Articles tagged with Protein Coding Genes
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Researchers discovered that specific RNAs interact with multiple proteins, promoting aggregation and altering RNA splicing. This finding has implications for understanding complex diseases like Fragile X Tremor Syndrome.
Researchers discovered a correlation between mRNA codon composition and protein abundance, revealing the importance of gene sequence optimization for efficient translation. The study's findings have significant implications for medicine and bioengineering, offering new avenues for treating diseases and boosting biotech applications.
Researchers at UNIGE have deciphered the fundamental role of the Not1 protein in regulating ribosome activity, allowing proteins to assemble at the right time and place. This discovery sheds light on a crucial element of cellular machinery and its potential link to diseases.
Researchers discovered that people with bipolar disorder have lower levels of the CPG2 protein, which regulates glutamate receptor numbers at excitatory synapses. Genetic variations in the SYNE1 gene, encoding the protein, undermine its expression and function in neurons.
In a breakthrough discovery, researchers found that compacted regions along the genome increase at protein-coding genes in mouse embryos, leading to rapid 'decisions' about which genes should be made into proteins. This study provides new insights into how genes are controlled in early animal development.
Researchers engineered E. coli to produce a heat-resistant protein using an expanded genetic code, evolving it through laboratory selection. The new protein outperformed the natural enzyme in extreme heat conditions, nearly doubling its thermal stability.
Researchers at InStem have identified distinct markers to distinguish ribosomes that are specialized for producing specific sets of proteins. These findings suggest a novel role for the Fragile X Mental Retardation Protein in modifying ribosomal RNA and regulating protein synthesis.
Researchers use cryo-electron microscopy to capture detailed snapshots of the TFIID molecule's dynamic structure as it interacts with DNA. The high-resolution images reveal new insights into the molecular mechanism and provide opportunities for developing drugs that target its structural changes.
Researchers have discovered previously unidentified mutations in the PfCoronin and PfKelch13 genes that confer artemisinin resistance in West African malaria strains. These findings provide potential insights into the molecular mechanisms of artemisinin resistance.
Researchers discovered a self-protection mechanism in failing heart cells that triggers the regulation of genes promoting heart failure. The study reveals that one fragment of the protein junctophilin-2 protects against damage by traveling to the cell nuclei.
A new study finds that long noncoding RNA lincRNA-Cox2 regulates the activity of genes involved in inflammation and immune system responses. It boosts production of the Cox2 enzyme and influences expression of other genes, shedding light on previously dismissed 'junk DNA' functions.
Researchers found that a genetic defect tied to ALS and other neurodegenerative diseases leads to increased lipid production in starved cells. The mutation alters the regulation of lipid metabolism pathways, increasing levels of enzymes like NOX2, which can damage cells.
Researchers identified a dominantly inherited mutation that makes cotton bollworms resistant to genetically engineered cotton. The study's findings suggest that this dominant gene is spreading rapidly and may soon threaten cotton production in China.
Researchers at York University discovered a new role for beta-catenin, a protein involved in cell regulation, in controlling messenger RNA translation. This finding could lead to the development of novel therapeutic interventions for cancers and neurological diseases.
A Japanese team of researchers found that early changes to synapse gene regulation, including the phosphorylation of SRRM2 protein, can lead to Alzheimer's disease. This discovery offers new insights into the pathology of AD and may suggest possibilities for gene therapies using virus vectors.
Researchers discovered rare functional variants in genes AAED1 and ATAD2 associated with ADHD risk. These findings may lead to the development of genetic diagnostic methods and a better understanding of the disorder's underlying mechanisms.
Scientists have identified the cause of Saul-Wilson syndrome, a rare type of dwarfism characterized by short stature and developmental delays. A single spontaneous gene change alters protein packaging in the cell's Golgi complex, affecting protein function and stability.
Researchers at UNIGE have identified a protein called RUP2 that blocks the effect of UV-B radiation on plant flowering, allowing plants to regulate their growth in response to seasonal changes. This discovery has significant implications for agriculture and our understanding of plant development.
Researchers found a new mechanism by which small snoRNAs regulate the splicing process of host genes, ensuring proper protein production. This breakthrough discovery opens a new avenue of research into gene expression and has implications for understanding diseases like cancer.
A study led by Prof. Erich Bornberg-Bauer revealed that de novo genes constantly emerge in non-coding DNA regions and can occasionally acquire functions in organisms over longer periods of time.
Researchers at Stanford Medicine have successfully developed a method to induce tolerance to gene therapy in mice, eliminating the autoimmune reaction that often occurs. This breakthrough could lead to effective treatments for single-gene disorders such as Duchenne muscular dystrophy.
