing mechanisms that break down protein clumps, preventing age-related diseases like Alzheimer's and Parkinson's. By modulating proteasome activity, scientists have found a potential therapeutic target for aging and related neurodegenerative disorders.
Researchers found that metformin + leucine (MET+LEU) treatment prevents myotube atrophy by reversing cellular senescence and improving proteostasis. The study used C2C12 myoblasts, aged mouse single myofibers, and human primary myotubes to demonstrate MET+LEU's skeletal muscle cell-autonomous properties.
Researchers found that protein modifier SUMO plays a key role in cellular adaptation to simulated microgravity. The study identified 37 proteins that physically interact with SUMO, including those involved in DNA damage repair and energy production.
A DNA designer drug restored levels of stathmin-2, a protein necessary for motor neurons to function, in both mouse and human studies. This finding could lead to clinical trials to delay paralysis in ALS patients by maintaining stathmin-2 levels.
Scientists discovered the molecular basis of CAMSAP3's role in stabilizing microtubules, which is critical for cell survival and various cellular processes. The findings provide a key concept to understanding how microtubule dynamics control cellular phenomena.
A protein complex formed of HuR and YB1 is crucial for messenger RNA stability during muscle-fiber formation. Further research could help scientists influence protein synthesis and develop novel therapeutics for muscle-related pathologies.
New study reveals that diseased plant cells produce more proteins before dying, alerting healthy cells to boost immunity and prevent disease spread. This 'deathbed rally' helps the rest of the plant stay healthy, paving the way for potential disease resistance strategies.
Researchers have discovered thousands of new miniproteins in human organs, which challenge the assumption that they are insignificant and functionless. The proteins were found to interact with older proteins, suggesting a key role in cellular functions.
Scientists at the University of Illinois Chicago have found a way to selectively degrade disease-causing proteins in specific parts of cells. By studying the movement of enzymes inside cells, they discovered that attaching or detaching a fat molecule can direct where these enzymes go.
A team of researchers has identified a molecular switch that regulates autophagy in plants, bridging two quality control pathways. The study reveals that this regulatory mechanism is conserved in eukaryotes and essential for preventing cells from 'eating' healthy cellular components.
Researchers discovered a cluster of enzymes in bacteria that can be reprogrammed to edit proteins and potentially treat human diseases such as Parkinson's and Crohn's. The study also identified key components of the bacterial immune system, including two on-off switches, that could be targeted therapeutically.
A team of researchers discovered that a mutation in the HMGB1 protein causes a rare disorder with severe malformations, suggesting a link between protein droplets and genetic disease. The study's findings could have implications for understanding congenital malformations, common diseases, and cancer.
A synthetic biosensor created at Cornell University enables the study of proteins in ways previously impossible, leading to potential applications in drug development and environmental sensing. The system uses cell-free synthesis to produce proteins directly into an artificial membrane, allowing for dual optical and electronic readouts.
Researchers at Tufts University School of Medicine found that p97 protein mutations can cause organelle miscommunication, leading to the accumulation of molecules on mitochondria-endoplasmic reticulum contacts. This miscommunication can modulate membrane rigidity and impact interorganelle interactions.
Researchers found that klotho has anti-inflammatory and neuroprotective effects on cultured glial cells, reversing increased secretion of pro-inflammatory cytokines. The study supports klotho's therapeutic potential in pathological processes with a neuroinflammatory component.
Researchers found a protein called Rac1 that triggers milk production in breast cells when lactation stops and the breast returns to its pre-pregnancy state. This process involves cell death and autophagy, but can be reversed upon suckling, providing a fail-safe mechanism for mammalian survival.
Researchers have developed a technique to record cellular events in a long protein chain, allowing them to reconstruct the timing of gene activation, response to drugs, and other processes. This method has potential applications in understanding memory formation, aging, and disease progression.