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The attachment of the small protein ubiquitin to other proteins (ubiquitination) regulates numerous biological processes, including signal transduction and metabolism / Scientists at the University of Cologne discover the link to aging and longevity.

Scientists have discovered that the protein ubiquitin plays an important role in the regulation of the aging process. Ubiquitin was previously known to control numerous processes, such as signal transduction and metabolism. Prof. Dr. David Vilchez and his colleagues at the CECAD Cluster of Excellence for Aging Research at the University of Cologne performed a comprehensive quantitative analysis of ubiquitin signatures during aging in the model organism Caenorhabditis elegans, a nematode worm which is broadly used for aging research.

This method — called ubiquitin proteomics — measures all changes in ubiquitination of proteins in the cell. The resulting data provide site-specific information and define quantitative changes in ubiquitin changes across all proteins in a cell during aging. A comparison with the total protein content of a cell (proteome) showed which changes have functional consequences in protein turnover and actual protein content during aging. The scientists thus discovered new regulators of lifespan and provide a comprehensive data set that helps to understand aging and longevity. The article, ‘Rewiring of the ubiquitinated proteome determines aging in C. elegans,‘has now been published in Nature.

Northwestern Medicine investigators have discovered that a subset of proteins in mitochondria of brain and heart cells are long-lived, supporting the long-term stability of mitochondrial complex architecture.

The study, published in the Journal of Cell Biology, was led by Jeffrey Savas, PhD, assistant professor in the Ken & Ruth Davee Department of Neurology’s Division of Behavioral Neurology, of Medicine the in Division of Nephrology and Hypertension, and of Pharmacology.

Previous work led by Savas discovered that nuclear pore complex proteins in post-mitotic neurons are exceptionally long-lived and persist for months in mouse and rat brains. These proteins, termed long-lived proteins, or LLPs, provide long-term stability and structure to the nuclear pore and subsequently to the nuclear envelope of neurons; however, this concept had never been considered for other intracellular organelles, until now.

Investigators who previously developed a recipe for turning skin cells into primitive muscle-like cells that can be maintained indefinitely in the lab without losing the potential to become mature muscle have now uncovered how this recipe works and what molecular changes it triggers within cells. The research, which was led by scientists at Massachusetts General Hospital (MGH) and is published in Genes & Development, could allow clinicians to generate patient-matched muscle cells to help treat muscle injuries, aging-related muscle degeneration, or conditions such as muscular dystrophy.

It’s known that expression of a muscle regulatory gene called MyoD is sufficient to directly convert skin cells into mature muscle cells; however, mature muscle cells do not divide and self-renew, and therefore they cannot be propagated for clinical purposes. “To address this shortcoming, we developed a system several years ago to convert skin cells into self-renewing muscle stem-like cells we coined induced myogenic progenitor cells, or iMPCs. Our system uses MyoD in combination with three chemicals we previously identified as facilitators of cell plasticity in other contexts,” explains senior author Konrad Hochedlinger, Ph.D., a principal investigator at the Center for Regenerative Medicine at MGH and a professor of medicine at Harvard Medical School.

In this latest study, Hochedlinger and his colleagues uncovered the details behind how this combination converts skin cells into iMPCs. They found that while MyoD expression alone causes skin cells to take on the identity of mature muscle cells, adding the three chemicals causes the skin cells to instead acquire a more primitive stem cell–like state. Importantly, iMPCs are molecularly highly similar to muscle tissue stem cells, and muscle cells derived from iMPCs are more stable and mature than muscle cells produced with MyoD expression alone.

“University Of The 3rd Age” — Seniors Staying Intellectually Challenged, Socially Engaged, And Physically And Mentally Healthy — Maya Abi Chahine, University for Seniors, American University of Beirut (AUB)

AUB (https://www.aub.edu.lb/seniors/Pages/default.aspx).

Continue reading “Maya Abi Chahine, Program Manager, University for Seniors, American University of Beirut” »

If you’ve ever seen a petunia with artfully variegated petals, then you’ve seen transposons at work. The flower’s showy color patterns are due to transposable elements, or DNA sequences that can move locations within a genome. Yet when it comes to transposons’ effects on humans, the results might not be as lovely or desirable.

As researchers learn more about these so-called mobile genetic elements, they’ve found increasing evidence that transposons influence and even promote aging and age-related diseases like cancer as well as neurogenerative and autoimmune disorders, says John Sedivy, a professor of biology and director of the Center on the Biology of Aging at Brown. Sedivy is the corresponding author of a new review article in Nature that discusses the latest thinking and research around transposons.

“Let’s put it this way: These things can be pretty dangerous,” said Sedivy. “If they are uncontrolled, and there are many examples of that, transposons can have profound consequences on most forms of life that we know of.”

The Conboys are looking at human trials soon but not with E5. it will be interesting to see how their trial compares to this E5 dog trial.

In this video Dr. Fahy shares his opinion on some of the up and coming anti-aging therapies, including NAD boosters, Hyperbaric Oxygen Chambers and senolytics.

Continue reading “E5 On Dogs Project: Validating The 54% Reduction In Epigenetic Age | Dr Greg Fahy Episode 8” »

Unlike humans, these eight-armed creatures can form crystal-clear memories even in their final weeks.

Immortal bacteria genetic mechanisms could be used in crispr to make humans truly Immortal: 3.

Researchers successfully resuscitated bacteria from the South Pacific Gyre that were buried under marine snow for 100 million years.

“So many genes are involved in DNA maintenance, FOXO3 for example, which is very interesting, but it cannot be a therapeutic target because it will trigger a lot of other things,” he explains. “SIRT6 is coding for only one protein and, because it’s a small protein, the cargo size is not too big and it can be easily delivered into cells, so it’s possible to use it as a gene therapy target.”

Some of the other factors that play in Genflow’s favour, says Leire, are that the world has reached a better understanding of the biology of aging, but also that gene therapy has also progressed well over the years.