Articles tagged with Protein Coding Genes
A team of researchers found that non-optimal codon usage slows translation of the genetic code into protein, allowing it to achieve its optimal structure. This discovery provides new insights into controlling the rates at which critically important proteins are synthesized and could lead to better understanding of cancers and diseases.
Scientists at Queen Mary University of London identified a gene linked to resistance in melanoma tumour cells. The gene TP63 was found to correlate significantly with a worse prognosis in melanoma patients.
A study by Vanderbilt University researchers found that cells can alter their biological clocks by using different synonymous codons in the genetic code. This adaptation allows cells to survive in changing environments, such as varying temperatures, and potentially has applications in biotechnology like biofuel production.
Researchers have identified a novel abnormal protein, C9RANT, that builds up in the brains of patients with ALS and FTD due to genetic abnormalities. Detecting C9RANT in cerebrospinal fluid may provide a valuable diagnostic tool for these diseases.
Scientists studied evolutionary rates of nearly 20,000 human genes and found that genes involved in the same biological pathways change their rate of evolution in parallel. This signature can help identify partner genes that may work together in biochemical pathways, providing clues to their function.
The R1441G mutation, known as the Basque mutation, is a genetic variation that increases the risk of developing Parkinson's disease. A study published in Neurogenetics and Movement Disorders found that individuals carrying this mutation have an 83% chance of developing the disease by age 80.
Researchers at OHSU found that epigenetic control, specifically DNA methylation and histone changes, play a crucial role in regulating puberty. By delaying puberty in female rats using targeted gene therapy, the study provides new insights into the complex protein/gene interactions involved.
Researchers found that the critical transcription factor TFIID can co-exist in two distinct structural states, enabling recognition and binding to DNA sequences. This discovery provides new insight into gene expression regulation, a process crucial for growth, development, health, and survival of all organisms.
Researchers have identified a new genetic mutation in the ARHGEF28 gene that is present in all cases of amyotrophic lateral sclerosis (ALS). The protein arising from this gene appears to play a critical role in the disease, and understanding its function could lead to targeted therapies.
The Biophysical Society has awarded Minority Affairs Committee Travel Awards to 14 students and postdoctoral fellows from diverse backgrounds, enabling them to present their research at the annual meeting. Recipients include Otonye Braide, Jackson Chief Elk, and others from universities across the US.
A defective protein called gigaxonin has been discovered as the cause of a rare and lethal childhood disease, giant axonal neuropathy (GAN). The protein plays a critical role in degrading intermediate filaments in nerve cells, leading to massive aggregations that disrupt normal functioning.
Researchers in Ghent have identified a new mutation in the CTNNA3 gene associated with arrhythmogenic right ventricular cardiomyopathy (ARVC), a hereditary heart condition that can lead to sudden cardiac death. The discovery could improve ARVC screening by including the CTNNA3 gene in genetic tests.
A collaborative research effort has pinpointed the genetic footprint that links fragile X syndrome and autism. The findings identify at least 93 genes controlled by the fragile X mental retardation protein, which are also linked to other neurologic syndromes.
A recent study found that nearly three-quarters of gene mutations occurred within the past 5,000 to 10,000 years, indicating a significant impact on human evolution.
Johns Hopkins researchers identified a protein called JMJD2C that helps breast cancer cells spread by unlocking genes. The discovery confirms the protein's role in breast cancer progression and offers a potential target for anti-cancer therapy.
Scientists have discovered a new method for identifying genes in animals, which could increase genetic information by 70-80%. This technique allows for direct observation of genes and proteins, enabling more efficient study of animal diseases and viruses.
Researchers at Gladstone and Stanford Institutes develop new tactic for treating neurodegenerative conditions like ALS by hijacking gene Dbr1 to reduce toxic TDP-43 levels. This breakthrough could have far-reaching implications for treating devastating diseases.
Researchers study circadian clocks in cultured cells and find that the transcription factor BMAL1 must die for the DBP gene to function. This discovery offers a possible explanation for how different genes have distinct daily cycles of expression.
A large Australian family's genetic mystery has been solved, revealing the cause of their rare intellectual disability as altered protein regulation. The study found that a specific gene and its regulation played a key role in triggering the disability, which affects only male family members.
Research reveals that gene length is crucial for protein expression, with shorter genes utilizing specialized terminators to avoid repression. This finding highlights the importance of gene ends in regulating gene activity.
Researchers successfully integrated a single functionalized photosynthetic protein system into an artificial photovoltaic device, retaining its biomolecular properties. This breakthrough demonstrates the potential for light-driven, highly efficient single-molecule electron pumps to act as current generators in nanoscale electric circuits.
