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Ample literature evidences confirm the suitability of this protein as a good target.
This mutant protein is more efficiently GPI-modified than any mutant AChE tested thus far.
The mutant protein appears to have a dominant negative effect, which could be due to it dimerising with the wild-type protein and inhibiting its activity, thus further reducing the levels of functional protein.
Increasing gene expression restored mutant fitness to varying degrees, demonstrating that the fitness disadvantage of synonymous mutants arose from a lack of beneficial protein rather than costs of protein production.
The high level of success shows that relatively "simple" computational methods can in some cases predict the behavior of mutant proteins with good reliability.
In some cases, therefore, it is possible that the mutant protein exerts a dominant negative effect.
In the case of interference, increased production of the wild-type protein may be therapeutic, but in the case of toxicity, suppression of the mutant protein may also be needed.
Cells of the mutant are viable, showing that the protein is dispensable for growth, but grow slower and have thickened cell walls.
Although this scheme requires no knowledge of the structure of a mutant protein, it is useful in predicting the activities of mutants.
The swapped mutant was destabilized by 3 kcal/mol per gene V protein dimer relative to the wild-type protein, demonstrating that factors other than hydrophobicity must make substantial contributions to the effects of mutations on the stability of the protein.

Related Questions

What is the impact of five missense mutations on the function of a protein?5 answersFive missense mutations in different proteins have been studied for their impact on protein function. The mutations in OPN3, desmoplakin, SMAD4, MERS-CoV S protein, and cytosolic proteins were found to have deleterious effects on protein structure and function. In OPN3, the p. I51T variant failed to effectively dock with 11‐cis‐retinal, leading to a loss of function. For desmoplakin, mutations rendered PRD proteins insoluble and compromised cytoskeletal linkages. In SMAD4, mutations resulted in deformed and unstable protein structures, affecting protein-ligand interactions. Mutations in MERS-CoV S protein affected protein stability and binding affinity with the DPP4 receptor. Additionally, SNVs in cytosolic proteins altered peroxisomal targeting signals, impacting protein import. These findings highlight the diverse ways missense mutations can disrupt protein function, providing insights for potential therapeutic interventions.
How does mutation testing work?5 answersMutation testing is a fault-based testing technique that evaluates the effectiveness of a test suite in detecting faults. It involves seeding faults into the program under test and then writing tests to reveal these faults. The goal is to create tests that can detect a large number of faults, including those that couple with the seeded faults. Several approaches have been proposed to improve the efficiency of mutation testing. One approach is to automate the process using tools like Mutta, which can automate the mutation testing process for web applications. Another approach is to scale mutation testing by using distributed systems and load distribution algorithms, which can significantly reduce the computational cost. Additionally, there are efforts to adapt mutation testing for deep learning models, such as Probabilistic Mutation Testing (PMT), which addresses the stochasticity inherent in training deep learning models and allows for more consistent and informed decisions on mutations.
Can mutations be inherited?5 answersMutations can be inherited from previous generations. Most gene variants in an individual's genome are not new mutations but have been passed down through generations. In the case of genetic diseases caused by a single mutation in one gene, such as cystic fibrosis, haemophilia, and achondroplasia, the inheritance of the abnormal gene variant follows simple Mendelian rules. Studies have shown that point mutations in male germ cells can be transmitted to the next generation without severe selection. In the context of upper tract urothelial carcinoma (UTUC), germline pathogenic/likely pathogenic mutations have been identified and found to significantly increase UTUC risk in Chinese populations. In the case of gynecological cancers, a genetic predisposition can contribute to up to 10% of cases, and risk-reducing surgery may be offered to high-risk individuals. In prostate cancer, germline pathogenic variants have been underestimated, and enhanced family history screening and genetic testing have been used to identify these variants.
Is there mutation load in bacteria?5 answersMutation load in bacteria refers to the accumulation of deleterious mutations in a population. Studies have shown that bacteria can exhibit mutation rate polymorphism, ranging from wild-type levels to significantly higher rates. Despite the presence of large numbers of deleterious mutations, beneficial mutations do arise but often do not reach fixation over long periods of time. This suggests that the dynamics of beneficial mutations in bacteria are not solely driven by constant positive selection, but rather by other evolutionary mechanisms such as negative frequency-dependent or temporally fluctuating selection. The low mutational load observed in bacteria is consistent with the pattern of genetic polymorphism observed in metagenomics studies of the human gut microbiota. Therefore, it can be concluded that while bacteria do experience mutation load, the presence of beneficial mutations and other evolutionary mechanisms contribute to the maintenance of genetic diversity and the long-term survival of bacterial populations.
Do mutated cells go through apoptosis?10 answers
Is mutation required for bank loan?10 answers

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How to reduction of antinutritional factor at pulses?
5 answers
Reduction of antinutritional factors in pulses can be achieved through various processing methods. Traditional techniques like soaking, dehulling, boiling, germination, and fermentation are effective in decreasing compounds such as phytate, protease inhibitors, phenolics, tannins, lectins, and saponins. Innovative methods like extrusion, microwave heating, and micronization have also shown promise in reducing antinutrient content, although results vary. Pressure cooking, among homemade methods, has been reported to result in the most significant reduction of antinutritional factors in pulses. However, it is important to note that while these processing techniques are valuable in reducing antinutritional factors, they can also have adverse effects on the protein content of pulses, particularly affecting albumin, globulin, and total proteins.