A new international collaboration led by the CNIO reveals that up to 20% of human genes may not be coding genes, but rather non-coding or pseudogenes, which could have significant effects on biomedicine. The study analyzed gene catalogs and found that many genes were more likely to be non-coding than previously thought.
Researchers have developed a new CRISPR technique that allows them to skip over specific parts of genes that can cause disease. This approach could potentially treat genetic diseases such as Duchenne's muscular dystrophy and Huntington's disease by eliminating mutated gene sequences and influencing their expression.
Researchers discover that PLD3 and PLD4 play a crucial role in degrading DNA and preventing autoimmune reactions. The proteins were found to regulate endosomal nucleic acid sensing, which may contribute to new approaches in cancer immunotherapy and treatment of autoimmune disorders.
Researchers have successfully engineered silkworms to produce high yields of spider silk using genome editing, a breakthrough that could pave the way for mass production of this versatile material. The transgenic silkworms produced fibers with improved elasticity and extensibility compared to wild-type silkworms.
A University of Wisconsin-Madison research team discovered a previously unknown mechanism for controlling cellular decisions, combining an on-and-off switch in a single protein. The protein EBS binds to two different chemical modifications on histones, promoting or preventing the transition to flowering.
A new genetic link has been found between the gene IRF2BPL and a previously undiagnosed neurological disorder characterized by progressive neurodevelopmental regression. Mutations in IRF2BPL were identified in seven individuals, including five with severe symptoms and two with milder characteristics.
Researchers found that variants of the LOXL1 gene are associated with increased levels of the protein, which clogs the outflow pathway and causes high pressure in the eye. The long non-coding RNA lncLOXL1 regulates the gene's expression and is thought to contribute to the disease progression.
A team of researchers has developed an analytical tool to predict genes that can cause disease due to the production of truncated or altered proteins. The tool identified 252 candidate 'disease genes,' some of which have already been linked to disease in previous studies, supporting its effectiveness.
A new AI framework, ExPecto, predicts the effects of genetic mutations in the 'dark matter' regions of the human genome. The framework pinpointed mutations potentially responsible for increasing the risk of several immune-related diseases, including chronic hepatitis B virus infection and Crohn's disease.
Scientists have identified a protein called SIRT7 that protects cells against senescence by keeping certain genes turned off. This function is crucial for preventing age-related deterioration and could lead to therapies targeting cellular senescence.
The study reveals the Spp42 protein plays a crucial role in regulating spliceosome components, essential for transforming genetic information into functional proteins. This understanding may lead to new drugs targeting the spliceosome function to treat diseases such as cancer and leukemia.
Researchers have identified the biological process of mineralization that occurs in young corals, shedding light on coral reef formation and the storage of atmospheric carbon dioxide. The discovery also holds implications for new biotechnological developments using coral extractions to regenerate human bones.
A study led by NYU School of Medicine researchers found that mice genetically engineered to lack the gamma-CaMKII shuttle protein took twice as long to form a memory needed to complete a simple task. The team restored learning ability by re-inserting the human version of the shuttle protein into mice.
A study published in Neuron has found that a neural precursor protein called PRDM16 plays a crucial role in shaping the organization of the cerebral cortex. The researchers discovered that when PRDM16 is active, it helps to regulate the migration of neurons and their ultimate positioning in the cortex.
Researchers at Massachusetts General Hospital identify SMCHD1 as critical regulator of X chromosome inactivation, allowing genes to be suppressed. The study's findings have implications for treating diseases associated with misfolded chromatin and hold promise for reactivating the inactive X chromosome.
Researchers have created a comprehensive genetic atlas of human plasma proteins, identifying nearly 2,000 genetic associations with almost 1,500 proteins. This discovery promises to aid in the development of new drugs and enhance our understanding of various diseases.
Research reveals that cells must grow large enough to produce four key proteins before committing to division. This mechanism, discovered in budding yeast cells, may hold clues for controlling abnormal cell growth and its link to diseases like cancer.
Researchers have discovered that the act of reading histone modifications leads to the modification of an oncoprotein called TRIM24 with a small protein tag called SUMO. This discovery suggests new ways to inhibit metastasis in cancer cells by targeting TRIM24's interactions with histones.
The researchers have identified a gene called Ankrd16 that prevents the production of harmful protein aggregates in neurological disorders such as Alzheimer's and Parkinson's disease. Elevating levels of Ankrd16 protects specific neurons from dying, while removing it leads to widespread buildup of abnormal proteins.
