Multiple articles focus on the progress of mitochondrial in-depth research!

In this paper, the small compilation of a number of research results, to jointly interpret scientists in the field of online granulal research has made important research results, share to everyone! Photo Credit: CC0 Public Domain: Small Proteins Also Have a Big Role! Mitochondrial proteins determine the production of energy! Doi: 10.1038/s41467-020-14999-2 Duke-2 Researchers of the National University of Singapore and their colleagues report in the journal Nature Communications that a small, newly discovered protein in mitochondria is critical to energy productionZebrafish, which lack the small protein (scientists call it BRAWNIN), have similar characteristics to the rare mitochondrial disease in humans, suggesting that further research into the protein may help explain these conditions and find possible treatmentsThe international team, led by Lena Ho, a cell and developmental biologist and assistant professor of cardiovascular and metabolic disease programats at duke-NUS School of Medicine, found 16 "open reading box-coded short peptides" (SEPs), whose genetic codes translate in the nucleus but then import edited into mitochondria, the cell's energy station"SEPs have been attracting the scientific community for years because they represent a microprotein group that has never been explored, a treasure trove of new gene functions," DrHo said"But there is no systematic study to confirm their functional and biological correlationsWe found that mitochondria are a hot topic because of their function, and we don't fully understand the reasonsScience Sub-journal: Revealing mitochondrial protein MICU1 controls sugar/fat conversion pathwaydoi: 10.1126/scisignal.aaz6206 In a new study, researchers from research institutions such as The University of Tempou and the University of Texas in the United States identified a sensing protein that limits how much sugar and fat our cells convert into energy during hungerThey say it is possible to fine-tune the protein to boost the conversion of sugar and fat into energy in patients with metabolic diseases such as diabetes, obesity and cardiovascular disease, who need to lose weight and lead healthier livesThe findings were recently published in the journal Science Signaling'We hope to provide a solution for the millions of people around the world with metabolic problems in the future, ' the researchers saidMillions of people eat too much food, while millions more are in poverty and depend on too little food for their livelihoodsWe are looking at what happens at the molecular level in both cases, with the goal of developing a drug to interveneOur bodies keep moving things between cells, which is a bit like roads and carsThe vehicle used to convert fat and sugar into energy is called mitochondrial calcium uniporter (mitochondrialal al-uniporter, MCU)Just as traffic transports people to their destinations, the speed at which MCU moves energy is crucialIf it is too slow, there will be obesity and other diseasesIf it is too fast, it can lead to malnutritionGenes and Devel: Uncovering the new mechanisms of cell aging in the body! Mitochondria may be able to communicate with the nucleus to induce cell aging doi: 10.1101/gad.331272.119, a recent study published in the international journal Genes and Development, scientists from the Sanford Burnham Preby Institute of Medical Discovery and other institutions found that The particles may induce cell aging by communicating with the nucleus of cells, and the researchers have identified an FDA-approved drug that may inhibit the aging and damage effects of mouse bodies and cells, and the results may help develop new treatments to promote healthy aging or inhibit the occurrence of many age-related diseases, such as cancer and Alzheimer's diseaseResearcher Peter Adams said the study could provide us with new ideas to develop drugs that extend the body's healthy life, and as millions of Americans get older, we will soon face significant social and economic resistance, so the sooner the intervention is done, the sooner the intervention is done, researchers must understand the underlying biological effects of aging, and the results may help researchers develop new strategies to effectively suppress or slow the occurrence of many age-related diseasesNat Genet: Uncovering the mysteries of the mitochondrial genome or promising to help develop new treatments for multiple cancers doi: 10.1038/s41588-019-0557-x, recently published in the international journal Nature Nature In the Genetics study, scientists from the University of Texas Anderson Cancer Center and others delinmoststudid the energy engineering of cells- mitochondria, which play a key role in tumor development, and further study of the mitochondria genome are critical to uncovering tumor mechanisms and developing new therapiesResearcher Han Liang said the study laid the groundwork for translating mitochondrial biology research into clinical applications, and our analysis provided the most definitive mutation blueprint for the mitochondrial genome and identified several high-level mutations that are significantly more concentrated in kidney, colorectal, and thyroid cancers, suggesting that activating special signaling pathways may have carcinogenic effectsCell Rep: Mitochondrial key components regulate muscle function doi: 10.1016/j.celrep.2019.09.063 Intense activity (e.gmarathon) can make our muscles tired, sore and even damagedOver time, our muscle fibers are self-healing through complex cellular processesA recent study by thomas Jefferson University's MitoCare Center in collaboration with the Children's Nhs Genetic Medicine Research Center in Washington, D.C., has identified the protein MICU1 in mitochondria as the "power source" of all cells, playing a key role in maintaining muscle size and function and repairing damaged muscle fibersThese findings point to the potential role of MICU1 in neuromuscular diseaseThe study was published recently in the journal Cell ReportsThe contraction and relaxation of our muscles depends on the balance of calcium ions in each muscle fiberSome of this calcium is absorbed by mitochondria to boost metabolism and generate energy, while the protein MICU1 acts as the main regulator of calcium intake in mitochondriaControlling the transport of calcium through MICU1 helps to coordinate the function of muscle fibers and their internal mitochondriaInterruptions of this connection prevent normal communication between mitochondria and muscles, making