A study in The Journal of General Physiology reveals that CFTR's mechanism is akin to ABC transporters, with ATP hydrolysis underlying its unidirectional cycling. This finding provides new evidence for the functionality of a protein crucial to cystic fibrosis research.
Researchers found that DNp63a employs epigenetics to silence anti-proliferative genes, keeping cancer cells alive independently of p53. This discovery opens up new possibilities for targeting the protein's partner enzymes to break its cancer-causing mechanism.
A UC San Diego study has identified a human gene called Human Schlafen 11 that produces a protein blocking the replication of HIV in infected cells. The research may lead to diagnostic tests and therapeutic drugs to prevent AIDS progression.
Bacteria use a reversible switching mechanism to adapt to environments lacking oxygen, revealing a new 'antioxidant' pathway for repairing damaged proteins. This discovery has implications for the development of new antibiotics and our understanding of iron-sulfur cluster proteins in various cellular processes.
An international team of scientists has shown at an unprecedented level of detail how cells prioritize the repair of genes containing potentially dangerous damage. Cells use proteins to detect and replace damaged DNA, with critical steps at individual protein reads likely critical for successful repair.
The GENCODE Consortium discovered a staggering array of genes in the human genome, including over 10,000 novel genes and 20,687 protein-coding genes. Long non-coding RNAs, a relatively new type of gene, were also found to play a significant role in human biology and disease.
A study by UC San Diego researchers identified LIN28 protein binding sites in 25% of human transcripts, causing widespread alternative splicing changes that can result in cancer or other diseases. The discovery suggests that LIN28 itself should be a therapeutic target for diseases.
Researchers at Rice University and MD Anderson Cancer Center offer a possible explanation for the existence of operons, jointly controlled clusters of genes found in bacterial chromosomes. The study suggests that operons help bacteria deal with noisy biochemical signals by suppressing noise in gene regulatory networks.
Researchers find that certain RNAs can pause without being degraded, enabling protein production, and suggesting multiple proteins could be made from the same mRNA
A team led by Richard Ulevitch has received a five-year project renewal from the National Institutes of Health to investigate the workings of the immune system. The grant aims to improve human diseases such as viral and bacterial infections, and inherited immune disorders.
A novel method using immune cells has been shown to induce tolerance to specific proteins in mice, allowing them to tolerate gene therapy designed to deliver the protein. This approach may prevent rejection and improve the long-term success of gene therapies for various diseases.
A novel gene therapy approach has been developed to increase frataxin protein levels in Friedreich's ataxia patients. The method, using TALE proteins, successfully boosted frataxin production by 2-3 fold, offering a potential solution for treating the genetic disorder.
Researchers at University of Pennsylvania develop new approach to making vesicles and fine-tuning their shapes using genetic engineering. They successfully assemble oleosin into vesicles, which offer significant advantages for oral-drug delivery due to their biocompatibility and ability to carry large payloads.
A gene variant in sortilin, responsible for higher protein expression in liver, has been found to reduce cholesterol levels. The study reveals two mechanisms: increased LDL degradation and decreased APOB secretion via lysosomal targeting.
Scientists at Scripps Research Institute discovered a simple and safe method to disrupt specific genes within cells, offering a potential HIV treatment. The new technique uses zinc finger nuclease proteins, which can be added directly to cells without viral delivery methods.
Researchers discovered that master regulator protein ATF6α brings a plethora of coactivators to gene expression sites, activating downstream genes involved in the ER stress response. The study suggests ways to dampen ER stress signaling molecularly and could reveal new targets for diseases like Alzheimer's and Huntington's Diseases.
University of Texas Medical Branch researchers developed a more effective Rift Valley fever vaccine by removing the NSs gene and introducing a dominant negative PKR, improving immune response in large animals and health workers. The new vaccine strain offers enhanced differentiation between infected and vaccinated animals.
Researchers at CNIO discover chimeric RNA, which combines information from multiple genes, and identify 175 transcripts and 12 new proteins. The study challenges the classical vision of genome storage and raises questions about the function and importance of this process.
Researchers at Brown University discovered over 800 tiny genetic loops, called lariats, in human tissues, providing new insights into RNA splicing decisions. The location of branchpoints on these lariats reliably predicts where splicing will occur, enabling the creation of an algorithmic model with 95.6% accuracy.
Researchers found that overexpressing 14-3-3 proteins can make tumors resistant to chemotherapy. The study, led by Julián Cerón and Simó Schwartz Jr., reveals a key role for the par-5 gene in DNA damage response and genomic stability.
