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Category: biotech/medical – Page 856

Here we address the important question of cross-talk between the mitochondria and cytosol. We show that the inner mitochondrial protein, MiNT, interacts with a protein on the outer mitochondrial membrane (mNT). This interaction occurs within the major outer membrane protein VDAC1. Inside the inner space of VDAC1, MiNT transfers its [2Fe-2S] clusters to mNT, which was shown to be a [2Fe-2S] cluster donor protein that donates its cluster(s) to apo-acceptor proteins residing in the cytosol. Hence, we suggest a pathway for transferring [2Fe-2S] clusters from inside the mitochondria to the cytosol.

Mitochondrial inner NEET (MiNT) and the outer mitochondrial membrane (OMM) mitoNEET (mNT) proteins belong to the NEET protein family. This family plays a key role in mitochondrial labile iron and reactive oxygen species (ROS) homeostasis. NEET proteins contain labile [2Fe-2S] clusters which can be transferred to apo-acceptor proteins. In eukaryotes, the biogenesis of [2Fe-2S] clusters occurs within the mitochondria by the iron–sulfur cluster (ISC) system; the clusters are then transferred to [2Fe-2S] proteins within the mitochondria or exported to cytosolic proteins and the cytosolic iron–sulfur cluster assembly (CIA) system. The last step of export of the [2Fe-2S] is not yet fully characterized. Here we show that MiNT interacts with voltage-dependent anion channel 1 (VDAC1), a major OMM protein that connects the intermembrane space with the cytosol and participates in regulating the levels of different ions including mitochondrial labile iron (mLI). We further show that VDAC1 is mediating the interaction between MiNT and mNT, in which MiNT transfers its [2Fe-2S] clusters from inside the mitochondria to mNT that is facing the cytosol. This MiNT–VDAC1–mNT interaction is shown both experimentally and by computational calculations. Additionally, we show that modifying MiNT expression in breast cancer cells affects the dynamics of mitochondrial structure and morphology, mitochondrial function, and breast cancer tumor growth. Our findings reveal a pathway for the transfer of [2Fe-2S] clusters, which are assembled inside the mitochondria, to the cytosol.

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Malaria, a mosquito-borne infectious disease mostly found in tropical climates, is now on American shores. Late Monday, the Centers for Disease Control and Prevention announced a spat of cases — one in Texas and four in Florida — discovered in May and June that were locally acquired versus acquired while traveling abroad. This is the first time this has happened since 2003.

The CDC said that all five patients received treatment and are recovering, but the agency remains on alert for any new cases. While malaria was once a public health threat in the US, its presence was eradicated in the early 1950s. The last major outbreak was in 2003 with eight patients in Palm Beach County, Florida, all of whom had significant outdoor exposure.

For now, the CDC says the risk of catching malaria in the US “remains extremely low.” However, the instance shouldn’t be taken lightly, especially as many of us will be spending more time outdoors and traveling during the summer. Here’s what you need to know.

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In an organism, different kinds of cells carry out specific, specialized functions. Scientists can grow and study various types of cells in the lab. For a long time, a source of many of those cell lines were cancer samples that could be easily cultured over many generations. But those cells were not always representative of a particular cell type. Now, following huge breakthroughs, scientists learned how to create stem cells from adult skin cells. This has allowed scientists to utilize adult cells like those from the skin to create induced pluripotent cells (iPSCs), which can then be made into virtually any cell type.

The creation of so-called iPSCs was made possible through changing gene expression in cells, often with certain molecules or specialized proteins. Cells can also now be directly reprogrammed in some ways, without needing to bring them to a pluripotent state. The number of cell types that can be generated in this way is also expanding, bringing new insights into how specialized cells function.

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It sucks that the primary reason this has not gone forward is because it is off patent.

This video is reproduced from a presentation I gave to the Euro-Geroscience Task Force “Challenges in Developing Geroscience Drug Trials” held March 23, 2022 in Toulouse, France. It gives an introduction to the state of research on rapamycin as a potential longevity and healthspan drug and some of the challenges and opportunities for clinical development.

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Year 2022 😗😁

Summary: A rare genetic mutation that causes blindness also appears to be associated with above-average intelligence, a new study reports.

Source: University of Leipzig

Synapses are the contact points in the brain via which nerve cells ‘talk’ to each other. Disturbances in this communication lead to diseases of the nervous system, since altered synaptic proteins, for example, can impair this complex molecular mechanism. This can result in mild symptoms, but also very severe disabilities in those affected.