them more vulnerable to damage and unable to exert too much pressurePhoto Source: CC0 Public Domain 6:Nature: Revealing mitochondrial quality control defects can lead to heart disease: 10.1038/s41586-019-1667-4 Mutations in a gene that encodes adenine nucleotide translocators (ade nuclenineotide translocator, ANT) can lead to many diseases, such as heart disease and eye muscle weakness, but how these mutations cause internal diseases, but how these mutations cause internal mechanisms Now, in a new study, researchers at the Perelman School of Medicine at the University of Pennsylvania have revealed a surprising new feature of ANT: ANT is essential to help ensure the integrity of the mitochondria network by removing damaged mitochondria ---,--- and to find that the ANT mutation that leads to defects in the quality control system eventually leads to heart disease The findings were recently published in the journal Nature ANT is a well-known protein that helps mitochondria produce the chemical energy needed to drive the proper functioning of cells in the body, or adenosine triphosphate (ATP) Although mutations in the ANT gene are known to cause diseases, including cardiomyopathy, a disease that makes it harder for the heart to pump blood to other parts of the body, studies have shown that these mutations do not affect ANT's ability to produce chemical energy, raising questions about how people will get sick In revealing the association between ANT and mitochondrial autophagy and the effect of ANT mutations on mitochondrial quality control, our findings change the way we think about these disease-causing mutations, allowing us to focus on the right path, the researchers said Now that we know that these diseases are caused by mitochondrial quality control deficiencies rather than ATP deficiency, we can begin to consider treatments to improve mitochondrial quality control Mol Cell: New research reveals that cell mitochondrial stress response doi: 10.1016/j.molcel.2019.09.026 cells need a organcalled a generator called "mitochondria" to harness the energy stored in food Most of the proteins needed to achieve this function are encoded in the nucleus, synthesized in the cytoplasm, and then transported to the mitochondria Proteins entering the mitochondria require the presence of a signal sequence, which is removed once the protein arrives So far, researchers have not fully understood the importance of mitochondrial protein elimination signal sequences, and why removal defects can lead to many diseases, such as heart or brain diseases In response, Nora V , from the Institute of Biochemistry and Molecular Biology at the University of Freiburg, said: "I'm not going to be able to do this Dr Gtle et al have found that removing defects in the signal sequence causes proteins to accumulate, causing them to accumulate in the online granules, the results of which were published in the recent journal Molecular Cell 8: New research challenges scientists' understanding of premature aging of the body Mitochondrial DNA dysfunction or accelerates the aging process doi: 10.1038/s42255-0120-1, a recent study In a study published in the international journal Nature Metabolism, scientists from the University of Eastern Finland found that mitochondrial DNA dysfunction may accelerate the body's aging process in a way that is different from previously thought; Mitochondria are small-to-medium-sized organelles with their own DNA-mitochondrial DNA (mtDNA), and for almost half a century, mitochondrial DNA mutations and oxidizing stress have been considered the main causes of aging in the body, a hypothesis put forward in the 1970s in the Mitochondrial Aging Theory, which has been presented in mtDNA The mutation was tested in the mouse body, where inactive DNA modification mechanisms were present, and these mice were able to accumulate mtDNA mutations and show accelerated aging, leading scientists to believe that mtDNA mutations lead to aging; Ebiomedicine: Mitochondrial regulator sororoid adjustment factor or new target for cancer treatment doi: 10.1016/j.ebiom.2019.09.017 Recently, researchers from the Wistar Institute found the role of mitochondrial fission factor (MFF) in controlling cancer cell survival, suggesting that the protein may represent a promising therapeutic target They also found that the expression of MFF was regulated by Myc The results were published online in the journal EBioMedicine Mitochondria are organelles that provide energy to our cells, which also control multiple cellular death mechanisms and play a complex role in cancer In addition, mitochondrial dynamics can coordinate the size, shape, and position of the inner granules of cells, which in turn affect tumor progression, but until now, its mechanism has not been fully articulated 'We know that reprogramming of mitochondrial function is critical to the development and metastasis of cancer, ' the researchers said Our findings reveal new participants and approaches to this process, opening up specific treatment opportunities for selective elimination of tumor cells in patients The mFF gene amplification in prostate cancer patients is associated with disease recurrence and decreased survival rates They also observed increased expression of MFF protein in mouse models of prostate cancer and tissue samples in patients with other cancer types, including lung cancer and multiple myeloma Nature: An ATP-sensitive potassium ion channel in an at-ion iodo: 10.1038/s41586-019-1498-3 In a new study, researchers from the University of Padua, Italy, confirmed that a protein complex present in the mitochondria mediates ATP-dependent current, known as ATTokatP The findings were recently published in the journal Nature The researchers found that the potassium ion channel mitoKATP is similar to their counterpart sina, consisting of a combination of co-genesand and ATP, which they call MITOK and MITOSUR, respectively The in vitro reconstruction of MITOK and MITOSUR summarizes the main characteristics of mitoKATP Overexpression of MITOK causes significant organatomial swelling, however the genetic removal of this subbase can lead to instability of the mitochondrial membrane potential, expansion of the intracavity (intracristal space) and reduced oxidation phosphorylation In mouse models, the absence of MITOK inhibited the heart protection effect caused by the pretreatment of the drug induced by the heavy nitrogen oxide (diazoxide) (BioValleyBioon.com) Bio Valley For More Great Counts! 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