Researchers at Cold Spring Harbor Laboratory have solved the atomic structure of a human protein bound to a microRNA guide, revealing its biological mechanism of action. The discovery could aid in understanding gene function and advancing RNAi as a therapeutic strategy.
A new study suggests that a protein called heat shock factor-1 (HSF-1) is involved in chemotherapy-related heart damage. Researchers propose targeting HSF-1 in the heart as a potential therapy to prevent cardiac damage, potentially leading to improved outcomes for cancer patients undergoing chemotherapy.
Scientists have mapped how the XIAP protein activates a vital component of the immune defense system, specifically fighting bacterial infections. The study provides important insights into X-linked lymphoproliferative syndrome type 2 (XLP2), a rare genetic disorder affecting male children.
The Chromosome-Centric Human Proteome Project (C-HPP) is an ambitious international initiative that aims to identify and profile all human proteins. The project, which involves 20 scientific teams, will focus on 'missing' proteins and determine their functions in health and disease.
A team at Cold Spring Harbor Laboratory has found a striking association between Fragile-X gene mutations and autism, identifying 60 new candidate genes. The study suggests that these genes are regulated by FMRP, a protein encoded by the Fragile-X gene, which plays a vital role in neural development and synaptic plasticity.
Researchers at Johns Hopkins identified a gene, methionine sulfoxide reductase (MSRA), that modifies the risk of newborns with cystic fibrosis developing neonatal intestinal obstruction. This study may lead to a better understanding of how intestines work and pave the way for identifying genes involved in secondary complications.
A UNC-led team reveals that gene switches don't simply flip on or off, but instead exhibit dynamic binding behavior involving stable and transient states. This discovery offers new insights into gene regulation and potential applications in genetic medicine.
A study published in Science reveals that a gene silencing protein plays a crucial role in completing the transcription process, which is essential for successful gene expression. The research found that the protein helps to terminate transcription, forming the correct gene product.
Researchers at UCSF find hidden genetic code layer influencing protein synthesis rates, even in 'silent' mutations. The discovery challenges long-held assumptions and may accelerate industrial protein production for biofuels and medicines.
Researchers at Baylor College of Medicine have developed a semi-automated protocol called pathwalking to generate initial models of protein folds from near-atomic resolution images. This approach enables the rapid generation of ensemble models that can be optimized for full atomic models.
Two proteins, Rif1 and Rif2, discovered to deactivate DNA repair surveillance system, preventing cell 'anti-enzyme shield' from malfunctioning. Telomeres provide molecular 'caps' protecting chromosome ends from accidental breaks.
A novel method has precisely pinpointed the location of proteins that read and regulate chromosomes, providing a high-resolution view into gene regulation. This breakthrough could lead to a deeper understanding of normal human development and disease mechanisms.
Researchers at Northwestern University identified nine core genes that protect cells from protein misfolding, a common cause of over 300 diseases. They also discovered seven classes of small molecules that restore proper protein folding and reduce disease progression.
Researchers have determined the 3-D structure of a TAL effector bound to DNA, allowing scientists to better understand its ability to recognize and stick to specific sequences. This discovery will improve scientists' ability to target the proteins to different locations in a genome and predict their binding to unintended sites.
Scientists at Albert Einstein College of Medicine have discovered a mechanism that controls the survival of messenger RNA in cells, which could lead to new treatments for cancer. The study found that mRNAs made from specific genes are born with molecular self-destruct timers that ultimately destroy them.
A team of researchers has pinpointed an amino acid variation in the immune response gene DRB1 as a key factor in ulcerative colitis. This association was confirmed using sophisticated association techniques and suggests that the gene plays a significant role in determining the human immune response to extracellular antigens.
Scientists have elevated little-studied cellular mechanism sulfenylation to potential drug target by showing its importance in cell signaling and cancer. A new chemical probe allowed detection of minute differences in sulfenylation rates, revealing a key role for hydrogen peroxide in activating epidermal growth factor receptor.
Researchers at Sanford-Burnham Medical Research Institute discovered a way to reprogram muscle cells to burn sugar more efficiently, resulting in increased athletic ability and reduced lactic acid production. This novel mechanism could lead to new prevention or treatment methods for obesity, metabolic syndrome, and diabetes.
Researchers discovered a molecular pathway driven by PDGFR-alpha that promotes the aggressive nature of a significant proportion of glioblastomas. Overexpressed in GBMs, this pathway triggers signaling cascades leading to tumor growth and invasion. Manipulating Dock180 phosphorylation disrupts this pathway, resulting in failed tumor pr...