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Findings from a recent research project, conducted by a Marshall University scientist and assistant professor in the Marshall University College of Science, with researchers in Texas, was recently published in the December issue of the prestigious online journal, Nature Communications.

Dr. Eugene Shakirov is studying the connection between ribosomes and telomeres in plants. Telomeres are the physical ends of chromosomes and they shorten with age in most cells. Accelerated shortening of telomeres is linked to age-related diseases and overly long telomeres are often linked to cancer.

Telomere length varies between individuals at birth and is known to predetermine cellular lifespan, but the genes establishing telomere length variations are largely unknown. The research being done by Shakirov, along with collaborators at the University of Texas at Austin, Texas A&M University, HudsonAlpha Institute for Biology and the Kazan Federal University in Russia focused on the study of the genetic and epigenetic causes of natural telomere length variation in Arabidopsis thaliana, a small flowering plant.

Shaking hands with BrainCo’s artificial intelligence-powered prosthetic hand is like shaking hands with an exciting, optimistic version of the future. Here’s what this amazing prosthesis is able to do, and how it promises to transform life for amputees all around the world.

Johns Hopkins researchers report that a type of biodegradable, lab-engineered nanoparticle they fashioned can successfully deliver a “suicide gene” to pediatric brain tumor cells implanted in the brains of mice. The poly(beta-amino ester) nanoparticles, known as PBAEs, were part of a treatment that also used a drug to kill the cells and prolong the test animals’ survival.

In their study, described in a report published January 2020 in the journal Nanomedicine: Nanotechnology, Biology and Medicine, the researchers caution that for safety and biological reasons, it is unlikely that the suicide gene herpes simplex virus type I thymidine kinase (HSVtk)—which makes tumor cells more sensitive to the lethal effects of the anti-viral drug ganciclovir—could be the exact therapy used to treat human medulloblastoma and atypical teratoid/rhabdoid tumors (AT/RT) in children.

So-called “suicide genes” have been studied and used in cancer treatments for more than 25 years. The HSVtk gene makes an enzyme that helps restore the function of natural tumor suppression.

Telomerase defers the onset of telomere shortening and cellular senescence by adding telomeric repeat DNA to chromosome ends, and its activation contributes to carcinogenesis. Telomerase minimally consists of the telomerase reverse transcriptase (TERT) and the telomerase RNA (TR). However, how telomerase assembles is largely unknown. Here, we demonstrate that PES1 (Pescadillo), a protein overexpressed in many cancers, forms a complex with TERT and TR through direct interaction with TERT, regulating telomerase activity, telomere length maintenance, and senescence. PES1 does not interact with the previously reported telomerase components Reptin, Pontin, p23, and Hsp90. PES1 facilitates telomerase assembly by promoting direct interaction between TERT and TR without affecting TERT and TR levels. PES1 expression correlates positively with telomerase activity and negatively with senescence in patients with breast cancer. Thus, we identify a previously unknown telomerase complex, and targeting PES1 may open a new avenue for cancer therapy.

Telomerase is a ribonucleoprotein (RNP) enzyme that adds telomeric repeat DNA to chromosome ends (1–3). This prevents progressive shortening of telomeres caused by the failure of the DNA replication machinery to duplicate the very end of each chromosome. Once telomeres are shortened to a certain length, cells enter replicative senescence or, alternatively, undergo apoptosis, a major tumor-suppressive mechanism. Telomerase, which is required for de novo telomeric repeat DNA synthesis and telomere maintenance, is expressed in approximately 90% of cancer cells but undetectable in the majority of normal somatic cells (4–6). Thus, telomerase is thought to be a relevant factor in distinguishing cancer cells from normal cells and has become a target for cancer therapy.

Telomerase is minimally composed of the telomerase reverse transcriptase (TERT) and the telomerase RNA (TR). Studies have shown in vitro assembly of active telomerase by combining the purified RNA component with the TERT synthesized in rabbit reticulocyte extract (7–9). A few accessory proteins have been identified to associate with the active telomerase RNP complex. The molecular chaperones p23 and Hsp90 bind to human TERT (hTERT), and chemical inhibition of Hsp90 decreases telomerase activity (10, 11). However, determining whether Hsp90 is required for active telomerase assembly is difficult because chemical inhibition of a key chaperone in human cells potentially has pleiotropic and indirect effects. Assembly of human TR (hTR) and hTERT into catalytically active telomerase is facilitated by the adenosine triphosphatases Reptin and Pontin (12). Pontin knockdown (KD) reduces telomerase activity and hTR levels.

A new unique signal discovered within the brain might be what makes us human:

https://science.sciencemag.org/content/367/6473/83

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Years of investment in basic science of cancer therapeutics are “starting to pay off,” an expert said.

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Stephen Hawking passed away on 14 March 2018. His work changed literally everything we know about the cosmos and our place in it. But his greatest contribution to our species wasn’t his theories on black holes or how quickly the universe was expanding, it was his humanity.

Professor Hawking was born on 8 January 1942. He would have been 78 years old today – a bit older than ‘boomer’ age, his generation was called the “Silent” one. In his early twenties he was diagnosed with Lou Gehrig’s disease (ALS). Eventually he became paralyzed and could only speak with the assistance a computer-generated audio device.