Researchers found that Celecoxib treatment increased utrophin protein levels and improved muscle function in DMD mouse models. The study suggests that Celecoxib may have therapeutic potential for addressing key features of Duchenne muscular dystrophy.
A preliminary study found an investigational drug, RG7916, to increase survival and function in babies with type 1 spinal muscular atrophy by up to 6.5 times the normal amount of SMN protein. The study, which is ongoing, aims to determine if this treatment will provide meaningful benefits for children with SMA.
Researchers found that auxin hormone controls stem cell division and WOX4 gene expression, essential for wood formation. The study revealed a direct regulation of WOX4 by auxin signaling factors, shedding light on the complex mechanism behind plant growth.
Researchers found that negative selection does not eliminate nonsense mutations entirely, but rather has a slight impact on some genes. They also discovered that alternative splicing allows some genes to preserve their functions despite the presence of nonsense mutations.
Scientists have generated a vast library of unique cyclic compounds that can bind to their targets with stability and effectiveness. The new compounds have the capacity to interrupt specific protein-protein interactions that play a role in disease, offering potential therapeutic agents for various conditions.
Researchers used CRISPR to identify genes that help neurons defend against toxic protein aggregates, which are thought to drive ALS progression. A handful of genes, including Tmx2, show promise as potential drug targets.
Researchers developed Recon3D, a comprehensive human metabolic network reconstruction integrating genes, proteins, and metabolites. The tool revealed 'mutation hotspots' where disease-causing mutations occur, and how drugs affect metabolic reactions.
Researchers applied quantum machine learning to a real-world biological problem, predicting the strength of binding sites for transcription factors. The study demonstrated the potential of quantum computing for biology, with results consistent with current understanding of gene regulation.
Researchers found that Rev-erb controls gene expression in mouse liver via interactions between on-and-off regions on the same chromosome. The study demonstrates how Rev-erb represses transcription by loosening chromosome loops, leading to circadian repression of transcription.
Researchers identified the role of Gimap5 in regulating T cell function and found that GSK3 inhibitors can improve immune system function in mice and restore normal T cell function in human cells. This discovery may lead to new treatments for autoimmune diseases such as Type 1 diabetes, systemic lupus erythematosus, or asthma.
A multidisciplinary team has developed software called Scikit-Ribo to more accurately determine when cells translate RNA into protein. This method uses advanced statistical modeling techniques and can filter out noise from previous data, providing a clearer picture of translation dynamics.
Researchers at the Salk Institute discovered that genes that normally sever connections between neurons are reactivated in aging astrocytes, leading to reduced neuronal communication. This may explain age-related cognitive decline and neurological disorders such as Alzheimer's and diabetes.
The study reveals that the genetic code, specifically silent nucleotide substitutions, plays a crucial role in determining the functions of vital proteins. Ribosome density on RNA is also found to be significantly higher for β-actin than γ-actin, enabling it to translate into protein faster.
Researchers have detected mobile genetic elements that can switch off gene expression, altering protein production in eukaryotic organisms. These elements are prevalent in genomes of plants and fungi, but their impact is often negative, leading to degeneration and reduced productivity.
Researchers found that Skn-1a is a key regulator for generating Trpm5-expressing chemosensory cells in various parts of the body, including respiratory system and digestive tract. This discovery provides new insights into the role of these sensory cells in protecting against bacteria and potentially harmful substances.
Researchers have visualized the atomic structures of Cpf1 and Cas9 proteins to analyze their properties and identify ideal tools for different applications in gene modification. The study suggests that Cpf1 is more suitable for inserting DNA fragments due to its ability to produce staggered complementary ends.
Scientists are exploring multi-functional gene-editing technology by analyzing molecular features of Cpf1 and Cas9 proteins. The study reveals the high-resolution structure of these molecular scissors to better understand their working mechanism, including target DNA recognition and cleavage.
A new study found that breast cancer proteins can have altered functions in tumor cells due to changes in protein interaction networks. This shift affects the number of genes performing each function, not their expression levels. The study predicts patient survival and cancer subtype based on these functional shifts.
Scientists at UW-Madison create novel molecular treatment for Friedreich's ataxia, a rare genetic disorder caused by DNA repeats. The 'molecular prosthesis' helps cellular machinery overcome the blockade posed by repeats, restoring expression of the frataxin protein.
Researchers have validated five new genes responsible for Amyotrophic Lateral Sclerosis (ALS), a fatal neurological disorder. The study uses AI-powered technology to accelerate the discovery of new treatments by identifying key proteins linked to the disease.