Why would the soybeans used for tempeh affect the protein content?
4 answers
The choice of soybeans used for making tempeh can significantly impact the protein content of the final product. Different soybean varieties exhibit varying protein levels, influencing the overall protein content of tempeh. For instance, local soybeans have been found to have higher protein content compared to black and imported soybeans, resulting in tempeh with elevated protein levels. Additionally, incorporating alternative sources like green beans, peanuts, or koro swords as substitutes for soybeans can lead to varying protein contents in tempeh, with soybeans generally preferred for their higher protein content and sensory acceptance. Furthermore, innovative approaches such as adding cheese powder during tempeh fermentation have been explored to enhance protein content, showcasing the potential for combining vegetable and animal proteins to enrich the nutritional profile of tempeh.
What analogues of L-Quisqualic acid were prepared?
5 answers
Several analogues of L-Quisqualic acid were synthesized in different studies. These include compounds 2-6 in the study by Venkatraman et al., where compounds 4, 5, and 6 showed no sensitization effect towards L-2-amino-6-phosphonohexanoic acid (L-AP6). In another study by Subasinghe et al., analogues maleimide 2, N-methylmaleimide 3, N-(carboxymethyl)maleimide 4, succinimides 5A and 5B, and imidazolidinedione 6 were prepared, with compounds 3 and 4 showing increased potencies in slices pretreated with L-quisqualic acid. Additionally, cyclobutane analogues (Z)- and (E)-1-amino-3-[2‘-(3‘,5‘-dioxo-1‘,2‘,4‘-oxadiazolidinyl)]cyclobutane-1-carboxylic acid, compounds 2 and 3, were synthesized in the study by Littman et al., stimulating phosphoinositide hydrolysis in the hippocampus.
What are the most common cancer antigens and peptides found in the tumor microenvironment?
5 answers
The tumor microenvironment (TME) harbors various antigens and peptides that can be targeted for cancer immunotherapy. Traditional tumor-associated antigens (TAAs) and tumor-specific antigens (TSAs) are common in the TME, with recent focus on patient-specific neoantigens that are highly immunogenic. Additionally, noncanonical antigens derived from sequences outside protein-coding regions have been identified through mass spectrometry-based immunopeptidomics, offering new targets for therapy. Peptide-based nanoparticles have shown promise in targeting tumor cells and stromal cells in the TME, including immune cells, fibrosis-related cells, and angiogenic vascular cells, for cancer treatment. Furthermore, the identification of cancer antigens, especially Major Histocompatibility Complex (MHC) class I antigens, is crucial for developing antigen-specific immunotherapy to induce tumor-specific effector T cells and memory T cells for controlling tumor growth and relapse.
Cancer associated antigens?
5 answers
Cancer-associated antigens play a crucial role in cancer immunotherapy. These antigens can be broadly categorized into aberrantly expressed self-antigens, mutated self-antigens, and tumor-specific antigens, providing targets for therapeutic interventions. Various studies have identified nucleic acid sequences expressed in cancers, such as gastrointestinal, kidney, and prostate cancers, which can be utilized for cancer identification and treatment. Monoclonal antibodies targeting specific epitopes on tumor antigens have been developed for diagnostic and therapeutic purposes in human cancers. Novel cancer-associated antigens have been discovered, along with their amino acid and nucleic acid sequences, binding proteins, and immunoconjugates, offering new avenues for cancer diagnosis and treatment. The diverse array of antigens recognized by tumor-reactive T cells presents both opportunities and challenges for developing more effective cancer immunotherapies.
Does growth hormone Improve shoulder surgery recovery?
5 answers
In the context of shoulder surgery recovery, the use of growth hormone has shown mixed results. Studies have indicated that systemic administration of recombinant growth hormone may enhance the early healing of rotator cuff tears in rats. However, in a rat model of acute tendon-bone injury repair, human growth hormone treatment did not significantly accelerate the strength of tendon-to-bone healing and even demonstrated negative biomechanical consequences. On the other hand, biosynthetic human growth hormone has shown benefits in protein conservation, fat oxidation, and tissue healing in surgical patients with major traumas. Therefore, while growth hormone may have potential benefits in certain aspects of shoulder surgery recovery, further research is needed to determine its precise impact and optimal dosages for human application.
Are dogs are resistant to prion infection?