The interest of the two neurobiologists Professor Tobias Langenhan and Professor Manfred Heckmann, from Leipzig and Würzburg respectively, was aroused when they read in a scientific publication about a mutation that damages a synaptic protein.

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The 2023 edition of the exclusive Longevity Investors Conference is fast approaching, bringing together investors, companies and researchers in Gstaad, Switzerland in September. One of the speakers at this year’s conference is scientist, writer and presenter Dr Andrew Steele, the author of the best-selling book Ageless: The new science of getting older without getting old. When it comes to his views on longevity, Steele sits firmly in the camp that aging, like cancer, is something that humanity should be focused on curing.

Longevity. Technology: Last year, Steele told us he was “absolutely convinced” curing aging is possible, but that significant questions remain around how quickly we can get there. As he prepares to speak to more than 100 investors at LIC, we caught up with Steele to see how his views on longevity have evolved, and what he would say to those considering investing in the field.

First and foremost, Steele, who recently published a new, free chapter of Ageless on the moral, ethical and social consequences of treating aging, believes that longevity represents a huge “human opportunity” for investors.

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Electron tunneling associated with ferritin was proposed as early as 1988, but it is still viewed skeptically despite substantial evidence that it occurs. In our recent paper published in IEEE Transactions on Molecular, Biological and Multi-Scale Communications, my co-authors and I review the evidence of electron tunneling in ferritin, as well as the evidence that such electron tunneling may be used by biological systems that include the retina, the cochlea, macrophages, glial cells, mitochondria and magnetosensory systems.

While these diverse systems fall in different fields of study, we hope that this article will raise awareness of the mechanism of electron tunneling associated with and encourage further research into that phenomenon in that incorporate ferritin, particularly where there is no apparent need for the iron storage functions of ferritin in those systems.

Ferritin is an iron storage protein that self-assembles into a 12-nanometer diameter spherical shell that is 2 nanometers thick, and it can store up to ~4,500 iron atoms in an 8-nanometer diameter core. With an evolutionary history that appears to stretch back more than 1.2 billion years, it might seem rather old, but it should be kept in mind that are believed to have first evolved ~3.5 billion years ago. As such, it may have taken more than 2 billion years for ferritin to evolve. When the first multicellular organisms evolved ~600 million years ago, members of the ferritin family of proteins were likely present, and they can be found today in almost all plants and animals.

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Do you ever mesh your other hobbies with the space stuff? Yes. I once turned the results of one of my experiments into a musical. In 2020, during the lockdowns, I put a scientific instrument on my balcony to measure light, sound and pollution before and after the pandemic. I ended up with several graphs and thought, Why not turn these into a musical? So, me and my brother got several musical instruments and played notes according to how high or low each point on the graph was. We actually submitted that to the NASA SpaceApps COVID-19 Challenge and became one of the top six global winners.

Do you think you’ll study space science at university when you’re older? I think so. Either aerospace or astrophysics, or maybe both.

Any other cool projects in the pipeline? Not right now, but I’m getting ready to go to Belgium this September, to represent Canada in the EU Contest for Young Scientists, which is an international science competition. I’ll be able to showcase this project there. But before then, I need to make a 10-page project report with figures, summaries and scientific documents. And I’ll need a poster!

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The first gene therapy that can treat Duchenne muscular dystrophy (DMD) has been approved by the U.S. Food and Drug Administration; it will be marketed as Elevidys (delandistrogene moxeparvovec-rokl) by Sarepta Therapeutics Inc. Children aged four to five with the disorder and confirmed gene mutations will be eligible to receive the one-time treatment if insurers approve, as the cost is $3.2 million per patient.

DMD is caused by mutations in a gene called dystrophin, which results in a serious lack of functional dystrophin protein. The gene therapy works by sending a gene that can produce a shortened version of the dystrophin protein to patients; the company has termed it Elevidys micro-dystrophin.

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In a new paper published today in Nature, researchers at the Francis Crick Institute have outlined the structure and function of a protein complex that is required to repair damaged DNA and protect against cancer.

Every time a cell replicates, mistakes can happen in the form of , but specialized proteins exist to repair the damaged DNA.

People with mutations in a DNA repair called BRCA2 are predisposed to breast, ovarian and , which often develop at a young age. In the clinic, these cancers are treated with a drug that inhibits PARP, another protein needed for DNA repair.

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