7 answers
Yes, dogs are resistant to prion infection, a phenomenon that has been substantiated through various studies focusing on genetic, biochemical, and experimental evidence. The resistance of dogs to prion diseases, despite their exposure to prion agents such as the bovine spongiform encephalopathy (BSE) agent, has been a subject of interest in prion research. A critical factor contributing to this resistance is the presence of a negatively charged amino acid residue at position 163 in the canine prion protein (PrP), which is distinct from the amino acids found in prion-susceptible species. Experimental evidence supporting this comes from studies where transgenic mice expressing the canine PrP, specifically with glutamic acid at position 163, were resistant to a range of prion isolates, including those derived from BSE. Substituting this residue with asparagine, common in susceptible species, rendered the mice susceptible to prion infection, highlighting the significance of this amino acid in conferring resistance. Further genetic studies have identified polymorphisms in the prion protein gene (PRNP) and its related gene, PRND, in dogs. However, unlike in prion-susceptible species, these polymorphisms do not establish a strong genetic linkage that could influence susceptibility, suggesting that the resistance in dogs may primarily be due to specific structural features of the PrP rather than genetic variability. Comparative studies on prion-resistant animals have pointed out that certain amino acids, including the one at position 163 in dogs, contribute to the structural stability and conformational properties of PrP, which in turn may prevent the misfolding process central to prion diseases. Moreover, research into other prion-resistant species and the structural analysis of their PrP has provided insights into the mechanisms of resistance. For instance, studies on raccoon dogs, which share a high homology with canine PrP, have shown similar resistance patterns, further emphasizing the role of specific amino acids and structural configurations in preventing prion disease. Additionally, investigations into the shadow of prion protein gene (SPRN) in dogs have revealed polymorphisms that, while not directly linked to prion diseases, contribute to the broader understanding of prion resistance mechanisms. Molecular dynamics studies on the NMR structure of dog PrP have also supported the hypothesis that specific residues, particularly D159 (equivalent to D163 considering species-specific numbering), are crucial for the resistance observed in canids. In summary, the resistance of dogs to prion infection is a multifaceted phenomenon rooted in the unique structural features of the canine PrP, particularly the presence of a negatively charged amino acid at a critical position, alongside a lack of genetic linkage between known prion susceptibility genes. This resistance is further supported by comparative genetic and structural analyses across different species, providing a comprehensive understanding of the factors that contribute to the exceptional prion resistance observed in dogs.
Has EMS been successfully applied to other crops besides onions?
5 answers
Yes, EMS has been successfully applied to various crops besides onions. Research has shown that EMS-induced mutagenesis has been effectively utilized in crops like maize, rice, and mungbean. Studies have highlighted the use of different concentrations of EMS to induce genetic variations, enhance stress tolerance, and create novel mutants in these crops. For instance, in maize, EMS mutagenesis resulted in the development of promising mutants recommended for future breeding programs. Similarly, in rice, the application of EMS led to a decrease in various growth parameters with increasing mutagen concentration, indicating successful mutagenesis. Therefore, EMS mutagenesis has proven to be a valuable tool in creating genetic diversity and improving traits in a variety of crops beyond just onions.
Do amyloid beta monoclonal antibodies reduce tau and neurodegeration?
4 answers
Monoclonal antibodies targeting amyloid beta (Aβ) have shown promising effects in reducing tau pathology and neurodegeneration. Specifically, anti-Aβ antibodies have been found to inhibit the spread of tau aggregates and reduce tau pathology in vivo. These antibodies enhance microglial activity around neuritic plaques, mitigating some tau-induced pathological manifestations. Additionally, the engagement of TREM2 with an agonistic antibody has resulted in reduced Tau burden, attenuated neurodegeneration, and cognitive decline in Tauopathy models. Furthermore, a novel monoclonal antibody recognizing β-sheet secondary structure on pathological oligomers of Aβ and tau has shown significant cognitive rescue and reductions in oligomeric forms of Aβ and tau, suggesting its potential as an effective therapeutic agent for Alzheimer's disease.
How can gene therapy assist in hereditary blindess?
5 answers
Gene therapy offers promising solutions for hereditary blindness by targeting inherited retinal diseases (IRDs) caused by mutations in over 250 genes. This approach involves replacing or editing disease-causing genes with functional copies to slow disease progression and potentially restore vision. Gene therapy has shown success in treating IRDs like Leber congenital amaurosis and choroideremia, leading to positive outcomes in patients. By utilizing gene supplementation strategies through subretinal or intravitreal injections, gene therapy aims to address the genetic heterogeneity of IRDs and provide potential clinical benefits to a wide range of patients. With ongoing and planned clinical trials targeting various IRDs such as retinitis pigmentosa, usher syndrome, and Stargardt disease, gene therapy holds significant promise in combating hereditary blindness and improving visual outcomes for affected individuals.
Role of CYP71B31 in arabidopsis thaliana?
4 answers
CYP71B31 in Arabidopsis thaliana is implicated in the oxygenation of terpenes produced by terpene synthases TPS10 and TPS14, leading to the formation of various oxygenated terpenoids like aldehydes lilas A and B, p-cymen-8-ol, α-terpineol, verbenone, and α-terpinyle acetate. This oxygenation process is crucial for the production of volatile compounds emitted by flowers, which play essential roles in attracting pollinators, seed dispersers, and defense against herbivores. CYP71B31's involvement in metabolizing linalool, a major product of TPS10 and TPS14, suggests its role in the biosynthesis of these oxygenated terpenoids. Additionally, CYP71B31 is part of the intricate network of cytochrome P450 enzymes in Arabidopsis involved in various metabolic pathways, including defense mechanisms against pathogens.